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1
Genova, M. P., K. Todorova-Ananieva, B. Atanasova, and K. Tzatchev. "Assessment of Beta-Cell Function During Pregnancy and after Delivery." Acta Medica Bulgarica 41, no. 1 (June 1, 2014): 5–12. http://dx.doi.org/10.2478/amb-2014-0001.
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Summary The aim of the present study was to assess β-cell function using homeostasis model (HOMA-B) and disposition index (DI) in pregnant women with/without gestational diabetes, and after delivery. A total of 102 pregnant women between 24-28 gestational weeks (53 with gestational diabetes mellitus (GDM) and 49 with normal glucose tolerance (NGT) and 22 GDM postpartum women (8-12 weeks after delivery) were included in the study. All postpartum women had a history of GDM. HOMA indexes (insulin resistance - HOMA-IR and HOMA-B for assessing β-cell function) were calculated from fasting glucose and insulin concentrations. To estimate insulin secretion independent of insulin sensitivity, DI was calculated using glucose and insulin levels at 0 and 60 min during the course of a 2 h 75g oral glucose tolerance test (OGTT). In GDM pregnant women HOMA-B was significantly lower compared to NGT women (p = 0.017), but there was no significant difference compared to women after birth (NS). There was difference between NGT and postpartum women (p < 0.05). DI was significantly lower for GDM pregnant women in comparison to NGT and postpartum women (p < 0.0001; p = 0.011), between NGT and women after birth (p < 0.04). In our study, comparison of НОМА-В in NGT and GDM pregnant women demonstrated that the OR of developing GDM was 0.989 (95% CI, 0.980-0.998, P = 0.013), and comparison of DI in healthy pregnant and GDM showed that the OR of developing GDM was 0.967 (95% CI, 0.947-0.988, P = 0.002). Therefore, HOMA-B and DI appear to be protective factors in the risk of developing GDM. According to our results, assessment of β-cell function, using HOMA-B and DI, showed that they are lower in GDM than NGT group and postpartum women. It is important to note that HOMA-B did not show significant difference between GDM pregnant and women after delivery with a history for GDM. We assume that pregnant women with GDM have a pancreatic β-cell defect that remains after birth. These women are at increased risk for developing diabetes mellitus, the most frequent type 2 diabetes, in the future after birth.
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Popovic, Ljiljana, Miroslava Zamaklar, Katarina Lalic, and Olga Vasovic. "Analysis of the effect of diabetes type 2 duration on beta cell secretory function and insulin resistance." Srpski arhiv za celokupno lekarstvo 134, no. 5-6 (2006): 219–23. http://dx.doi.org/10.2298/sarh0606219p.
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Diabetes type 2 is a chronic metabolic disorder. Pathogenesis of diabetes type 2 results from the impaired insulin secretion, impaired insulin action and increased endogenous glucose production. Diabetes evolves through several phases characterized by qualitative and quantitative changes of beta cell secretory function. The aim of our study was to analyze the impact of diabetes duration on beta cell secretory function and insulin resistance. The results indicated significant negative correlation of diabetes duration and fasting insulinemia, as well as beta cell secretory function assessed by HOMA ? index. Our study also found significant negative correlation of diabetes duration and insulin resistance assessed by HOMA IR index. Significant positive correlation was established between beta cell secretory capacity (fasting insulinemia and HOMA ?) and insulin resistance assessed by HOMA IR index, independently of diabetes duration. These results indicate that: beta cell secretory capacity, assessed by HOMA ? index, significantly decreases with diabetes duration. In parallel with decrease of fasting insulinemia, reduction of insulin resistance assessed by HOMA IR index was found as well.
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Al-Hakeim, Hussein Kadhem, and Mohammed Saied Abdulzahra. "Correlation Between Glycated Hemoglobin and Homa Indices in Type 2 Diabetes Mellitus: Prediction of Beta-Cell Function from Glycated Hemoglobin / Korelacija Između Glikoliziranog Hemoglobina I Homa Indeksa U Dijabetes Melitusu Tipa 2: Predviđanje Funkcije Beta Ćelija Na Osnovu Glikoliziranog Hemoglobina." Journal of Medical Biochemistry 34, no. 2 (April 1, 2015): 191–99. http://dx.doi.org/10.2478/jomb-2014-0033.
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Summary Background: The present study aimed to determine the most efficient insulin resistance function related to gly - cemic control expressed as glycated hemoglobin (HbA1c) in type 2 diabetes mellitus patients (T2DM). The other aim is to derive equations for the prediction of beta cell functions containing HbA1c as a parameter in addition to fasting glucose and insulin. Methods: T2DM Patients were grouped according to the following: (1) degree of control (good, fair, and poor control) and (2) insulin resistance as observed in obtained data and significant differences revealed by the homeostasis model assessment (HOMA) of related parameters (insulin resistance = HOMA2IR, beta-cell function = HOMA%B, and in sulin sensitivity = HOMA%S) among groups. Corre - lations and forecasting regression analysis were calculated. Results: HbA1c was found to be correlated with insulin resistance parameters in T2DM subgroups. This correlation was also significantly correlated with HOMA%B and the quantitative insulin sensitivity check index (QUICKI) in fair and poor control groups. Regression analysis was used to predict the forecasting equations for HOMA%B. The best applicable equations were derived for healthy control (HOMA2%B=-1.76*FBG+5.00*Insulin+4.69*HbA1c+189.84) and poor control groups (HOMA2%B=0.001* FBG+0.5*Insulin-8.67*HbA1c+101.96). These equations could be used to predict b-cell function (HOMA%B) after FBG, insulin and HbA1c values were obtained for healthy and poor control groups. In the good and fair control groups, the applicability of the HOMA model fails to yield appropriate results. Conclusions: Beta-cell function is correlated with QUICKI and HbA1c and could be predicted properly from HbA1c, insulin, and glucose in the healthy and poor control groups. New regression equations were established that involve HbA1c.
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Putera, Bayu Winata, Cynthia Retna Sartika, and Andi Wijaya. "The Dynamic Roles of Visfatin and Obestatin Serum Concentration in Pancreatic Beta Cells Dysfunction (HOMA-beta) and Insulin Resistance (HOMA-IR) in Centrally Obese Men." Indonesian Biomedical Journal 4, no. 1 (April 1, 2012): 43. http://dx.doi.org/10.18585/inabj.v4i1.161.
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BACKGROUND: Obesity is a major health problem in the world today. Obesity is closely associated with insulin resistance and type 2 diabetes. Epidemiological studies have shown that obese persons are in a state of insulin resistance, however, most of them do not progress to type 2 diabetes. This occurs because the beta cell function is still good enough for maintaining normal glucose level. Obestatin and visfatin are cytokines that are known to have a role in beta cell function. The aim of this study was to assess the relationship between visfatin and obestatin and Homeostasis Model Assessment of beta cell function (HOMA-β) and Homeostasis Model Assessment of insulin resistance (HOMA-IR).METHODS: This was a cross-sectional study involving 80 central obesity men with waist circumference >90 cm, age 30-65 years old. Visfatin and obestatin were measured by ELISA method. Beta pancreas cell dysfunction and insulin resistance were calculated by HOMA model.RESULTS: Our study showed a correlation between visfatin and HOMA-β (r=0.244 and p = 0.029) and visfatin with HOMA-IR (r=0.287 and p=0.001) and no correlation was found between obestatin with HOMA-β (r=0.010 and p=0.990) and obestatin with HOMA-IR (r=0.080 and p=0.480). We also found visfatin and obestatin concentrations were fluctuative depending on the measurements of the waist circumferences.CONCLUSIONS: High visfatin and low obestatin concentration were independently associated with increased beta pancreas cell dysfunction and insulin resistance.KEYWORDS: obesity. visfatin, obestatin, beta cell dysfunction (HOMA-β), insulin resistance (HOMA-IR)
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Rahman, Miftakh Nur, Indriyanti Rafi Sukmawati, Irma Melyani Puspitasari, and Miswar Fattah. "Serum Free Zinc as A Predictor for Excessive Function of Pancreatic Beta-Cells in Central-Obese Men." Indonesian Biomedical Journal 11, no. 3 (December 3, 2019): 262–6. http://dx.doi.org/10.18585/inabj.v11i3.618.
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BACKGROUND: Central obesity is known as a risk factor for type 2 diabetes mellitus (T2DM). Its development is influenced by many factors such as a progressive failure of pancreatic beta cell function. The beta cells increase their function to secret insulin along T2DM development to compensate before it becomes exhausted. Zinc (Zn) plays a crucial role in beta cell function and insulin secretion. The majority of Zn in serum are bound to protein which is not readily available interact with cells. The free Zn in serum has been suggested as being more representative than total Zn in beta cell function. This research aimed to investigate the correlation between serum free Zn and homeostasis model assessment for beta cell function (HOMA-B) and to predict the pancreatic beta cell function in the development of T2DM.METHODS: This study was designed as an observational with a cross-sectional approach. The subjects were centrally obese men aged 30-50 years and who had met the inclusion and exclusion criteria from the screening tests. Control subjects were lean men without T2DM. Serum free Zn and serum total Zn were measured by using inductively coupled plasma-mass spectrometry (ICP-MS).RESULTS: There was positive correlation between serum free Zn and HOMA-B (R=0.361, p-value<0.001) but there was no correlation between serum total Zn and HOMA-B (R=-0.062, p-value=0.563). This study found that if the concentration of serum free Zn >1.7 ug/dL in central obese men was suggested as an excessive function of pancreatic beta cell and as an early warning before its exhausted.CONCLUSION: This study suggested that serum free Zn had a correlation with beta cell function and had a predictive ability for beta cell excessive function before its exhausted.KEYWORDS: Type 2 diabetes mellitus, HOMA-B, serum free zinc, central obesity
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Huang, Rong, Yu Dong, Anne Monique Nuyt, Emile Levy, Shu-Qin Wei, Pierre Julien, William D. Fraser, and Zhong-Cheng Luo. "Large birth size, infancy growth pattern, insulin resistance and β-cell function." European Journal of Endocrinology 185, no. 1 (July 1, 2021): 77–85. http://dx.doi.org/10.1530/eje-20-1332.
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Objective Large birth size programs an elevated risk of type 2 diabetes in adulthood, but data are absent concerning glucose metabolic health impact in infancy. We sought to determine whether the large birth size is associated with insulin resistance and β-cell function in infancy and evaluate the determinants. Design and participants In the Canadian 3D birth cohort, we conducted a nested matched (1:2) study of 70 large-for-gestational-age (LGA, birth weight >90th percentile) and 140 optimal-for-gestational-age (OGA, 25th–75th percentiles) control infants. The primary outcomes were homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-β) at age 2-years. Results HOMA-IR and HOMA-β were similar in LGA and OGA infants. Adjusting for maternal and infant characteristics, decelerated growth in length during early infancy (0–3 months) was associated with a 25.8% decrease (95% confidence intervals 6.7–41.0%) in HOMA-β. During mid-infancy (3–12 months), accelerated growth in weight was associated with a 25.5% (0.35–56.9%) increase in HOMA-IR, in length with a 69.3% increase (31.4–118.0%) in HOMA-IR and a 24.5% (0.52–54.3%) increase in HOMA-β. Decelerated growth in length during late infancy (1–2 years) was associated with a 28.4% (9.5–43.4%) decrease in HOMA-IR and a 21.2% (3.9–35.4%) decrease in HOMA-β. Female sex was associated with higher HOMA-β, Caucasian ethnicity with lower HOMA-IR, and maternal smoking with lower HOMA-β. Conclusions This study is the first to demonstrate that large birth size is not associated with insulin resistance and β-cell function in infancy but infancy growth pattern matters. Decelerated infancy growth may be detrimental to beta-cell function.
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Malamug, Lou Rose, Rudruidee Karnchanasorn, Raynald Samoa, and Ken C. Chiu. "The Role ofHelicobacter pyloriSeropositivity in Insulin Sensitivity, Beta Cell Function, and Abnormal Glucose Tolerance." Scientifica 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/870165.
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Infection, for example,Helicobacter pylori(H. pylori), has been thought to play a role in the pathogenesis of type 2 diabetes mellitus (T2DM). Our aim was to determine the role ofH. pyloriinfection in glucose metabolism in an American cohort. We examined data from 4,136 non-Hispanic white (NHW), non-Hispanic black (NHB), and Mexican Americans (MA) aged 18 and over from the NHANES 1999-2000 cohort. We calculated the odds ratios for states of glucose tolerance based on theH. pyloristatus. We calculated and compared homeostatic model assessment insulin resistance (HOMA-IR) and beta cell function (HOMA-B) in subjects without diabetes based on theH. pyloristatus. The results were adjusted for age, body mass index (BMI), poverty index, education, alcohol consumption, tobacco use, and physical activity. TheH. pyloristatus was not a risk factor for abnormal glucose tolerance. After adjustment for age and BMI and also adjustment for all covariates, no difference was found in either HOMA-IR or HOMA-B in all ethnic and gender groups except for a marginally significant difference in HOMA-IR in NHB females.H. pyloriinfection was not a risk factor for abnormal glucose tolerance, nor plays a major role in insulin resistance or beta cell dysfunction.
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Garg, MK, Namita Mahalle, and MK Dutta. "Study of beta-cell function (by HOMA model) in metabolic syndrome." Indian Journal of Endocrinology and Metabolism 15, no. 5 (2011): 44. http://dx.doi.org/10.4103/2230-8210.83059.
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Volpe, Alessandro, Chang Ye, Anthony J. Hanley, Philip W. Connelly, Bernard Zinman, and Ravi Retnakaran. "Changes Over Time in Uric Acid in Relation to Changes in Insulin Sensitivity, Beta-Cell Function, and Glycemia." Journal of Clinical Endocrinology & Metabolism 105, no. 3 (November 13, 2019): e651-e659. http://dx.doi.org/10.1210/clinem/dgz199.
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Abstract Context Serum uric acid has been linked to risk of type 2 diabetes (T2DM), but debate persists as to whether it plays a causal role. Indeed, it is unclear if changes in uric acid relate to the pathophysiologic determinants of T2DM (insulin resistance, beta-cell dysfunction), as would be expected if causal. Objective To evaluate the impact of changes in uric acid over 2 years on changes in insulin sensitivity, beta-cell function, and glycemia in women with and without recent gestational diabetes (GDM), a model of the early natural history of T2DM. Design/Setting/Participants At both 1 and 3 years postpartum, 299 women (96 with recent GDM) underwent uric acid measurement and oral glucose tolerance tests that enabled assessment of insulin sensitivity/resistance (Matsuda index, homeostasis model assessment of insulin resistance [HOMA-IR]), beta-cell function (insulin secretion-sensitivity index-2 [ISSI-2], insulinogenic index/HOMA-IR [IGI/HOMA-IR]), and glucose tolerance. Results Women with recent GDM had higher serum uric acid than their peers at both 1 year (281 ± 69 vs 262 ± 58 µmol/L, P = 0.01) and 3 years postpartum (271 ± 59 vs 256 ± 55 µmol/L, P = 0.03), coupled with lower insulin sensitivity, poorer beta-cell function, and greater glycemia (all P < 0.05). However, on fully adjusted analyses, neither uric acid at 1 year nor its change from 1 to 3 years was independently associated with any of the following metabolic outcomes at 3 years postpartum: Matsuda index, HOMA-IR, ISSI-2, IGI/HOMA-IR, fasting glucose, 2-hour glucose, or glucose intolerance. Conclusion Serum uric acid does not track with changes over time in insulin sensitivity, beta-cell function, or glycemia in women with recent GDM, providing evidence against causality in its association with diabetes.
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Lee, Sohyae, Jin-young Min, and Kyoung-bok Min. "Caffeine and Caffeine Metabolites in Relation to Insulin Resistance and Beta Cell Function in U.S. Adults." Nutrients 12, no. 6 (June 15, 2020): 1783. http://dx.doi.org/10.3390/nu12061783.
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The relationship between caffeine and insulin resistance (IR) has been assessed only in terms of caffeine intake, and the association between caffeine and beta cell function (BCF) remains unclear. This study examines the association between urinary caffeine and its metabolites, IR, and BCF in nondiabetic, noninstitutionalized US adults in order to account for the inter-individual differences in caffeine metabolism. Data on urinary caffeine and its metabolites, IR and BCF from adults aged 20 years and older who participated in the 2009–2010 and 2011–2012 National Health and Nutrition Examination Surveys were analyzed (n for caffeine = 994). IR and BCF were assessed using homeostatic model assessment (HOMA) and urinary caffeine and its metabolites were measured using high-performance liquid chromatography-electrospray ionization-tandem quadrupole mass spectrometry. After adjusting for all covariates, increases in urinary 1,3-DMU, 1,7-DMU, 1,3,7-TMU, theophylline, paraxanthine, caffeine, and AAMU were significantly associated with increased HOMA-IR and HOMA-β (HOMA of insulin resistance and beta cell function). Compared with individuals in the lowest quartile of urinary 1,3-DMU, 1,7-DMU, 1,3,7-TMU, theophylline, paraxanthine, caffeine, and AAMU, the regression coefficients for HOMA-IR and HOMA-β were significantly higher among those in the highest quartile. After stratification by prediabetes status, HOMA-IR and HOMA-β showed significant positive associations with urinary caffeine and its metabolites among subjects with normal fasting plasma glucose levels. Our cross-sectional study showed that caffeine and its metabolites were positively related to IR and BCF.
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Yan, Li-hui, Biao Mu, Da Pan, Ya-nan Shi, Ji-hong Yuan, Yue Guan, Wang Li, Xiao-yi Zhu, and Lei Guo. "Association between small intestinal bacterial overgrowth and beta-cell function of type 2 diabetes." Journal of International Medical Research 48, no. 7 (July 2020): 030006052093786. http://dx.doi.org/10.1177/0300060520937866.
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Aims Previous studies suggest that small intestinal bacterial overgrowth (SIBO) is associated with type 2 diabetes. However, few studies have evaluated the association between SIBO and beta-cell function in type 2 diabetes. The aim of this study was to evaluate whether beta-cell function was associated with SIBO. Materials and methods One hundred four patients with type 2 diabetes were included in this study. Based on the presence of SIBO, the patients were divided into SIBO-positive and SIBO-negative groups. Oral glucose tolerance tests were performed. Insulin sensitivity was measured using 1/homeostasis model assessment of insulin resistance (1/HOMA-IR) and the insulin sensitivity index (ISIM). Insulin release was calculated by HOMA-β, early-phase insulin secretion index InsAUC30/GluAUC30, and total-phase insulin secretion index InsAUC120/GluAUC120. Results Compared with the SIBO-negative group, patients in the SIBO-positive group showed a higher glucose level at 120 minutes, HbA1c, 1/HOMA-IR, and ISIM and a lower HOMA-β level, early-phase InsAUC30/GluAUC30, and total-phase InsAUC120/GluAUC120. Multiple linear regression analysis showed that body mass index, glucose at 0 minutes, and SIBO were independently associated with the early-phase and total-phase insulin secretion. Conclusion SIBO may be involved in lower levels of insulin release and worse glycemic control.
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Sokup, Alina, Barbara Ruszkowska-Ciastek, Małgorzata Walentowicz-Sadłecka, Marek Grabiec, and Danuta Rość. "Gestational Diabetes Mellitus Worsens the Profile of Cardiometabolic Risk Markers and Decrease Indexes of Beta-Cell Function Independently of Insulin Resistance in Nondiabetic Women with a Parental History of Type 2 Diabetes." Journal of Diabetes Research 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/743495.
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Background. Women with a history of both parental type 2 diabetes (pt2DM) and previous gestational diabetes (pGDM) represent a group at high risk of cardiovascular events. We hypothesized that pGDM changes cardiometabolic risk markers levels as well as theirs associations with glucose indices in nondiabetic pt2DM women.Methods. Anthropometric parameters, glucose regulation (OGTT), insulin resistance (HOMA-IR), beta-cell function, lipid levels, parameters of endothelial dysfunction, and inflammation were evaluated in 55 women with pt2DM, 40 with both pt2DM and pGDM 2–24 months postpartum, and 35 controls.Results. Prediabetes was diagnosed more frequently in women with both pt2DM and pGDM in comparison with women with only pt2DM (10 versus 8,P=0.04). The pGDM group had higher LDL-cholesterol, sICAM-1, tPa Ag, fibrinogen, and lower beta-cell function after adjustment for HOMA-IR, in comparison with pt2DM group. In pt2DM group postchallenge glucose correlated independently with hsCRP and in pGDM group fasting glucose with HOMA-IR.Conclusions. pGDM exerts a combined effect on cardiometabolic risk markers in women with pt2DM. In these women higher LDL-cholesterol, fibrinogen, sICAM-1, tPa Ag levels and decreased beta cell function are associated with pGDM independently of HOMA-IR index value. Fasting glucose is an important cardiometabolic risk marker and is independently associated with HOMA-IR.
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Aref, Abdel-Baset M., Osama M. Ahmed, Lobna A. Ali, and Margit Semmler. "Maternal Rat Diabetes Mellitus Deleteriously Affects Insulin Sensitivity and Beta-Cell Function in the Offspring." Journal of Diabetes Research 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/429154.
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This study was designed to assess the effect of maternal diabetes in rats on serum glucose and insulin concentrations, insulin resistance, histological architecture of pancreas and glycogen content in liver of offspring. The pregnant rat females were allocated into two main groups: normal control group and streptozotocin-induced diabetic group. After birth, the surviving offspring were subjected to biochemical and histological examination immediately after delivery and at the end of the 1st and 2nd postnatal weeks. In comparison with the offspring of normal control dams, the fasting serum glucose level of offspring of diabetic mothers was significantly increased at the end of the 1st and 2nd postnatal weeks. Serum insulin level of offspring of diabetic dams was significantly higher at birth and decreased significantly during the following 2 postnatal weeks, while in normal rat offspring, it was significantly increased with progress of time. HOMA Insulin Resistance (HOMA-IR) was significantly increased in the offspring of diabetic dams at birth and after 1 week than in normal rat offspring, while HOMA insulin sensitivity (HOMA-IS) was significantly decreased. HOMA beta-cell function was significantly decreased at all-time intervals in offspring of diabetic dams. At birth, islets of Langerhans as well as beta cells in offspring of diabetic dams were hypertrophied. The cells constituting islets seemed to have a high division rate. However, beta-cells were degenerated during the following 2 post-natal weeks and smaller insulin secreting cells predominated. Vacuolation and necrosis of the islets of Langerhans were also observed throughout the experimental period. The carbohydrate content in liver of offspring of diabetic dams was at all-time intervals lower than that in control. The granule distribution was more random. Overall, the preexisting maternal diabetes leads to glucose intolerance, insulin resistance, and impaired insulin sensitivity andβ-cell function in the offspring at different postnatal periods.
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Biswas, Subrata Kumar, Sabreena Mohtarin, Sonchita Rani Mudi, Taznuva Anwar, Laila Anjuman Banu, Sheikh Md Khorshed Alam, Md Fariduddin, and M. Iqbal Arslan. "Relationship of Soluble RAGE with Insulin Resistance and Beta Cell Function during Development of Type 2 Diabetes Mellitus." Journal of Diabetes Research 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/150325.
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This study examined whether circulating levels of soluble receptor for advanced glycation end products (sRAGE) alter in prediabetes and correlate with insulin resistance (IR) and beta cell function in prediabetes and newly diagnosed type 2 diabetes mellitus (T2DM). Subjects without previous history of diabetes were recruited and grouped as control, prediabetes, and newly diagnosed T2DM. The control subjects (n=40) and people with prediabetes (n=52) and diabetes (n=66) were similar in terms of age, sex, BMI, systolic and diastolic BP, and fasting insulin level. HOMA-IR was found significantly higher in people with diabetes than control subjects (p<0.001) and people with prediabetes (p=0.005); and HOMA-%B was found significantly deteriorated in people with diabetes (p<0.001) compared to control subjects and people with prediabetes. However, serum sRAGE levels did not show any significant alteration in people with prediabetes compared to control subjects. Moreover, univariate and multivariate analyses did not identify any significant correlation and statistical association of sRAGE with HOMA-IR and HOMA-%B in people with prediabetes and newly diagnosed T2DM. Our data suggest that serum sRAGE levels do not alter in people with prediabetes compared to control subjects and do not correlate or associate with IR and beta cell function during development of T2DM.
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Sathyapalan, Thozhukat, Anne-Marie Coady, Eric S. Kilpatrick, and Stephen L. Atkin. "The effect of atorvastatin on pancreatic beta cell requirement in women with polycystic ovary syndrome." Endocrine Connections 6, no. 8 (November 2017): 811–16. http://dx.doi.org/10.1530/ec-17-0217.
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Background There is an increased risk of developing T2DM in women with polycystic ovary syndrome (PCOS), and there is evidence that statins improve metabolic parameters in these patients. However, there are some data to show that statins increase the risk of incipient diabetes. Materials and methods We have previously shown that 12 weeks of atorvastatin improves insulin resistance when measured using HOMA-IR. This post hoc analysis was designed to look at the effect of atorvastatin on pancreatic β cell function using HOMA-β in the same study. In this randomised, double-blind placebo controlled study, 40 medication-naïve patients with PCOS were randomised to either atorvastatin 20 mg daily or placebo for 3 months. A 3-month extension study for both groups of patients was undertaken with metformin 1500 mg daily after completing initial 3 months of atorvastatin or placebo. Results There was a significant reduction in HOMA-β (240 ± 3.2 vs 177 ± 2.3; P value <0.01) after 12 weeks of atorvastatin treatment, which was maintained by metformin in the subsequent 12 weeks. There were no changes in HOMA-β after the placebo or after subsequent metformin treatment. There was no linear correlation between reduction in HOMA-β with improvement of free androgen index (FAI) (r2 = 0.02; P = 0.72), testosterone (r2 = 0.13; P = 0.49), SHBG (r2 = 0.22; P = 0.48), hsCRP (r2 = 0.19; P = 0.64), triglycerides (r2 = 0.09; P = 0.12), total cholesterol (r2 = 0.11; P = 0.32) or LDL-C (r2 = 0.19; P = 0.38). Conclusion Treatment with atorvastatin for 12 weeks in women with PCOS significantly reduced HOMA-β. This could be potentially due to fall in β-cell requirement with improvement of insulin resistance rather than a reduction of β-cell function.
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Polic, Melita, Maja Miskulin, Martina Smolic, Kristina Kralik, Ivan Miskulin, Maja Berkovic, and Ines Curcic. "Psoriasis Severity—A Risk Factor of Insulin Resistance Independent of Metabolic Syndrome." International Journal of Environmental Research and Public Health 15, no. 7 (July 13, 2018): 1486. http://dx.doi.org/10.3390/ijerph15071486.
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Background: It is still debatable whether psoriasis increases cardiovascular risk indirectly since it is associated with metabolic syndrome or is an independent cardiovascular risk factor. The aim of this study was to evaluate psoriasis severity as an independent predictor of insulin resistance (IR) irrespective of the presence of metabolic syndrome (MetS). Methods: This was a case control study including 128 patients stratified into two groups: patients with psoriasis and metabolic syndrome vs. patients with psoriasis and no metabolic syndrome. MetS was diagnosed according to ATP III criteria with homeostatic model assessment of insulin resistance (HOMA-IR), as well as a homeostatic model assessment of beta cell function (HOMA-β) were calculated. Results: Compared to subjects without metabolic syndrome, patients with metabolic syndrome had a significantly higher Psoriasis Area Severity Index (PASI) values (p < 0.001). The strongest correlation was established for HOMA-IR and the PASI index (p < 0.001), even after adjustment for body mass index (BMI) in regression analysis model. In patients without MetS and severe forms of disease, the HOMA-IR and HOMA-β values were significantly higher compared to mild forms of disease (p < 0.001 for all) while in subjects with MetS no difference was established for HOMA-IR or HOMA-β based on disease severity. Conclusions: Psoriasis severity is an independent risk factor of HOMA-IR, the strongest association being present in the non-MetS group, who still had preserved beta cell function suggesting direct promotion of atherosclerosis via insulin resistance depending on the disease severity, but irrespective of the presence of metabolic syndrome.
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Santos, Carla Danusa da Luz, Ana Paula Grotti Clemente, Vinicius José Baccin Martins, Maria Paula Albuquerque, and Ana Lydia Sawaya. "Adolescents with Mild Stunting Show Alterations in Glucose and Insulin Metabolism." Journal of Nutrition and Metabolism 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/943070.
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Purpose. To evaluate glucose and insulin profiles in adolescents with mild stunting and overweight in order to assess the possibility of increased predisposition to diabetes.Subjects and Methods. The study population consisted of 66 pubertal adolescents classified as mildly stunted (height-for-age z scores ≥−2 and <−1) or of normal stature, as well as overweight (body mass index ≥85th percentile) or normal weight. Beta-cell function and insulin resistance were evaluated according to the homeostasis model assessment (HOMA).Results. In the group with mild stunting, glucose, insulin, and HOMA-IR levels were significantly higher in overweight adolescents compared with those of normal weight, whereas HOMA-B levels were significantly lower. Adolescents with mild stunting showed significantly higher accumulations of body and abdominal fat than their normal stature counterparts.Conclusions. The presence of mild stunting was associated with higher levels of glucose and insulin, diminished function of beta cells, and increased insulin resistance. These results reinforce the need for intervention in adolescents with mild stunting.
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Chandrika A., Mary, and B. Shanthi. "A study of insulin resistance and pancreatic beta cell function in diabetics and non-diabetics." Biomedicine 39, no. 3 (November 14, 2020): 497–502. http://dx.doi.org/10.51248/.v39i3.178.
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Introduction and Aim: The most common non-communicable disease affecting large population is type 2 diabetes mellitus. This metabolic disorder is characterized by hyperglycemia with disturbances of carbohydrate, fat and protein metabolism. The causes of diabetes mellitus can vary greatly but always include either defects in insulin secretion of the pancreas or the cells of the body not responding properly to the insulin produced or in both at some point in the course of the disease.
Materials and Methods: 200 participants who were divided into two groups, non-diabetics with and without family history of diabetes were involved in this study. The outcomes of fasting plasma glucose, postprandial plasma glucose, glycated hemoglobin, fasting plasma insulin, serum c-peptide, HOMA -IR, HOMA-B were compared between both the groups.
Results: All these parameters were significantly correlated between the groups with the level of significance p<0.05%. Non-diabetic off-springs of type 2 diabetes were found to have hyperinsulinemia, increased level of serum c-peptide level, moderate insulin resistance and pancreatic beta cell dysfunction than non-diabetics without the family history of diabetes. The fasting hyperinsulinemia, known to reflect decreased insulin sensitivity constitute the strongest independent predictor of type 2 diabetes.
Conclusion: The above findings show that insulin resistance is the primary abnormality in type 2 Diabetes Mellitus.
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Adamska, Agnieszka, Agnieszka Łebkowska, Małgorzata Jacewicz, Anna Krentowska, Justyna Hryniewicka, Sławomir Wołczyński, Maria Górska, and Irina Kowalska. "Serum Concentrations of Betatrophin and Its Association with Indirect Indices of Insulin Resistance and Beta Cell Function in Women with Polycystic Ovary Syndrome." International Journal of Endocrinology 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/2316986.
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Introduction. Data underline the role of betatrophin in glucose homeostasis. Polycystic ovary syndrome (PCOS) is characterized by insulin resistance (IR). The aim of our study was to investigate the relationship of serum betatrophin concentrations with indirect indices of IR and insulin secretion in women with PCOS, compared to the control group. Methods. The study group comprised 43 women with PCOS and 16 controls. IR was assessed by HOMA-IR and Matsuda index. Insulin secretion was evaluated with HOMA-B. An oral glucose tolerance test (OGTT) with estimation of serum betatrophin concentrations was performed. Results. Glucose load resulted in an increase in serum betatrophin concentrations in the control group (p=0.02). Serum betatrophin concentrations at 120 min of OGTT were lower in women with PCOS than in the control group (p=0.02). We observed positive correlations between baseline serum betatrophin concentrations and HOMA-IR (r=0.39, p=0.008), negative correlations with Matsuda index (r=−0.31, p=0.004), and a positive relationship with HOMA-B (r=0.38, p=0.01) in women with PCOS. Multiple regression analysis revealed that HOMA-B (β=0.47, p=0.001) was an independent factor connected to serum betatrophin levels in PCOS. Conclusions. Serum concentrations of betatrophin are connected with insulin resistance and beta cell function and did not change after glucose load in women with PCOS.
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Dixon, J. B., A. F. Dixon, and P. E. O'Brien. "Improvements in insulin sensitivity and beta-cell function (HOMA) with weight loss in the severely obese." Diabetic Medicine 20, no. 2 (February 2003): 127–34. http://dx.doi.org/10.1046/j.1464-5491.2003.00889.x.
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Rubi, Dianandha Septiana, and Ahmad Hamim Sadewa. "The Effect of Pumpkin on GLP-1 and HOMA-β in Hypercholesterolemic Rats." Romanian Journal of Diabetes Nutrition and Metabolic Diseases 23, no. 1 (March 1, 2016): 19–25. http://dx.doi.org/10.1515/rjdnmd-2016-0003.
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AbstractBackground and aim: High fat and fructose diet may impair β cell function through oxidative stress that is induced by subsequent hypercholesterolemia. The β cell function is usually quantified by homeostatic model assessment beta-cell function (HOMA-β). Oxidative stress may be decreased by β-carotene from pumpkin (Cucurbita maxima). This study aimed to evaluate the effects of pumpkin powder on glucagon-like peptide-1 (GLP-1) level and HOMA-β in rats with high fat and fructose diet.Material and method: A total 25 rats were administered a high fat and fructose diet during 25 days. They were divided into five groups 1) normal, 2) hypercholesterolemic rats 3) hypercholesterolemic rats with 0.16 g pumpkin/200g bodyweight (BW); 4) hypercholesterolemic rats with 0.32 g pumpkin/200 g BW, and 5) hypercholesterolemic rats with 0.64 g of pumpkin/200 g BW. The lipid levels were measured before and after administration of pumpkin for 4 weeks, and at the end of the study, GLP-1 level and HOMA-β were analyzed.Results: Administration of pumpkin to the rats on a high fat and fructose diet reduced total cholesterol, triglyceride, and increased HDL levels. Changes were positively correlated with the amount of pumpkin intake. The decrease of cholesterol levels was positively associated with GLP-1 level, and negatively correlated with HOMA-βConclusions: This study suggested that pumpkin can improve the HOMA-β and decrease GLP-1 levels, possibly by reducing cholesterol levels.
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Wallensteen, Lena, Leif Karlsson, Valeria Messina, Anna Nordenström, and Svetlana Lajic. "Perturbed Beta-Cell Function and Lipid Profile After Early Prenatal Dexamethasone Exposure in Individuals Without CAH." Journal of Clinical Endocrinology & Metabolism 105, no. 7 (April 20, 2020): e2439-e2448. http://dx.doi.org/10.1210/clinem/dgaa280.
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Abstract Background Prenatal treatment with dexamethasone (DEX) reduces virilization in girls with congenital adrenal hyperplasia (CAH). The treatment is effective but may result in long-lasting adverse effects. In this study we explore the effects of DEX on metabolism in individuals not having CAH but treated with DEX during the first trimester of fetal life. Method All DEX-treated participants (n = 40, age range 5.1-26.4 years) and controls (n = 75, age range 4.5-26.6 years) were assessed with fasting blood samples to measure blood count, renal function, glucose homeostasis, and serum lipid profiles. Results There were no significant differences between DEX and control participants for birth parameters, weight and height, or body mass index at the time of testing. Analyzing the entire cohort, we found no significant effects of DEX on blood count, renal function, or serum lipid profiles. However, a lower HOMA-β index in the DEX-treated individuals (U = 893.0; P = 0.049) was observed. Post hoc analyses revealed an effect in girls (U = 152.5; P = 0.024) but not in boys (U = 299.5; P = 0.550). The effect on HOMA-β persisted (U = 117.5; P = 0.048) after analyzing data separately in the participants < 16 years of age. In addition, we observed higher plasma glucose levels (F = 14.6; P = 0.001) in the DEX-treated group. The participants ≥ 16 years of age in the DEX-treated group had significantly higher total plasma cholesterol (F = 9.8; P = 0.003) and higher low-density lipoprotein cholesterol levels (F = 7.4; P = 0,009). Conclusion Prenatal DEX exposure in early pregnancy has negative effects on beta-cell function and lipid profile in individuals without CAH already at a young age.
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Stefan, Diana Simona, Andrada Mihai, Daiana Bajko, Daniela Lixandru, Laura Petcu, Ariana Picu, Bogdan Smeu, Catalin Copaescu, Constantin Ionescu Tirgoviste, and Cristian Guja. "Comparison of Sleeve Gastrectomy and Conservatory Treatment Effect on Biochemical and Hormonal Profile of Obese Type 2 Diabetes Subjects: CREDOR Randomized Controlled Study Results." Revista de Chimie 68, no. 7 (August 15, 2017): 1622–27. http://dx.doi.org/10.37358/rc.17.7.5730.
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Metabolic surgery is the most efficacious method for the treatment of morbid obesity and was recently included among the antidiabetes treatments recommended in obese type 2 diabetes (T2D) patients. The aim of this study was to compare in a randomized controlled trial the effect of sleeve gastrectomy (SG) to that of intensive lifestyle intervention plus pharmacologic treatment on some markers of insulin resistance and beta cell function as well as some appetite controlling hormones in a group of male obese T2D subjects. The study groups comprised 20 subjects for SG and 21 control subjects. Fasting blood glucose, insulin, proinsulin, adiponectin, leptin, ghrelin, HOMA-IR, HOMA-%B, proinsulin-to-insulin ratio and proinsulin-to-adiponectin ratio were evaluated at baseline and after one year follow-up. Overall, patients in the SG group lost 78.98% of excess weight loss (%EWL) in comparison with 9.45% in the control group. This was accompanied by a significant improvement of insulin resistance markers, including increase of adiponectin and decrease of HOMA-IR, while no changes were recorded in the control group. Weight loss was also associated with a significant improvement of proinsulin-to-insulin and proinsulin-to-adiponectin ratio, both surrogate markers of beta cell dysfunction. These also improved in the control group, but were only marginally significant. Our findings suggest that improved insulin resistance and decreased beta cell dysfunction after sleeve gastrectomy might explain diabetes remission associated with metabolic surgery.
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Taverna, M. J., N. Pacher, F. Bruzzo, G. Slama, and J. L. Selam. "Beta-cell function evaluated by HOMA as a predictor of secondary sulphonylurea failure in Type 2 diabetes." Diabetic Medicine 18, no. 7 (July 2001): 584–88. http://dx.doi.org/10.1046/j.1464-5491.2001.00534.x.
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Hsu, Wei-Hao, Chin-Wei Tseng, Yu-Ting Huang, Ching-Chao Liang, Mei-Yueh Lee, and Szu-Chia Chen. "Common Risk Factors in Relatives and Spouses of Patients with Type 2 Diabetes in Developing Prediabetes." Healthcare 9, no. 8 (August 6, 2021): 1010. http://dx.doi.org/10.3390/healthcare9081010.
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Prediabetes should be viewed as an increased risk for diabetes and cardiovascular disease. In this study, we investigated its prevalence among the relatives and spouses of patients with type 2 diabetes or risk factors for prediabetes, insulin resistance, and β-cell function. A total of 175 individuals were included and stratified into three groups: controls, and relatives and spouses of type 2 diabetic patients. We compared clinical characteristics consisting of a homeostatic model assessment for insulin resistance (HOMA-IR) and beta cell function (HOMA-β), a quantitative insulin sensitivity check index (QUICKI), and triglyceride glucose (TyG) index. After a multivariable linear regression analysis, the relative group was independently correlated with high fasting glucose, a high TyG index, and low β-cell function; the relatives and spouses were independently associated with a low QUICKI. The relatives and spouses equally had a higher prevalence of prediabetes. These study also indicated that the relatives had multiple factors predicting the development of diabetes mellitus, and that the spouses may share a number of common environmental factors associated with low insulin sensitivity.
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Bonadonna, Riccardo C., Lawrence Blonde, Mikhail B. Antsiferov, Rachele Berria, Pierre Gourdy, Mensud Hatunic, Viswanathan Mohan, and Michael Horowitz. "13. Lixisenatide as add-on treatment among patients with different beta-cell function levels as assessed by HOMA-beta index (1018-P)." Nederlands Tijdschrift voor Diabetologie 12, no. 4 (October 2014): 17. http://dx.doi.org/10.1007/s12467-014-0038-x.
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Wu, Kunrong, Xiaoli Li, Yuedong Xu, Xiaoqian Zhang, Ziwan Guan, Shufang Zhang, and Yan Li. "SLC22A1 rs622342 Polymorphism Predicts Insulin Resistance Improvement in Patients with Type 2 Diabetes Mellitus Treated with Metformin: A Cross-Sectional Study." International Journal of Endocrinology 2020 (May 8, 2020): 1–7. http://dx.doi.org/10.1155/2020/2975898.
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Background. Metformin is the most widely used oral antidiabetic agent and can reduce insulin resistance (IR) effectively. Organic cation transporter 1 (encoded by SLC22A1) is responsible for the transport of metformin, and ataxia-telangiectasia-mutated (ATM) is a gene relating to the DNA repair and cell cycle control. The aim of this study was to evaluate if the genetic variants in SLC22A1 rs622342 and ATM rs11212617 could be effective predictors of islet function improvement in patients with type 2 diabetes mellitus (T2DM) on metformin treatment. Methods. This cross-sectional study included 111 patients with T2DM treated with metformin. Genotyping was performed by the dideoxy chain-termination method. The homeostatic indexes of IR (HOMA-IR) and beta-cell function (HOMA-BCF) were determined according to the homeostasis model assessment. Results. Fasting plasma glucose (FPG) levels, HbA1c levels, and HOMA-IR were significantly higher in patients with the rs622342 AA genotype than in those with C allele (P<0.05). However, these significant differences were not observed between rs11212617 genotype groups. Further data analysis revealed that the association between the rs622342 polymorphism and HOMA-IR was gender related, and so was rs11212617 polymorphism and HOMA-BCF. HOMA-IR was significantly higher in males with rs622342 AA genotype than in those with C allele (P=0.021), and HOMA-BCF value was significantly higher in females carrying rs11212617 CC genotype than in those with A allele (P=0.038). The common logarithm (Lg10) of HOMA-BCF was positively correlated with the reciprocal of HbA1c (r = 0.629, P<0.001) and negatively associated with Lg10 FPG (r = −0.708, P<0.001). Conclusions. The variant of rs622342 could be a predictor of insulin sensitivity in patients with T2DM treated with metformin. The association between the rs622342 polymorphism and HOMA-IR and the association between the rs11212617 polymorphism and HOMA-BCF were both gender related.
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Wang, Jie, Xinye Jin, Ping An, Songyan Yu, and Yiming Mu. "The Effects of Exenatide Once Weekly (EXQW) and Exenatide Twice a Day (EXBID) on Beta-Cell Function in Type 2 Diabetes: A Systematic Review and Network Meta-Analysis." Journal of Diabetes Research 2019 (October 28, 2019): 1–9. http://dx.doi.org/10.1155/2019/8083417.
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Background. In patients with type 2 diabetes mellitus (T2DM) and poor glycemic control receiving metformin (MET), glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are recommended as the adjunctive therapy. However, there are only a few studies involving the comparative effects of exenatide twice a day (EXBID) and exenatide once weekly (EXQW) on HOMA-β. This meta assessed the comparative effects of EXQW and EXBID on HOMA-β among T2DM patients. Materials and Methods. PubMed, Cochrane Library, and Embase databases were searched to collect randomized controlled trials (RCTs). Network meta-analysis was performed, and network diagrams were constructed to evaluate the effects. The primary outcome is HOMA-β, and the secondary outcomes are fasting blood glycose (FBG), glycated hemoglobin (HbA1c), and weight loss. Results. A total of 8 studies with 3506 subjects were included. Compared with other antidiabetic agents, EXQW has a greater improvement in HOMA-β than EXBID (weight mean difference WMD=‐0.46, 95% confidence interval (CI) [-0.64, -0.28], P=0.001). The effect of EXQW on HbA1c is superior to that of sitagliptin (SITA) (WMD=0.51, 95% CI [0.03, 0.99], P=0.037). The significant reduction of weight was detected for EXBID in comparison with EXQW (WMD=‐0.73, 95% CI [-1.13, -0.33], P=0.001), and no significant difference was found between EXQW and MET. Conclusions. EXQW shows a greater improvement in HOMA-β than EXBID. Moreover, the efficacy of EXQW on glycemic control is similar to other antidiabetic agents including EXBID. It is an advisable treatment for diabetic patients to improve HOMA-β and has an advantage of fewer number of injections compared with EXBID, to increase patients’ adherence and quality of life.
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Meng, Chuchen, Min Sun, Zhixiao Wang, Qi Fu, Mengdie Cao, Zhenxin Zhu, Jia Mao, et al. "Insulin Sensitivity and Beta-Cell Function Are Associated with Arterial Stiffness in Individuals without Hypertension." Journal of Diabetes Research 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/151675.
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Aim. We investigated the relationship between brachial-ankle pulse wave velocity (baPWV) and glucose levels, insulin sensitivity, and beta-cell function in Chinese individuals with or without hypertension.Methods. We recruited 3137 nondiabetic individuals whose age, body mass index (BMI), glucose levels, blood pressure (BP), lipids, hemoglobin A1C (HbA1c), baPWV, and insulin levels were measured.Results. In normotensive group, 2 h glucose levels (β=0.046,P<0.001) associated with baPWV, showed a significant increase in patients with NG as compared to those with DM (P=0.032). The hypertensive group showed no such differences. The Matsuda index (β=0.114,P<0.001) and HOMA-β(β=0.045,P<0.001) were negatively correlated with baPWV while lnHOMA-IR (β=0.196,P=0.076) and the Quantitative Insulin Sensitivity Check Index (QUICKI) (β=0.226,P=0.046) showed a borderline negative correlation. BaPWV significantly decreased (P=0.032) with an increase in insulin sensitivity in individuals with both normal BP and glucose tolerance.Conclusions. BaPWV was significantly associated with 2 h glucose levels, insulin sensitivity and beta-cell function in normotensive population, whereas in hypertensive individuals, BP was the dominant factor influencing arterial stiffness. Individuals with abnormal insulin sensitivity in the absence of diabetes and hypertension are also at an increased risk of arterial stiffness.
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Ke, Weijian, Liehua Liu, Juan Liu, Ailing Chen, Wanping Deng, Pengyuan Zhang, Xiaopei Cao, et al. "Effects of Liraglutide Combined with Short-Term Continuous Subcutaneous Insulin Infusion on Glycemic Control and Beta Cell Function in Patients with Newly Diagnosed Type 2 Diabetes Mellitus: A Pilot Study." Journal of Diabetes Research 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/6839735.
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The objective of this paper is to investigate the effects of liraglutide in combination with short-term continuous subcutaneous insulin infusion (CSII) therapy on glycemic control and beta cell function in patients with newly diagnosed type 2 diabetes mellitus (T2DM). Thirty-nine eligible newly diagnosed T2DM patients were recruited and randomized to receive either of two therapies: short-term CSII alone (CSII alone group) or CSII in combination with liraglutide (CSII + Lira group) for 12 weeks. Blood glucose control, homeostasis model assessment (HOMA) indices, and acute insulin response (AIR) were compared between the two groups. The patients in CSII + Lira group achieved euglycemia with equivalent insulin dosage in shorter time (1 (0) versus 2 (3) days,P=0.039). HbA1c at the end of study was comparable between two groups (6.3±0.7% versus6.0±0.5%, for CSII alone group and CSII + Lira group, resp.,P=0.325). The increment of AIR was higher in CSII + Lira group (177.58 (351.57) μU·min/mL versus 58.15 (51.30) μU·min/mL,P<0.001). However, after stopping liraglutide, its effect on beta cell function disappeared completely. Liraglutide combined with short-term CSII was effective in further improving beta cell function, but the beneficial effects did not sustain after suspension of the therapy.
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Caldas, Amanda D. A., Adriana Lofrano Porto, Lucilia Domingues Casulari da Motta, and Luiz Augusto Casulari. "Relationship between insulin and hypogonadism in men with metabolic syndrome." Arquivos Brasileiros de Endocrinologia & Metabologia 53, no. 8 (November 2009): 1005–11. http://dx.doi.org/10.1590/s0004-27302009000800015.
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OBJECTIVE: To evaluate the incidence of hypogonadism in men with metabolic syndrome and its correlation with serum insulin levels. METHODS: Observational, transversal study with 80 men with metabolic syndrome. The individuals were divided into two groups: Group 1: 56 patients (70%) with total testosterone > 300 ng/dL (normal gonadal function); Group 2: 24 patients (30%) with total testosterone < 300 ng/dL (hypogonadic). RESULTS: The subjects from Group 2 compared to Group 1 presented higher body mass index (BMI), waist and hip circumferences, insulin, homeostasis model assessment insulin resistance index (Homa-IR) and beta cell (Homa-β), and triglycerides, but lower SHBG and free testosterone values. Inverse correlations between insulin levels and total testosterone and SHBG, as well as between Homa-IR and total testosterone were observed. CONCLUSION: In this series of men with metabolic syndrome, hypogonadism was associated with insulin resistance and may be a marker of metabolic abnormalities.
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Kanti, Georgia, Evrim Anadol-Schmitz, Pavel Bobrov, Klaus Strassburger, Sabine Kahl, Oana P. Zaharia, Theresia Sarabhai, et al. "Vitamin B12 and Folate Concentrations in Recent-onset Type 2 Diabetes and the Effect of Metformin Treatment." Journal of Clinical Endocrinology & Metabolism 105, no. 6 (March 27, 2020): e2222-e2231. http://dx.doi.org/10.1210/clinem/dgaa150.
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Abstract Context Vitamin B12 and folate deficiency are not only linked to hematological, neurological, and cardiovascular diseases, but are also associated with insulin resistance. Metformin can decrease vitamin B12 and folate concentrations. Objective To examine (1) effects of short-term metformin treatment on serum holotranscobalamin (holoTC) and folate and (2) their association with insulin sensitivity in recent-onset type 2 diabetes. Design This cross-sectional analysis comprised patients (known disease duration <12 months) on metformin monotherapy (MET, n = 123, 81 males, 53 ± 12 years) or nonpharmacological treatment (NPT, n = 126, 77 males, 54 ± 11 years) of the German Diabetes Study. Main Outcome Measures HoloTC (enzyme-linked immunosorbent assay), cobalamin, and folate (electrochemiluminescence); beta-cell function and whole-body insulin sensitivity, measured during fasting (HOMA-B, HOMA-IR) and intravenous glucose tolerance tests combined with hyperinsulinemic–euglycemic clamp tests. Results HoloTC (105.4 [82.4, 128.3] vs 97 [79.7, 121.9] pmol/L) and folate concentrations (13.4 [9.3, 19.3] vs 12.7 [9.3, 22.0] nmol/L) were similar in both groups. Overall, holoTC was not associated with fasting or glucose-stimulated beta-cell function and insulin-stimulated glucose disposal. Cobalamin measurements yielded similar results in representative subgroups. In NPT but not MET, folate levels were inversely correlated with HOMA-IR (r = –0.239, P = .007). Folate levels did not relate to insulin sensitivity or insulin secretion in the whole cohort and in each group separately after adjustment for age, body mass index, and sex. Conclusions Metformin does not affect circulating holoTC and folate concentrations in recent-onset type 2 diabetes, rendering monitoring of vitamin B12 and folate dispensable, at least during the first 6 months after diagnosis or initiation of metformin.
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Chari, Suresh T., Mauricio Zapiach, Dhiraj Yadav, and Robert A. Rizza. "Beta-cell function and insulin resistance evaluated by HOMA in pancreatic cancer subjects with varying degrees of glucose intolerance." Pancreatology 5, no. 2-3 (January 2005): 229–33. http://dx.doi.org/10.1159/000085276.
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Pattan, Vishwanath, Maria Chang Villacreses, Rudruidee Karnchanasorn, Wei Feng, Raynald Samoa, and Ken C. Chiu. "Comparison of Serum Copper, Selenium and Zinc Concentrations Among the States of Glucose Tolerance." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A319—A320. http://dx.doi.org/10.1210/jendso/bvab048.651.
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Abstract Trace element is essential for the proper growth, development, and physiology of the organism and the primary source of trace element is dietary intake. Among trace elements, the role of copper (Cu), selenium (Se), and zinc (Zn) in the pathogenesis of diabetes have been widely recognized. However, there is little information available about these 3 trace elements across the different states of glucose tolerance. We examined associations between serum levels of trace elements - Cu, Zn, and Se with various stages of glucose tolerance in a representative, cross-sectional sample of US adults. Our sample included 5,087 adults (≥20 years) with available serum concentrations of Cu, Zn and Se as well as states of glucose tolerance, defined by history, HbA1c, fasting, and 2-hour plasma glucose concentrations. Serum concentrations of trace elements were compared with glucose tolerance status with the consideration of covariates. Regression analyses was used to examine the relationship of trace elements with HOMA-IR, HOMA-B, and BMI in non-diabetic subjects with the consideration of appropriate covariates. Serum Se (P<0.0001) and Zn (P<0.0001) concentrations differed significantly among 3 groups based on the states of glucose tolerance, while no difference was noted in serum Cu concentration. In non-diabetic subjects, serum Cu concentration was positively correlated with BMI (P<0.0001) with a possible compensatory increased beta cell function (P=0.018). Serum Se concentration was negatively correlated with insulin resistance (P=0.016) but not with beta cell function or BMI. Serum Zn concertation was negatively correlated with beta cell function (P=0.0023) and BMI (P=0.018), but not with insulin resistance. We found that a higher serum concentration of trace elements was associated with negative glucose and fuel homeostasis in a non-deficiency population possibly through different mechanisms. Although the casual relationship remains to be elucidated, we recommend against trace element supplementation in a non-deficiency population.
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Phan, Thi To Nhu, and Trung Vinh Hoang. "Investigation of the progress in the women with gestational diabetes mellitus postpartum." Vietnam Journal of Diabetes and Endocrinology, no. 40 (January 28, 2021): 45–51. http://dx.doi.org/10.47122/vjde.2020.40.8.
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Aims: Our aim was to evaluate the uptake of postpartum screening, the prevalence and the risk factors for glucose intolerance in women with a recent history of gestational diabetes mellitus (GDM). Methods: All women with a history of GDM are advised to undergo a 75g oral glucose tolerance test (OGTT) around 6 - 12 weeks postpartum. Indices of insulin sensitivity (the Matsuda index and the reciprocal of the homeostasis model assessment of insulin resistance, HOMA-IR) and an index of beta-cell function, the Insulin Secretion-Sensitivity Index-2 (ISSI-2) were calculated based on the OGTT postpartum. Multivariable logistic regression was used to some factors. Results: Of all women (135) who received an OGTT postpartum, 42.2% (57) had glucose intolerance (11.8% impaired fasting glucose, 24.4% impaired glucose tolerance and 6.0% both impaired fasting and impaired glucose tolerance) and 1.5% (2) had overt diabetes. Compared to women with a normal OGTT postpartum, women with glucose intolerance and diabetes were older (32.5 ± 4.3 vs. 30.8 ± 4.8 years, p = 0.049), were more often obese (34.5% vs. 17.3%, p = 0.023). In the multivariable logistic regression, an EM background [OR = 2.76 (1.15 - 6.62), p = 0.023] and the HbA1c level at the time of the OGTT in pregnancy [OR = 4.78 (1.19 - 19.20), p = 0.028] remained significant predictors for glucose intolerance postpartum. Women with glucose intolerance and diabetes postpartum had a similar insulin sensitivity [Matsuda index 0.656 (0.386 - 1.224) vs. 0.778 (0.532 - 1.067), p = 0.709; HOMA-IR 0.004 (0.002 - 0.009) vs. 0.064 (0.003 - 0.007), p = 0.384] but a lower beta-cell function compared to women with a normal OGTT postpartum, remaining significant after adjustment for confounders [ISSI-2 1.6 (1.2 - 2.1) vs. 1.9 (1.7 - 2.4), p = 0.002]. Conclusions: Glucose intolerance is very frequent in early postpartum in women with GDM these women have an impaired beta-cell function. Nearly one third of women did not attend the scheduled OGTT postpartum and these women have an adverse risk profile. More efforts are needed to engage and stimulate women with GDM to attend the postpartum OGTT.
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Asanaliyar, Meharban, and Pratibha Nadig. "In -Vivo Anti-Diabetic Activity of Hydro-Ethanolic Seed Extract of Syzygium Cumini (L.)." Biomedical and Pharmacology Journal 14, no. 1 (March 28, 2021): 241–47. http://dx.doi.org/10.13005/bpj/2119.
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Introduction: Diabetes mellitus continues to be a major health problem in India and across the world. Over centuries, numerous herbal extracts have been used in the Indian traditional medicine to control elevated blood sugar levels in patients with diabetes. Different aqueous and organic extracts of Syzygium cumini (L.) Skeels have found widespread use owing to their anti-diabetic activity. A systematic study was undertaken to characterise and evaluate the effects of a hydro-ethanolic seed extract (SCE) of Syzygium cumini in a rodent model of experimental type 2 diabetes mellitus. Methods: An established model of diabetes mellitus with a combination of streptozotocin and high fat diet (over 12 weeks) in adult male Wistar albino rats, was used in this study. The onset of diabetes mellitus in rats was confirmed with a fasting blood glucose (FBG) of >200 mg/dl. The diabetic rats were allocated into five experimental groups and treated as follows: with vehicle alone, pioglitazone (10 mg/kg), 100mg/kg or 200mg/kg or 400 mg/kg of SCE, respectively for 21 days. The pre and post treatment levels of fasting blood glucose, insulin and lipids were measured from serum obtained from the various treatment groups. In order to measure insulin resistance, a homeostasis model assessment of insulin resistance (HOMA IR) and for measuring the beta cell function a homeostasis model assessment were employed. The results obtained from these studies were analysed using the Analysis of variance (ANOVA) method. Results: Our study demonstrates the SCE preparation to induce a statistically significant dose-dependent reduction in FBG, serum lipid levels and HOMA IR with a concomitant increase in the serum insulin levels and HOMA B. Conclusions: Wistar rats dosed with SCE at 100 and 200 mg/kg body weight demonstrated statistically significant anti-diabetic activity by virtue of improving the pancreatic beta cell function and reduction in insulin resistance.
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Tarantino, Giovanni, Vincenzo Citro, Clara Balsano, and Domenico Capone. "Could SCGF-Beta Levels Be Associated with Inflammation Markers and Insulin Resistance in Male Patients Suffering from Obesity-Related NAFLD?" Diagnostics 10, no. 6 (June 11, 2020): 395. http://dx.doi.org/10.3390/diagnostics10060395.
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One of the pathologic hallmarks of obesity is macrophage infiltration of adipose tissue that has been confirmed as source of multipotent adult stem cells. Stem cell growth factor-beta (SCGF-β) shows activity on granulocyte/macrophage progenitor cells in combination with granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF). Obesity-associated inflammation induces insulin resistance (IR), which is central to nonalcoholic fatty liver disease (NAFLD) or hepatic steatosis (HS). We searched for relationship between levels of SCGF-β and those of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-β (TNF-β), interleukin-12p40 (IL-12p40), interleukin-10 (IL-10), ferritin, GM-CSF and M-CSF and between SCGF-β concentrations and IR in obese patients with HS. Eighty obese patients were retrospectively studied. Serum cytokines levels were appreciated by magnetic bead-based multiplex immunoassays. IR was evaluated by homeostatic model assessment (HOMA), HOMA-derived β-cell function (HOMA-B%), quantitative insulin sensitivity check Index (QUICKI) and single point insulin sensitivity estimator (SPISE). HS and spleen volume were assessed by ultrasonography (US). SCGF-β and IL-6 levels predicted HOMA values (p = 0.032 and 0.041, respectively) only in males. In male patients, CRP and IL-6 levels (p = 0.007) predicted SCGF-β concentrations (p = 0.03 and 0.007, respectively), which in turn predicted HS at US, p = 0.037. SCGF-β levels were linked to IR and HS severity with the mediation role of CRP. IL-10 levels negatively predicted SCGF-β concentrations (p = 0.033). M-CSF levels predicted serum concentration of both TNF-β and IL-12p40 (p = 0.00), but did not predict serum IL-10 (p = 0.30). Prediction of HOMA values by SCGF-β levels, likely mediated by markers of inflammation, characterizes this study, shedding some light on mechanisms inducing/worsening IR of male patients with obesity-related NAFLD.
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Tasnim, Masuma, Qazi Shamima Akhter, Salma Akhter, Nasreen Sultana Lovely, Khadiza Begum, and Susmita Sinha. "Insulin Secretory Status in Obese Female." Journal of Bangladesh Society of Physiologist 9, no. 2 (March 30, 2015): 72–77. http://dx.doi.org/10.3329/jbsp.v9i2.22800.
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Background: In obesity insulin hypersecretion is a key feature indicating the abnormal pancreatic beta cell function which is the fundamental defect in the development of NIDDM, hypertension and cardiovascular diseases. Objective: To assess the secretory status of insulin in adult obese female. Methods: The present study was a cross sectional analytical study and conducted in the Department of Physiology, Dhaka Medical College, Dhaka from July 2012 to June 2013. 50 obese female subjects of 20-40 years were included from Out-patient Department (Obesity clinic) of BIRDEM Hospital, Dhaka and by personal contact from different areas of Dhaka city. 50 age matched, healthy non-obese female subjects selected as controls . Fasting serum insulin level was measured by ELISA and fasting glucose level was measured by Glucose oxidase method. The insulin secretory status was calculated by HOMA-%B using HOMA software. For statistical analysis unpaired Students t test and Pearsons correlation coefficient (r) test were performed as applicable . Result: Mean fasting serum insulin and HOMA%B (P<0.001) were higher in the obese than that non obese. Fasting serum insulin level and HOMA%B showed significantly positive correlation with WHR. Conclusion: This study concludes that obese individual develops a state of insulin hypersecretion and hyperinsulinemia. DOI: http://dx.doi.org/10.3329/jbsp.v9i2.22800 Bangladesh Soc Physiol. 2014, December; 9(2): 72-77
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Ma, Xiao-yu, Fen-qin Chen, Hong Hong, Xiu-juan Lv, Ming Dong, and Qiu-yue Wang. "The Relationship between Serum Osteocalcin Concentration and Glucose and Lipid Metabolism in Patients with Type 2 Diabetes Mellitus - The Role of Osteocalcin in Energy Metabolism." Annals of Nutrition and Metabolism 66, no. 2-3 (2015): 110–16. http://dx.doi.org/10.1159/000370198.
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Background: Recent animal studies have found that the osteocalcin secreted by osteoblasts could participate in glucose and lipid metabolism. Our study aimed to investigate the relationship between serum osteocalcin concentration and glucose and lipid metabolism in patients with type 2 diabetes mellitus. Methods: 985 patients with type 2 diabetes were divided into the male group (n = 495) and the postmenopausal female group (n = 490). The average ages were 54.42 ± 10.535 and 64.93 ± 9.277, respectively. We collected the parameters of age, duration, fasting plasma glucose, HbA1c, fasting insulin, fasting C peptide, blood lipid, 25 (OH) VD3, parathyroid hormone (PTH), Alkaline phosphatase (ALP), procollagen type 1 N-terminal propeptide (P1NP), β-C-terminal telopeptide of type I collagen (β-CTx), osteocalcin, HOMA-IR, HOMA-β, body mass index (BMI), and waist-to-hip ratio (WHR). The relationship of osteocalcin and these parameters were analyzed by Pearson/Spearman correlation analysis and stepwise multiple regression analysis. Results: Osteocalcin was negatively correlated with HbA1c (p < 0.05) and it was also an independent relevant factor affecting HbA1c in both groups. Osteocalcin was positively correlated with HOMA-β and it was an independent relevant factor affecting HOMA-β in male group (p < 0.01). Conclusions: These findings indicate the association between serum osteocalcin and glucose metabolism and beta cell function. No relationship was found between osteocalcin and insulin resistance and lipid metabolism in type 2 diabetes.
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Miao, Tian, Bangliang Huang, Niexia He, Lihua Sun, Guangsheng Du, Xiaoli Gong, Yong Xu, Yi Zheng, Hongting Zheng, and Hua Qu. "Decreased Plasma Maresin 1 Concentration Is Associated with Diabetic Foot Ulcer." Mediators of Inflammation 2020 (April 16, 2020): 1–7. http://dx.doi.org/10.1155/2020/4539035.
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Aims. To assess the maresin 1 (MaR1) contents in type 2 diabetic patients with or without diabetic foot ulcer and to analyze the association of MaR1 concentrations with several metabolism-related parameters. Methods. Plasma MaR1 concentrations were analyzed in 96 subjects with normal glucose tolerant (NC, n=43), type 2 diabetes (T2DM, n=40), or diabetic foot ulcer (DFU, n=13). The intravenous glucose tolerance test (IVGTT) and biochemical parameters were measured in all participants. Results. Plasma MaR1 concentrations were significant decreased in type 2 diabetes patient with or without DFU compared with NC (both P<0.001) and were lowest in DFU patients among these 3 groups. (DFU vs. T2DM, P<0.05). Plasma MaR1 concentrations were negatively correlated with BMI, waist circumference (Wc), waist hip ratio (WHR), systolic blood pressure (SBP), diastolic blood pressure (DBP), LDL-c, FPG, 2hPG, HbA1c, and homeostasis model assessment for insulin resistance (HOMA-IR) (all P<0.05) and were positively correlated with HDL-c, acute insulin response (AIR), area under the curve of the first-phase (0-10 min) insulin secretion (AUC), and homeostasis model assessment for beta-cell function (HOMA-β) (all P<0.05). After adjusting for age and sex, Wc, WHR, TG, FPG, 2hPG, HbA1c, HOMA-IR, AIR, AUC, and HOMA-β remain statistically significant (all P<0.05). Conclusions. Plasma MaR1 concentration were decreased in T2DM with or without DFUs and were the lowest in DFU patients. The decreased plasma MaR1 strongly associated with obesity, impaired glucose and lipid metabolism, reduced first-phase of glucose-stimulated insulin secretion, and enhanced insulin resistance.
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Pan, A., SS Nag, BC Mondal, A. Anindya Dasgupta, and P. Piyali Mitra. "Status of glucose metabolism including insulin resistance and beta cell function in overtly iron loaded Thalassemia patients." Journal of College of Medical Sciences-Nepal 10, no. 3 (June 17, 2015): 29–36. http://dx.doi.org/10.3126/jcmsn.v10i3.12774.
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BACKGROUND Abnormality of glucose metabolism is a frequent complication in Thalassemia patients. Both insulin deficiency and insulin resistance has been proposed in its pathogenesis. Some form of abnormality in glucose metabolism is expected at an earlier age in these patients in developing countries like India and Nepal where iron overload is excessive due to lack of chelation therapy.MATERIALS AND METHODS Fasting serum glucose and fasting serum insulin (FSI) were measured in 40 beta-thalassemia major patients, 40 Ebeta- thalassemia patients and 40 controls, all aged between 5 and 12 years. 2 hours after an appropriate dose of oral glucose feed (Children ingested 1.75 g/kg body weight maximum 75 gram dissolved in 250 to 300 ml water) blood samples were drawn again to measure post prandial serum glucose. Iron overload was assessed by measuring liver size, spleen size, total amount of packed cells transfused and serum ferritin. Insulin resistance (IR), insulin sensitivity (%S) and beta cell functions (%B) were derived from the measured laboratory parameters using the latest version of Homeostatic Model Assessment (HOMA) calculator software.RESULTS No one had impaired glucose metabolism or diabetes mellitus beta-thalassemia major patients showed evidence of insulin resistance in the form of significantly higher fasting serum insulin (p value 0.002), IR (p value 0.003), %B (p value 0.017) and significantly lower %S (0.002) when compared with controls. FSI showed positive correlation with total amount of packed cells received (r=0.372, p=0.018), serum ferritin (r=0.345, p=0.029) and spleen size (r=0.427, p=0.006). Similarly, IR also showed positive correlation with total amount of packed cells received (r=0.388, p=0.013), serum ferritin (r=0.336, p=0.034) and spleen size (r=0.425, p=0.005). %S showed negative correlation with all these parameters. %B didn’t show any statistically significant correlation with these parameters.Ebeta- thalassemia patients didn’t have any statistically significant difference in FSI, IR, %S and %B than controls.CONCLUSION Insulin resistance develops as the earliest abnormality in glucose metabolism in overtly iron loaded beta thalassemia major patients at an early age. Ebeta- thalassemia patients with milder phenotype do not develop dysfunction of glucose metabolism at such an early age.Journal of College of Medical Sciences-Nepal, 2014, Vol-10, No-3, 29-36
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Preumont, V., M. P. Hermans, S. Brichard, and M. Buysschaert. "Six-month exenatide improves HOMA hyperbolic product in type 2 diabetic patients mostly by enhancing beta-cell function rather than insulin sensitivity." Diabetes & Metabolism 36, no. 4 (September 2010): 293–98. http://dx.doi.org/10.1016/j.diabet.2010.02.001.
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Yassin, Mohamed A., Ahmed M. Elawa, and Ashraf T. Soliman. "Detection of Glycemic Abnormalities in Young Adult Patients with Beta Thalassemia Major Using Continuous Glucose Monitoring System (CGMS) and Oral Glucose Tolerance Test (OGTT)." Blood 118, no. 21 (November 18, 2011): 2158. http://dx.doi.org/10.1182/blood.v118.21.2158.2158.
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Abstract Abstract 2158 Introduction: Both insulin deficiency and insulin resistance are reported in patients with β thalassemia major (BTM). The use of continuous blood glucose monitoring system (CGMS) among the different methods for early detection of glycaemic abnormalities has not been studied thoroughly in these patients. Aims: The aims of this study were: 1. to detect glycaemic abnormalities, if any, in young adults with BTM using fasting blood glucose (FBG), oral glucose tolerance test (OGTT), 72-h continuous glucose concentration by CGMS system, and serum insulin and C-peptide concentrations 2. To compare the results of these two methods in detecting glycaemic abnormalities in these patients and 3. To calculate homeostatic model assessment (HOMA), and the quantitative insulin sensitivity check index (QUICKI) in these patients. In order to evaluate whether glycaemic abnormalities are due to insulin deficiency and/or resistance. Materials and methods: Randomly selected young adults (n = 14) with BTM were the subjects of this study. All patients were investigated using a standard oral glucose tolerance test (OGTT) (using 75 gram of glucose) and 72-h continuous glucose concentration by CGM system (Medtronic system). Fasting serum insulin and C-peptide concentrations were measured and HOMA-B, HOMA-IR were calculated accordingly. Results: Using OGTT, 5 patients had impaired fasting glucose (IFG) (Fasting BG from 5.6 to 6.9 mmol/L). Two of them had impaired glucose tolerance IGT (BG from 7.8 and < 11.1 mmol/L) and one had BG = 16.2 mmol/L after 2-hrs (diabetic). Using CGMS in addition to the glucose data measured by glucometer (3–5 times/ day), 6 patients had IFG. The maximum (postprandial) BG recorded exceeded 11.1 mmol/L in 4 patients (28.5%) (Diabetics) and was > 7.8 but < 11.1 mmol/L in 8 patients (57%) (IGT). The mean values of HOMA and QUICKI in patients with BTM were < 2.6 (1.6± 0.8) and > 0.33 (0.36±0.03) respectively ruling out significant insulin resistance in these adolescents. There was a significant negative correlation between the β-cell function (B %) on the one hand and the fasting and the 2-h BG (r= −0.6, and − 0.48, P< 0.01 respectively) on the other hand. Serum insulin concentrations were not correlated with fasting BG or ferritin levels. The average and maximum BG levels recorded by CGMS were significantly correlated with the fasting BG (r= 0.69 and 0.6 respectively with P < 0.01) and with the BG at 2-hour after oral glucose intake (r= 0.87and 0.86 respectively with P < 0.01). Ferritin concentrations were positively correlated with the fasting BG and the 2-h BG levels in the OGTT (r= 0.69, 0.43 respectively, P < 0.001) as well as with the average and the maximum BG recorded by CGM (r =0.75, and 0.64 respectively with P < 0.01). Ferritin concentrations were negatively correlated with the β-cell function (r= −0.41, P< 0.01). Conclusion: CGMS has proved to be superior to OGTT for the diagnosis of glycaemic abnormalities in young adult patients with BTM. In our patients, defective β-cell function rather than insulin resistance appeared to be the cause for these abnormalities. The significant correlations between serum ferritin concentrations and the beta cell functions suggested the importance of adequate chelation to prevent β-cell dysfunction Disclosures: No relevant conflicts of interest to declare.
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Borges-Canha, Marta, João Sérgio Neves, Fernando Mendonça, Maria Manuel Silva, Cláudia Costa, Pedro Cabral, Vanessa Guerreiro, et al. "Is Insulin Resistance at Baseline a Predictor of Weight Loss After Bariatric Surgery?" Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A18—A19. http://dx.doi.org/10.1210/jendso/bvab048.034.
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Abstract Background: Obesity is a multifactorial disease that is strongly associated to other metabolic disorders, such as insulin resistance and type 2 diabetes. Bariatric surgery is nowadays considered the most effective treatment of morbid obesity. The role of insulin resistance (IR) in weight loss after bariatric surgery is highly unknown. Aim: To evaluate the association between Insulin Resistance (IR) and percentage of excess weight loss (EWL%) one, two, three and four years after bariatric surgery in patients with morbid obesity. Methods: Retrospective longitudinal study in patients with morbid obesity followed in our centre between January 2010 and July 2018 were included. Patients were excluded if they had diabetes. We evaluated baseline Homeostatic Model Assessment of IR (HOMA-IR), Homeostatic Model Assessment of β-cell function (HOMA-beta), Quantitative Insulin Sensitivity Check Index (QUICKI) and Matsuda and DeFronzo index, and performed a linear regression concerning each year’s EWL%. Results: After applying the exclusion criteria, 1723 patients were included in this analysis. The logarithm of HOMA-beta was negatively associated with EWL% at second-, third- and fourth-years post-surgery (β=-1.04 [-1.82 to -0.26], p<0.01; β=-1.16 [-2.13 to -0.19], p=0.02; β=-1.29 [-2.64 to 0.06], p=0.061, respectively), adjusting for age, sex, body mass index and type of surgery. This was not observed in the first-year post-surgery nor for the other indexes. Glycaemia at baseline was also positively associated to EWL% at second- and third-years post-surgery. Conclusion: IR at baseline seems to be associated to long term weight loss, explicitly after the first year post bariatric surgery.
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Vrbikova, J., M. Hill, L. Starka, D. Cibula, B. Bendlova, K. Vondra, J. Sulcova, and M. Snajderova. "The effects of long-term metformin treatment on adrenal and ovarian steroidogenesis in women with polycystic ovary syndrome." European Journal of Endocrinology 144, no. 6 (June 1, 2001): 619–28. http://dx.doi.org/10.1530/eje.0.1440619.
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OBJECTIVE: To evaluate adrenal and ovarian steroidogenesis before and after long-term treatment with metformin in women with polycystic ovary syndrome (PCOS). DESIGN AND METHODS: Twenty-four women with PCOS were evaluated before and after treatment (27+/-4 weeks) with metformin (1000 mg/day) using adrenocorticotrophin (ACTH), GnRH analogue and oral glucose tolerance (oGTT) tests. For statistical evaluation, ANOVA and Wilcoxon's test were used. RESULTS: In 58% of the women a significant improvement in menstrual cyclicity was observed. No significant change in basal steroid levels was found. After ACTH stimulation, a significant decrease in the activity of 3 beta-hydroxysteroid dehydrogenase in C(21) steroids (P<0.05) and in 17 beta-hydroxysteroid dehydrogenase (P<0.01) was observed, as was an increase in the activity of C17,20-lyase in the Delta(4) pathway (P<0.01). A significant growth in the dehydroepiandrosterone (DHEA)/DHEA-sulfate ratio (P<0.05) was detected. With regard to ovarian steroidogenesis, a significant decrease in the stimulated levels of testosterone (P<0.05), index of free testosterone (P<0.01), LH (P<0.05) and oestradiol (P<0.01), and an increase in the levels of 17-hydroxypregnenolone (P<0.05) were detected. In the indices of ovarian enzyme activities, we observed a significant decrease in 3 beta-hydroxysteroid dehydrogenase in C21 steroids (P<0.01), in C17,20-lyase in the Delta 5 pathway (P<0.01), in 17 beta-hydroxysteroid dehydrogenase (P<0.05) and in aromatase. In glucose metabolism, a tendency towards reduction in the homeostasis model assessment (HOMA)-R (for insulin resistance) and HOMA-F (for beta cell function) was detected. In addition, an increase in the levels of C peptide during oGTT was observed (P<0.01). CONCLUSIONS: Long-term metformin treatment reduced various steroid enzymatic activities both in the ovary and the adrenal glands, without apparent changes in basal steroid levels and in insulin sensitivity.
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Kartikawati, Anggi, Yani Lina, and Andi Wijaya. "25(OH)D was Correlated with Increased Risk of Insulin Resistance, but Not Mediated by Adiponectin and hsCRP." Indonesian Biomedical Journal 4, no. 2 (August 1, 2012): 84. http://dx.doi.org/10.18585/inabj.v4i2.166.
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BACKGROUND: Studies have shown that change of calcium and vitamin D homeostasis is associated with insulin resistance, decreased beta cell function, metabolic syndrome, glucose intolerance and diabetes. Evidence suggests that vitamin D insufficiency is inversely related to risk of metabolic disorders including type-2 Diabetes Mellitus (T2DM), although the underlying mechanisms are not yet understood. Hence, current study was conducted to investigate correlation between 25(OH)D and insulin resistance through adiponectin or High Sensitivity C-Reactive Protein (hsCRP) in centrally obese men.METHODS: This was a cross-sectional study involving 80 centrally obese men with waist circumference (WC) >90 cm and age 30-60 years. Total 25(OH)D concentration was measured by Enzyme-Linked Immunosorbent Assay (ELISA) method. Insulin resistance was calculated by HOMA model.RESULTS: This study showed there was no correlation of 25(OH)D-WC (r=0.006 and p=0.957), 25(OH)D-adiponectin (r=0.179 and p=0.111) abd 25(OH)D-hsCRP (r=-0.223 and p=0.334), but we observed statistically significant negative correlation between 25(OH)D and insulin resistance index (HOMA-IR) (r=0.461 and p=0.041).CONCLUSIONS: We conclude that low 25(OH)D concentration was significantly associated with increased risk of insulin resistance. Since the adiponectin or hsCRP was not correlated, the possible pathways need to be futher investigated.KEYWORDS: central obesity, 25(OH)D, adiponectin, hsCRP, insulin resistance (HOMA-IR)
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Sarkar, Jit, Sujay Krishna Maity, Abhishek Sen, Titli Nargis, Dipika Ray, and Partha Chakrabarti. "Impaired compensatory hyperinsulinemia among nonobese type 2 diabetes patients: a cross-sectional study." Therapeutic Advances in Endocrinology and Metabolism 10 (January 2019): 204201881988902. http://dx.doi.org/10.1177/2042018819889024.
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Aims: Obesity associated prolonged hyperinsulinemia followed by β-cell failure is well established as the pathology behind type 2 diabetes mellitus (T2DM). However, studies on nonobese T2DM have reported it to be a distinct clinical entity with predominant insulin secretory defect. We, therefore, hypothesized that compensatory hyperinsulinemia in response to weight gain is impaired in nonobese subjects. Methods: This was a cross-sectional study from a community-based metabolic health screening program. Adiposity parameters including body mass index (BMI), waist circumference (WC), body fat percentage, plasma leptin concentration and metabolic parameters namely fasting insulin, glucose, total cholesterol, and triglycerides were measured in 650 individuals (73% healthy, 62% nonobese with a BMI <25). Results: In contrast to obese T2DM, nonobese T2DM patients did not exhibit significant hyperinsulinemia compared with the nonobese healthy group. Age, sex, and fasting glucose adjusted insulin levels, homeostatic model assessment of insulin resistance (HOMA-IR) and HOMA-beta cell function (HOMA-B) were increased in obese T2DM compared with nonobese T2DM. Although adiposity parameters showed strong correlation with fasting insulin in obese healthy ( r = 0.38, 0.38, and 0.42, respectively; all p values < 0.001) and T2DM ( r = 0.54, 0.54, and 0.66, respectively; all p < 0.001), only BMI and leptin showed a weak correlation with insulin in the nonobese healthy group (0.13 and 0.13, respectively; all p < 0.05) which were completely lost in the nonobese T2DM. Conclusions: Compensatory hyperinsulinemia in response to weight gain is impaired in the nonobese population making insulin secretory defect rather than IR the major pathology behind nonobese T2DM.
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Meisinger, Christa, Jakob Linseisen, Michael Leitzmann, Hansjoerg Baurecht, and Sebastian Edgar Baumeister. "Association of physical activity and sedentary behavior with type 2 diabetes and glycemic traits: a two-sample Mendelian randomization study." BMJ Open Diabetes Research & Care 8, no. 2 (December 2020): e001896. http://dx.doi.org/10.1136/bmjdrc-2020-001896.
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IntroductionObservational studies suggest that physical activity lowers and sedentary behavior increases the risk of type 2 diabetes. Despite of some supportive trial data for physical activity, it is largely unresolved whether these relations are causal or due to bias.ObjectiveWe investigated the associations between accelerometer-based physical activity and sedentary behavior with type 2 diabetes and several glycemic traits using two-sample Mendelian randomization analysis.Research design and methodsSingle nucleotide polymorphisms (SNPs) associated at p<5×10−8 with accelerometer-based physical activity average accelerations, vigorous physical activity (fraction of accelerations >425 milligravities), and sedentary behavior (metabolic equivalent task ≤1.5) in a genome-wide analysis of the UK Biobank served as instrumental variables.OutcomesType 2 diabetes, hemoglobin A1c (HbA1c), fasting glucose, homeostasis model assessment of beta-cell function (HOMA-B), and homeostasis model assessment of insulin resistance (HOMA-IR).ResultsPhysical activity and sedentary behavior were unrelated to type 2 diabetes, HbA1c, fasting glucose, HOMA-B, and HOMA-IR. The inverse variance weighted ORs per SD increment for the association between average accelerations and vigorous physical activity with type 2 diabetes were 1.00 (95% CI 0.94 to 1.07, p=0.948) and 0.83 (95% CI 0.56 to 1.23, p=0.357), respectively. These results were confirmed by sensitivity analyses using alternative MR-methods to test the robustness of our findings.ConclusionsBased on these results, genetically predicted objectively measured average or vigorous physical activity and sedentary behavior is not associated with type 2 diabetes risk or with glycemic traits in the general population. Further research is required to deepen the understanding of the biological pathways of physical activity.
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Huțanu, Adina, Mihaela Zaharia, Lenard Farczadi, Ionela Maria Pașcanu, Raluca Monica Pop, and Minodora Dobreanu. "Evaluation of Plasma AA/DHA+EPA Ratio in Obese Romanian Children." Revista Romana de Medicina de Laborator 29, no. 2 (April 1, 2021): 165–78. http://dx.doi.org/10.2478/rrlm-2021-0002.
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Abstract The aim of the study was to evaluate the plasma profile of arachidonic acid (AA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), as well to analyze the relationship of Omega 6/Omega 3 ratio with anthropo-metric parameters and insulin resistance markers. Material and methods: Plasma levels of free fatty acids (FFAs) were measured using a high-throughput LC-MS AB Sciex4600 in 202 children (127 obese and 75 non-obese), age and sex-matched. Lipid and glucose profiles were assessed with current laboratory methods, while insulin resistance and beta-cell function were evaluated using HOMA-IR and HOMA-β respectively. Results: In obese children, AA and AA/(DHA+EPA) ratio were significantly higher regardless of age and gender. In the lowest quartile of DHA, there was a clear trend for insulin resistance, with plasma insulin level, HOMA-IR, and HOMA-β significantly higher compared to the highest quartile of DHA. After adjustment for age and gender DHA remains a negative predictive factor for insulin resistance. Waist-to-height ratio (WHtR), a marker of visceral obesity was higher in children with a higher AA/(DHA+EPA) ratio. Conclusions: In obese children, the AA is higher in concordance with insulin resistance. Additionally, children with a higher AA/(DHA+EPA) ratio have greater BMI, fat mass, waist circumference, and WHtR, important indicators of central adiposity, and cardio-metabolic disorders. LC/MS is a versatile tool for Omega ratio assessment, especially in children where the sample size is a limiting factor for metabolic and nutrition evaluation.
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Cockcroft, Emma, Craig Williams, Sarah Jackman, Neil Armstrong, and Alan Barker. "Agreement and Reliability of Fasted and Oral Glucose Tolerance Test-Derived Indices of Insulin Sensitivity and Beta Cell Function in Boys." International Journal of Sports Medicine 38, no. 06 (May 8, 2017): 411–17. http://dx.doi.org/10.1055/s-0043-104932.
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AbstractAssessment of plasma insulin and glucose outcomes is important in paediatric studies aimed at reducing future risk of type 2 diabetes and cardiovascular disease. The aims of this study are to determine the between-method agreement and the day-to-day reliability of fasting and oral glucose tolerance test (OGTT)-derived estimates of insulin sensitivity and β-cell function in healthy boys. Fasting and OGTT assesments of insulin resistance and β-cell function were performed on 28 boys (12.3±2.9 years). Measurements were repeated after 1 week (fasting, n=28) and 1 day (OGTT, n=8). Agreement between estimates of insulin resistance and β-cell function was examined using Pearson’s correlation coefficient. Reliability was assessed using change in the mean, Pearson’s correlation coefficient, and typical error expressed as a coefficient of variation (CV). The Matsuda index was positively related with QUICKI (r=0.88, P<0.001) and negatively related to HOMA-IR (r=−0.76, P<0.001). The Cederholm index was not significantly related with fasting estimates of insulin resistance (all r<0.40, P>0.05). For reliability, QUICKI had the lowest CV% for the fasting (4.7%) and the Cederholm index for the OGTT (6.4%) estimates. The largest CV% was observed in fasting insulin (30.8%) and insulinogenic index 30’ (62.5%). This study highlights differences in between-method agreement and day-to-day reliability for estimates of insulin resistance in youth. The low CV supports the use of the FGIR (fasting) and Cederholm (OGTT) indices in this population.