Academic literature on the topic 'HOMA Beta-Cell Function'

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.

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.

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.

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)

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

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.

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.

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 &lt; 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.

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.

Background: African-Americans are a vulnerable population group with disproportionately elevated rates of type 2 Diabetes Mellitus (DM). Resistant starch is a promising food ingredient that has the potential to reduce the risk factors involved in the development of type 2 DM. To date, there is a dearth of published research studies on the effect of resistant starch on African-Americans who are at increased risk for type 2 DM. Objective: The major objective of this study was to determine if daily consumption of approximately twelve grams of high-maize™ 260 resistant starch (RS) added to bread improved glucose homeostasis by monitoring changes in fasting plasma glucose, fructosamine, hemoglobin A1c, insulin, glucagon-like peptide-1, C-reactive protein, homeostasis model assessment insulin resistant (HOMA- IR) and beta-cell function (HOMA-Beta), serum acetate, propionate, and butyrate levels. Design: A fourteen-week, randomized, double-blind, within-subject crossover design feeding study was carried out in African-American males (n=8) and females (n=7) at increased risk for type 2 DM who resided in Southwest Virginia. All participants consumed bread containing added RS or control bread (no added RS) for six-weeks. RS and control bread feedings were separated by a two-week washout period. Results: Fasting Plasma Glucose (FPG) levels were significantly lower (P = 0.0179) after six-week control bread feedings compared to baseline. FPG levels were also significantly lower (P < 0.0001) after two-week washout period than at baseline. FPG levels were significantly higher (P < 0.0001) after six-week resistant starch bread feeding than at washout. FPG levels due to consumption of resistant starch versus control bread approached significance (P = 0.0574). Fructosamine levels were significantly lower (P = 0.0054) after control bread and resistant starch bread (P < 0.0012) consumption compared to baseline. No significant differences were found in fructosamine levels due to resistant bread intake versus control (P = 0.9692). Mean baseline HbA1c levels were 6.9% (n=15). This value was slightly lowered to 6.79% (n=14) at the end of the fourteen-week study, although statistical significance was not found. Mean ± standard errors for HbA1c values were 6.9% ± 0.18% and 6.9% ± 0.14% at baseline for the sequence groups, resistant starch first (n=7) and control treatment first (n=8) groups, respectively. Mean ± standard error HbA1c values were 6.7% ± 0.27% and 6.9% ± 0.27% at the conclusion of fourteen-week study for sequence groups, resistant starch first group (n=7) and control treatment first group, respectively. Baseline mean and standard errors C-reactive Protein (CRP) levels for male and female combined results were 0.62 ± 0.16 mg/dL (n=15). Mean CRP levels were 0.53 ± 0.12 mg/dL for resistant starch bread and 0.64 ± 0.21 mg/dL for control bread feeding periods. No significant differences were found for treatment, gender, or sequence effects for C-reactive protein levels during the fourteen-week study (P > 0.05). Mean HOMA-IR levels following six-week resistant starch and control bread consumption decreased to normal values (> 2.5), although no significant differences were found for treatment (P = 0.5923). Conclusions: Eighty-seven grams of Hi- maize™ 260 Resistant Starch added to baked loaves of bread consumed by a free-living African-American population at increased risk for type 2 diabetes did not consistently show significance in all clinical indicators and biochemical markers assessed. On the basis of the evidence in this study we do not have evidence that this amount of resistant starch in this population's diet will prevent the onset of diabetes. However, results are suggestive that higher levels of resistant starch in a more controlled experiment could reduce clinical risk factors for type 2 diabetes.
Ph. D.