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Готові списки джерел за темами / Cardioautonomic function, beta cell insulin secretion, type 2 diabetes / Статті в журналах

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Статті в журналах з теми "Cardioautonomic function, beta cell insulin secretion, type 2 diabetes"

Автор: Grafiati

Опубліковано: 11 березня 2023

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1

Khin, Phyu Phyu, Jong Han Lee, and Hee-Sook Jun. "Pancreatic Beta-cell Dysfunction in Type 2 Diabetes." European Journal of Inflammation 21 (January 30, 2023): 1721727X2311541. http://dx.doi.org/10.1177/1721727x231154152.

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Pancreatic β-cells produce and secrete insulin to maintain blood glucose levels within a narrow range. Defects in the function and mass of β-cells play a significant role in the development and progression of diabetes. Increased β-cell deficiency and β-cell apoptosis are observed in the pancreatic islets of patients with type 2 diabetes. At an early stage, β-cells adapt to insulin resistance, and their insulin secretion increases, but they eventually become exhausted, and the β-cell mass decreases. Various causal factors, such as high glucose, free fatty acids, inflammatory cytokines, and isle

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2

Masoodi, Shariq Rashid. "Decline in Beta-Cell Function among Adolescents with Type 2 Diabetes Mellitus." JMS SKIMS 20, no. 2 (2017): 115–16. http://dx.doi.org/10.33883/jms.v20i2.211.

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It is well known that beta-cell function declines over time in adults with type 2 diabetes mellitus (T2DM). The beta-cell dysfunction, initially characterized by impairment in the first phase of insulin secretion following glucose stimulation, advances to a decline in second phase insulin secretion as the disease progresses. But whether this decline in beta-cell function occurs in adolescents with T2DM is uncertain. Investigators prospectively compared beta-cell functioning over time between 39 adolescents with newly diagnosed T2DM (mean age, 15 years; body-mass index z-score, 2.4) and 32 obes

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3

Yan, Li-hui, Biao Mu, Da Pan, et al. "Association between small intestinal bacterial overgrowth and beta-cell function of type 2 diabetes." Journal of International Medical Research 48, no. 7 (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

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4

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 H

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5

Konenkov, Vladimir Iosifovich, Vadim Valerievich Klimontov, Svetlana Viktorovna Michurina, M. A. Prudnikova, and I. Ju Ishenko. "Melatonin and diabetes: from pathophysiology to the treatment perspectives." Diabetes mellitus 16, no. 2 (2013): 11–16. http://dx.doi.org/10.14341/2072-0351-3751.

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Pineal hormone melatonin synchronizes insulin secretion and glucose homeostasis with solar periods. Misalliance between melatonin-mediated circadian rhythms and insulin secretion characterizes diabetes mellitus type 1 (T1DM) and type 2 (T2DM). Insulin deficiency in T1DM is accompanied by increased melatonin production. Conversely, T2DM is characterized by diminished melatonin secretion. In genome-wide association studies the variants of melatonin receptor MT2 gene (rs1387153 and rs10830963) were associated with fasting glucose, beta-cell function and T2DM. In experimental models of diabetes me

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6

Shvarts, V. "Inflammation of adipose tissue. Part 2. Pathogenetic role in type 2 diabetes mellitus." Problems of Endocrinology 55, no. 5 (2009): 43–48. http://dx.doi.org/10.14341/probl200955543-48.

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This review deals with the role of adipose tissue inflammation (ATI) in the development of type 2 diabetes mellitus (DM2). ATI is regarded as a link between obesity and DM2. The review illustrates the involvement of main adipokines in pathogenesis of DM2 and provides a detailed description of such factors as impaired adiponectin and stimulation of cytokine production responsible for metabolic disorders, activation of lipolysis, in adipocytes, increased fatty acid and triglyceride levels, suppression of insulin activity at the receptor and intracellular levels. Adipokines, in the first place cy

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7

Makaji, Emilija, Sandeep Raha, Michael G. Wade, and Alison C. Holloway. "Effect of Environmental Contaminants on Beta Cell Function." International Journal of Toxicology 30, no. 4 (2011): 410–18. http://dx.doi.org/10.1177/1091581811405544.

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There is an increasing concern that chemicals in the environment are contributing to the global rise in the prevalence of type 2 diabetes (T2D). However, there is limited evidence for direct effects of these chemicals on beta cell function. Therefore, the goals of this study were (1) to test the hypothesis that environmental contaminants can directly affect beta cell function and (2) examine mechanistic pathways by which these contaminants could affect beta cell function. Using mouse beta TC-6 cells, we examined the acute effects of 6 substances (benzo[a]pyrene, bisphenol A [BPA], propylparabe

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8

Tarlton, Jamie M. R., Steven Patterson, and Annette Graham. "MicroRNA Sequences Modulated by Beta Cell Lipid Metabolism: Implications for Type 2 Diabetes Mellitus." Biology 10, no. 6 (2021): 534. http://dx.doi.org/10.3390/biology10060534.

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Alterations in lipid metabolism within beta cells and islets contributes to dysfunction and apoptosis of beta cells, leading to loss of insulin secretion and the onset of type 2 diabetes. Over the last decade, there has been an explosion of interest in understanding the landscape of gene expression which influences beta cell function, including the importance of small non-coding microRNA sequences in this context. This review sought to identify the microRNA sequences regulated by metabolic challenges in beta cells and islets, their targets, highlight their function and assess their possible re

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9

Kim, Yong Kyung, Lori Sussel, and Howard W. Davidson. "Inherent Beta Cell Dysfunction Contributes to Autoimmune Susceptibility." Biomolecules 11, no. 4 (2021): 512. http://dx.doi.org/10.3390/biom11040512.

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The pancreatic beta cell is a highly specialized cell type whose primary function is to secrete insulin in response to nutrients to maintain glucose homeostasis in the body. As such, the beta cell has developed unique metabolic characteristics to achieve functionality; in healthy beta cells, the majority of glucose-derived carbons are oxidized and enter the mitochondria in the form of pyruvate. The pyruvate is subsequently metabolized to induce mitochondrial ATP and trigger the downstream insulin secretion response. Thus, in beta cells, mitochondria play a pivotal role in regulating glucose st

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10

Grubelnik, Vladimir, Jan Zmazek, Rene Markovič, Marko Gosak, and Marko Marhl. "Mitochondrial Dysfunction in Pancreatic Alpha and Beta Cells Associated with Type 2 Diabetes Mellitus." Life 10, no. 12 (2020): 348. http://dx.doi.org/10.3390/life10120348.

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Type 2 diabetes mellitus is a complex multifactorial disease of epidemic proportions. It involves genetic and lifestyle factors that lead to dysregulations in hormone secretion and metabolic homeostasis. Accumulating evidence indicates that altered mitochondrial structure, function, and particularly bioenergetics of cells in different tissues have a central role in the pathogenesis of type 2 diabetes mellitus. In the present study, we explore how mitochondrial dysfunction impairs the coupling between metabolism and exocytosis in the pancreatic alpha and beta cells. We demonstrate that reduced

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11

Suleiman, Mara, Lorella Marselli, Miriam Cnop, et al. "The Role of Beta Cell Recovery in Type 2 Diabetes Remission." International Journal of Molecular Sciences 23, no. 13 (2022): 7435. http://dx.doi.org/10.3390/ijms23137435.

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Type 2 diabetes (T2D) has been considered a relentlessly worsening disease, due to the progressive deterioration of the pancreatic beta cell functional mass. Recent evidence indicates, however, that remission of T2D may occur in variable proportions of patients after specific treatments that are associated with recovery of beta cell function. Here we review the available information on the recovery of beta cells in (a) non-diabetic individuals previously exposed to metabolic stress; (b) T2D patients following low-calorie diets, pharmacological therapies or bariatric surgery; (c) human islets i

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12

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 (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 f

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13

Glaser, Benjamin, Gil Leibovich, Rafael Nesher, Svend Hartling, Christian Binder, and Erol Cerasi. "Improved beta-cell function after intensive insulin treatment in severe non-insulin-dependent diabetes." Acta Endocrinologica 118, no. 3 (1988): 365–73. http://dx.doi.org/10.1530/acta.0.1180365.

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Abstract. In Type II, non-insulin-dependent diabetes, insulin secretion is often reduced to the point where oral hypoglycaemic agents fail to control the plasma glucose level. We studied 12 patients (age 41–66 years; 4 lean, 8 obese) with Type II diabetes mellitus for 1–25 years who were uncontrolled despite maximal dose glibenclamide and metformin. After withdrawal of medication, blood glucose control was determined by measuring glucose before and 2 h after each meal for 48 h, and beta-cell function by insulin or C-peptide response to glucagon and to iv glucose. Following these tests, intensi

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14

So, Wing Yan, Wai Nam Liu, Adrian Kee Keong Teo, Guy A. Rutter, and Weiping Han. "Paired box 6 programs essential exocytotic genes in the regulation of glucose-stimulated insulin secretion and glucose homeostasis." Science Translational Medicine 13, no. 600 (2021): eabb1038. http://dx.doi.org/10.1126/scitranslmed.abb1038.

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The paired box 6 (PAX6) transcription factor is crucial for normal pancreatic islet development and function. Heterozygous mutations of PAX6 are associated with impaired insulin secretion and early-onset diabetes mellitus in humans. However, the molecular mechanism of PAX6 in controlling insulin secretion in human beta cells and its pathophysiological role in type 2 diabetes (T2D) remain ambiguous. We investigated the molecular pathway of PAX6 in the regulation of insulin secretion and the potential therapeutic value of PAX6 in T2D by using human pancreatic beta cell line EndoC-βH1, the db/db

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15

Brüning, Dennis, Kathrin Hatlapatka, Verena Lier-Glaubitz, et al. "Pharmacological inhibition of thioredoxin reductase increases insulin secretion and diminishes beta cell viability." Naunyn-Schmiedeberg's Archives of Pharmacology 394, no. 6 (2021): 1133–42. http://dx.doi.org/10.1007/s00210-020-02046-2.

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AbstractApparently, both a decrease in beta cell function and in beta cell mass contribute to the progressive worsening of type 2 diabetes. So, it is of particular interest to define factors which are relevant for the regulation of insulin secretion and at the same time for the maintenance of beta cell mass. The NADPH-thioredoxin system has a candidate role for such a dual function. Here, we have characterized the effects of a highly specific inhibitor of thioredoxin reductase, AM12, on the viability and function of insulin-secreting MIN6 cells and isolated NMRI mouse islets. Viability was che

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16

Sanlioglu, Ahter D., Bahri Karacay, Mustafa Kemal Balci, Thomas S. Griffith, and Salih Sanlioglu. "Therapeutic potential of VIP vs PACAP in diabetes." Journal of Molecular Endocrinology 49, no. 3 (2012): R157—R167. http://dx.doi.org/10.1530/jme-12-0156.

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Type 2 diabetes (T2D) is characterized by chronic insulin resistance and a progressive decline in beta-cell function. Although rigorous glucose control can reduce morbidity and mortality associated with diabetes, achieving optimal long-term glycemic control remains to be accomplished in many diabetic patients. As beta-cell mass and function inevitably decline in T2D, exogenous insulin administration is almost unavoidable as a final outcome despite the use of oral antihyperglycemic agents in many diabetic patients. Pancreatic islet cell death, but not the defect in new islet formation or beta-c

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17

Ladwa, Meera, Oluwatoyosi Bello, Olah Hakim, et al. "Ethnic differences in beta cell function occur independently of insulin sensitivity and pancreatic fat in black and white men." BMJ Open Diabetes Research & Care 9, no. 1 (2021): e002034. http://dx.doi.org/10.1136/bmjdrc-2020-002034.

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IntroductionIt is increasingly recognized that type 2 diabetes (T2D) is a heterogenous disease with ethnic variations. Differences in insulin secretion, insulin resistance and ectopic fat are thought to contribute to these variations. Therefore, we aimed to compare postprandial insulin secretion and the relationships between insulin secretion, insulin sensitivity and pancreatic fat in men of black West African (BA) and white European (WE) ancestry.Research design and methodsA cross-sectional, observational study in which 23 WE and 23 BA men with normal glucose tolerance, matched for body mass

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18

Chen, Xi, Enrique Maldonado, Ralph A. DeFronzo, and Devjit Tripathy. "Impaired Suppression of Glucagon in Obese Subjects Parallels Decline in Insulin Sensitivity and Beta-Cell Function." Journal of Clinical Endocrinology & Metabolism 106, no. 5 (2021): 1398–409. http://dx.doi.org/10.1210/clinem/dgab019.

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Abstract Aim To examine the relationship between plasma glucagon levels and insulin sensitivity and insulin secretion in obese subjects. Methods Suppression of plasma glucagon was examined in 275 obese Hispanic Americans with varying glucose tolerance. All subjects received a 2-hour oral glucose tolerance test (OGTT) and a subset (n = 90) had euglycemic hyperinsulinemic clamp. During OGTT, we quantitated suppression of plasma glucagon concentration, Matsuda index of insulin sensitivity, and insulin secretion/insulin resistance (disposition) index. Plasma glucagon suppression was compared betwe

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19

Kahleova, Hana, Andrea Tura, Marta Klementova, et al. "A Plant-Based Meal Stimulates Incretin and Insulin Secretion More Than an Energy- and Macronutrient-Matched Standard Meal in Type 2 Diabetes: A Randomized Crossover Study." Nutrients 11, no. 3 (2019): 486. http://dx.doi.org/10.3390/nu11030486.

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Diminished postprandial secretion of incretins and insulin represents one of the key pathophysiological mechanisms behind type 2 diabetes (T2D). We tested the effects of two energy- and macronutrient-matched meals: A standard meat (M-meal) and a vegan (V-meal) on postprandial incretin and insulin secretion in participants with T2D. A randomized crossover design was used in 20 participants with T2D. Plasma concentrations of glucose, insulin, C-peptide, glucagon-like peptide-1 (GLP-1), amylin, and gastric inhibitory peptide (GIP) were determined at 0, 30, 60, 120, and 180 min. Beta-cell function

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20

Robles-Cervantes, J. A., M. G. Ramos-Zavala, M. González-Ortiz, et al. "Relationship between Serum Concentration of Uric Acid and Insulin Secretion among Adults with Type 2 Diabetes Mellitus." International Journal of Endocrinology 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/107904.

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To determine the relationship between serum concentrations of uric acid and insulin secretion with hyperglycaemic clamp technique among adults with type 2 diabetes mellitus (DM2) without hyperuricemia, we carried out a cross-sectional study on 45 patients of both gender. We observed correlation between uric acid with male genderr=0.710(P=0.001). Also correlation between uric acid and total insulin secretion was positiver=0.295(P=0.049). As well as a positive correlation adjusted for body mass index was demonstrated for the first, second, and total phases of insulin secretion, respectively,r=0.

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21

Zhang, Irina X., Jianhua Ren, Suryakiran Vadrevu, Malini Raghavan, and Leslie S. Satin. "ER stress increases store-operated Ca2+ entry (SOCE) and augments basal insulin secretion in pancreatic beta cells." Journal of Biological Chemistry 295, no. 17 (2020): 5685–700. http://dx.doi.org/10.1074/jbc.ra120.012721.

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Type 2 diabetes mellitus (T2DM) is characterized by impaired glucose-stimulated insulin secretion and increased peripheral insulin resistance. Unremitting endoplasmic reticulum (ER) stress can lead to beta-cell apoptosis and has been linked to type 2 diabetes. Although many studies have attempted to link ER stress and T2DM, the specific effects of ER stress on beta-cell function remain incompletely understood. To determine the interrelationship between ER stress and beta-cell function, here we treated insulin-secreting INS-1(832/13) cells or isolated mouse islets with the ER stress–inducer tun

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22

Mohtarin, Sabreena, Md Matiur Rahman, Subrata Kumar Biswas, Forhadul Hoque Mollah, and M. Iqbal Arslan. "Study of phases of insulin secretion in pre-diabetes and newly diagnosed type 2 diabetes mellitus." Bangabandhu Sheikh Mujib Medical University Journal 8, no. 2 (2016): 85. http://dx.doi.org/10.3329/bsmmuj.v8i2.28927.

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<p><strong>Background:</strong> Insulin is released from the pancreas in a biphasic manner in response to arterial glucose concentration. The assumption has been generally made that the 30-minute response reflected first-phase insulin release, whereas the 120-minute response reflected second-phase insulin release.</p><p><strong>Objectives:</strong> The aim of this study was to identify the defect in first and second phases of insulin secretion in pre-diabetes and newly diagnosed T2DM.</p><p><strong>Methods:</strong> This case-co

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23

Sjöstrand, M., K. Carlson, H. J. Arnqvist, et al. "Assessment of beta-cell function in young patients with type 2 diabetes: arginine-stimulated insulin secretion may reflect beta-cell reserve." Journal of Internal Medicine 275, no. 1 (2013): 39–48. http://dx.doi.org/10.1111/joim.12116.

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24

Ladwa, M., O. Hakim, S. A. Amiel, and L. M. Goff. "A Systematic Review of Beta Cell Function in Adults of Black African Ethnicity." Journal of Diabetes Research 2019 (October 20, 2019): 1–17. http://dx.doi.org/10.1155/2019/7891359.

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Background. Understanding ethnic differences in beta cell function has important implications for preventative and therapeutic strategies in populations at high risk of type 2 diabetes (T2D). The existing literature, largely drawn from work in children and adolescents, suggests that beta cell function in black African (BA) populations is upregulated when compared to white Europeans (WE). Methods. A systematic literature search was undertaken in June 2018 to identify comparative studies of beta cell function between adults (>age 18 years) of indigenous/diasporic BA and WE ethnicity. All cate

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25

Ibfelt, Tobias, Christian P. Fischer, Peter Plomgaard, Gerrit van Hall та Bente Klarlund Pedersen. "The Acute Effects of Low-Dose TNF-αon Glucose Metabolism andβ-Cell Function in Humans". Mediators of Inflammation 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/295478.

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Type 2 diabetes is characterized by increased insulin resistance and impaired insulin secretion. Type 2 diabetes is also associated with low-grade inflammation and increased levels of proinflammatory cytokines such as TNF-α. TNF-αhas been shown to impair peripheral insulin signalingin vitroandin vivo. However, it is unclear whether TNF-αmay also affect endogenous glucose production (EGP) during fasting and glucose-stimulated insulin secretion (GSIS)in vivo. We hypothesized that low-dose TNF-αwould increase EGP and attenuate GSIS. Recombinant human TNF-αor placebo was infused in healthy, nondia

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26

Puddu, Alessandra, Roberta Sanguineti, Fabrizio Montecucco, and Giorgio Luciano Viviani. "Evidence for the Gut Microbiota Short-Chain Fatty Acids as Key Pathophysiological Molecules Improving Diabetes." Mediators of Inflammation 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/162021.

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In type 2 diabetes, hyperglycemia, insulin resistance, increased inflammation, and oxidative stress were shown to be associated with the progressive deterioration of beta-cell function and mass. Short-chain fatty acids (SCFAs) are organic fatty acids produced in the distal gut by bacterial fermentation of macrofibrous material that might improve type 2 diabetes features. Their main beneficial activities were identified in the decrease of serum levels of glucose, insulin resistance as well as inflammation, and increase in protective Glucagon-like peptide-1 (GLP-1) secretion. In this review, we

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27

Cabanas, E. Ann. "Maturity-Onset Diabetes of the Young: Recent Findings Indicate Insulin Resistance/Obesity Are Not Factors." Diabetes Educator 24, no. 4 (1998): 477–80. http://dx.doi.org/10.1177/014572179802400405.

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Maturity-onset diabetes of the young (MODY) is a relatively rare subtype of type 2 diabetes characterized by an early age of onset and autosomal dominant inheritance. Unlike type 2 diabetes, which is often associated with insulin resistance, MODY is caused by a primary defect in pancreatic beta-cell function resulting in a decrease in insulin secretion. Obesity is not a feature of MODY. However, environmental stressors that increase the demand for insulin, such as illness or puberty, may unmask the genetically limited insulin secretory reserve of the undiagnosed MODY patient. Euglycemia is the

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Edlund, A., M. Barghouth, M. Hühn, et al. "Defective exocytosis and processing of insulin in a cystic fibrosis mouse model." Journal of Endocrinology 241, no. 1 (2019): 45–57. http://dx.doi.org/10.1530/joe-18-0570.

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Cystic fibrosis-related diabetes (CFRD) is a common complication for patients with cystic fibrosis (CF), a disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR). The cause of CFRD is unclear, but a commonly observed reduction in first-phase insulin secretion suggests defects at the beta cell level. Here we aimed to examine alpha and beta cell function in the Cftr tm1 EUR/F508del mouse model (C57BL/6J), which carries the most common human mutation in CFTR, the F508del mutation. CFTR expression, beta cell mass, insulin granule distribution, hormone secreti

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McCarty, Mark F., and James J. DiNicolantonio. "Maintaining Effective Beta Cell Function in the Face of Metabolic Syndrome-Associated Glucolipotoxicity—Nutraceutical Options." Healthcare 10, no. 1 (2021): 3. http://dx.doi.org/10.3390/healthcare10010003.

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In people with metabolic syndrome, episodic exposure of pancreatic beta cells to elevated levels of both glucose and free fatty acids (FFAs)—or glucolipotoxicity—can induce a loss of glucose-stimulated insulin secretion (GSIS). This in turn can lead to a chronic state of glucolipotoxicity and a sustained loss of GSIS, ushering in type 2 diabetes. Loss of GSIS reflects a decline in beta cell glucokinase (GK) expression associated with decreased nuclear levels of the pancreatic and duodenal homeobox 1 (PDX1) factor that drives its transcription, along with that of Glut2 and insulin. Glucolipotox

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Lin, Edward, S. Scott Davis, Jahnavi Srinivasan, et al. "Dual Mechanism for Type-2 Diabetes Resolution after Roux-en-Y Gastric Bypass." American Surgeon 75, no. 6 (2009): 498–503. http://dx.doi.org/10.1177/000313480907500608.

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Resolution of Type-2 diabetes mellitus (DM) after weight loss surgery is well documented, but the mechanism is elusive. We evaluated the glucose-insulin metabolism of patients undergoing a Roux-en-Y gastric bypass (RYGB) using the intravenous glucose tolerance test (IVGTT) and compared it with patients who underwent laparoscopic adjustable gastric band (AB) placement. Thirty-one female patients (age range, 20 to 50 years; body mass index, 47.2 kg/m2) underwent RYGB. Nine female patients underwent AB placement and served as control subjects. All patients underwent IVGTT at baseline and 1 month

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Velikova, Tsvetelina V., Plamena P. Kabakchieva, Yavor S. Assyov, and Tsvetoslav А. Georgiev. "Targeting Inflammatory Cytokines to Improve Type 2 Diabetes Control." BioMed Research International 2021 (September 13, 2021): 1–12. http://dx.doi.org/10.1155/2021/7297419.

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Type 2 diabetes (T2D) is one of the most common chronic metabolic disorders in adulthood worldwide, whose pathophysiology includes an abnormal immune response accompanied by cytokine dysregulation and inflammation. As the T2D-related inflammation and its progression were associated with the balance between pro and anti-inflammatory cytokines, anticytokine treatments might represent an additional therapeutic option for T2D patients. This review focuses on existing evidence for antihyperglycemic properties of disease-modifying antirheumatic drugs (DMARDs) and anticytokine agents (anti-TNF-α, ant

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Okura, Tsuyoshi, Risa Nakamura, Yuichi Ito, et al. "Significance of pancreatic duodenal homeobox-1 (PDX-1) genetic polymorphism in insulin secretion in Japanese patients with type 2 diabetes." BMJ Open Diabetes Research & Care 10, no. 5 (2022): e002908. http://dx.doi.org/10.1136/bmjdrc-2022-002908.

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IntroductionPancreatic and duodenal homeobox factor-1 (PDX-1) is an imperative gene for insulin secretion in maturity-onset diabetes of the young 4. PDX-1 gene polymorphism was associated with lower first-phase insulin secretion in a genome-wide association study of intravenous glucose tolerance test. It was not associated with type 2 diabetes risk and insulin secretion in a genome-wide oral glucose tolerance test study. However, there have been no reports of overt type 2 diabetes and insulin resistance evaluation using a glucose clamp. We investigated PDX-1 polymorphism, insulin secretion, an

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Schultz, Julia, Rica Waterstradt, Tobias Kantowski, et al. "Precise expression of Fis1 is important for glucose responsiveness of beta cells." Journal of Endocrinology 230, no. 1 (2016): 81–91. http://dx.doi.org/10.1530/joe-16-0111.

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Mitochondrial network functionality is vital for glucose-stimulated insulin secretion in pancreatic beta cells. Altered mitochondrial dynamics in pancreatic beta cells are thought to trigger the development of type 2 diabetes mellitus. Fission protein 1 (Fis1) might be a key player in this process. Thus, the aim of this study was to investigate mitochondrial morphology in dependence of beta cell function, after knockdown and overexpression of Fis1. We demonstrate that glucose-unresponsive cells with impaired glucose-stimulated insulin secretion (INS1-832/2) showed decreased mitochondrial dynam

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Kufe, Clement N., Lisa K. Micklesfield, Maphoko Masemola, et al. "Increased risk for type 2 diabetes in relation to adiposity in middle-aged Black South African men compared to women." European Journal of Endocrinology 186, no. 5 (2022): 523–33. http://dx.doi.org/10.1530/eje-21-0527.

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Aims Despite a higher prevalence of overweight/obesity in Black South African women compared to men, the prevalence of type 2 diabetes (T2D) does not differ. We explored if this could be due to sex differences in insulin sensitivity, clearance and/or beta-cell function and also sex-specific associations with total and regional adiposity. Methods This cross-sectional study included 804 Black South African men (n = 388) and women (n = 416). Dual-energy X-ray absorptiometry was used to measure total and regional adiposity. Insulin sensitivity (Matsuda index), secretion (C-peptide index) and clear

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Bonora, Enzo, Maddalena Trombetta, Marco Dauriz, et al. "Chronic complications in patients with newly diagnosed type 2 diabetes: prevalence and related metabolic and clinical features: the Verona Newly Diagnosed Type 2 Diabetes Study (VNDS) 9." BMJ Open Diabetes Research & Care 8, no. 1 (2020): e001549. http://dx.doi.org/10.1136/bmjdrc-2020-001549.

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IntroductionWe explored the presence of chronic complications in subjects with newly diagnosed type 2 diabetes referred to the Verona Diabetes Clinic. Metabolic (insulin secretion and sensitivity) and clinical features associated with complications were also investigated.Research design and methodsThe comprehensive assessment of microvascular and macrovascular complications included detailed medical history, resting ECG, ultrasonography of carotid and lower limb arteries, quantitative neurological evaluation, cardiovascular autonomic tests, ophthalmoscopy, kidney function tests. Insulin sensit

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Oh, Yoon Sin, and Hee-Sook Jun. "Role of Bioactive Food Components in Diabetes Prevention: Effects on Beta-Cell Function and Preservation." Nutrition and Metabolic Insights 7 (January 2014): NMI.S13589. http://dx.doi.org/10.4137/nmi.s13589.

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Bioactive compounds found in fruits and vegetables can have anti-oxidant, anti-inflammatory, and anti-carcinogenic effects and can be protective against various diseases and metabolic disorders. These beneficial effects make them good candidates for the development of new functional foods with potential protective and preventive properties for type 1 and type 2 diabetes. This review summarizes the most relevant results concerning the effects of various bioactive compounds such as flavonoids, vitamins, and carotenoids on several aspects of beta-cell functionality. Studies using animal models wi

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Oberhauser, Lucie, and Pierre Maechler. "Lipid-Induced Adaptations of the Pancreatic Beta-Cell to Glucotoxic Conditions Sustain Insulin Secretion." International Journal of Molecular Sciences 23, no. 1 (2021): 324. http://dx.doi.org/10.3390/ijms23010324.

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Over the last decades, lipotoxicity and glucotoxicity emerged as established mechanisms participating in the pathophysiology of obesity-related type 2 diabetes in general, and in the loss of β-cell function in particular. However, these terms hold various potential biological processes, and it is not clear what precisely they refer to and to what extent they might be clinically relevant. In this review, we discuss the basis and the last advances of research regarding the role of free fatty acids, their metabolic intracellular pathways, and receptor-mediated signaling related to glucose-stimula

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Marrano, Nicola, Rosaria Spagnuolo, Giuseppina Biondi, et al. "Effects of Extra Virgin Olive Oil Polyphenols on Beta-Cell Function and Survival." Plants 10, no. 2 (2021): 286. http://dx.doi.org/10.3390/plants10020286.

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Extra virgin olive oil (EVOO) is a major component of the Mediterranean diet and is appreciated worldwide because of its nutritional benefits in metabolic diseases, including type 2 diabetes (T2D). EVOO contains significant amounts of secondary metabolites, such as phenolic compounds (PCs), that may positively influence the metabolic status. In this study, we investigated for the first time the effects of several PCs on beta-cell function and survival. To this aim, INS-1E cells were exposed to 10 μM of the main EVOO PCs for up to 24 h. Under these conditions, survival, insulin biosynthesis, gl

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Deep, Hardeep Singh, Barjinder Pal Singh, and Shalinder Pal Singh. "Evaluation of serum c-peptide levels in type 2 diabetics in Punjabi population." International Journal of Advances in Medicine 4, no. 4 (2017): 1026. http://dx.doi.org/10.18203/2349-3933.ijam20173225.

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Background: Diabetes mellitus is a chronic metabolic and endocrine disorder characterized by chronic hyperglycemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action or both. It is a major cause of mortality and morbidity worldwide. Human insulin and c-peptide are synthesized as a single polypeptide chain known as Proinsulin in the pancreatic beta cells. Serum insulin measurement gives a wrong value of insulin secretion, because insulin after its secretion into the portal vein, passes through the liver where approximately 5

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Bosma, Karin J., Cecilia E. Kaiser, Michelle E. Kimple, and Maureen Gannon. "Effects of Arachidonic Acid and Its Metabolites on Functional Beta-Cell Mass." Metabolites 12, no. 4 (2022): 342. http://dx.doi.org/10.3390/metabo12040342.

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Arachidonic acid (AA) is a polyunsaturated 20-carbon fatty acid present in phospholipids in the plasma membrane. The three primary pathways by which AA is metabolized are mediated by cyclooxygenase (COX) enzymes, lipoxygenase (LOX) enzymes, and cytochrome P450 (CYP) enzymes. These three pathways produce eicosanoids, lipid signaling molecules that play roles in biological processes such as inflammation, pain, and immune function. Eicosanoids have been demonstrated to play a role in inflammatory, renal, and cardiovascular diseases as well type 1 and type 2 diabetes. Alterations in AA release or

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Voĭchik, É. A. "Victosa: the experience with clinical application in patients with type 2 diabetes mellitus." Problems of Endocrinology 57, no. 3 (2011): 37–41. http://dx.doi.org/10.14341/probl201157337-41.

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Type 2 diabetes mellitus that comes from insulin resistance and deficit of insulin secretion has recently been described as associated with reduced incretin effect. The efficiency of traditional hypoglycemic therapy (metformin, secretagogues, glitazones, insulin) gradually decreases due to progressive loss of functioning beta-cell mass. The achievement of target blood glucose levels for the prevention of complications and cardiovascular pathology as a rule leads to such adverse events as increased body weight and hypoglycemia. The search for an «ideal» drug included the study and the use of in

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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 (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

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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 (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 a

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Bronczek, Gabriela Alves, Gabriela Moreira Soares, Carine Marmentini, Antonio Carlos Boschero, and José Maria Costa-Júnior. "Resistance Training Improves Beta Cell Glucose Sensing and Survival in Diabetic Models." International Journal of Molecular Sciences 23, no. 16 (2022): 9427. http://dx.doi.org/10.3390/ijms23169427.

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Resistance training increases insulin secretion and beta cell function in healthy mice. Here, we explored the effects of resistance training on beta cell glucose sensing and survival by using in vitro and in vivo diabetic models. A pancreatic beta cell line (INS-1E), incubated with serum from trained mice, displayed increased insulin secretion, which could be linked with increased expression of glucose transporter 2 (GLUT2) and glucokinase (GCK). When cells were exposed to pro-inflammatory cytokines (in vitro type 1 diabetes), trained serum preserved both insulin secretion and GCK expression,

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Picton, Sally F., Peter R. Flatt, and Neville H. McClenaghan. "Differential Acute and Long Term Actions of Succinic Acid Monomethyl Ester Exposure on Insulin-Secreting BRIN-BD11 Cells." International Journal of Experimental Diabetes Research 2, no. 1 (2001): 19–27. http://dx.doi.org/10.1155/edr.2001.19.

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Esters of succinic acid are potent insulin secretagogues, and have been proposed as novel antidiabetic agents for type 2 diabetes. This study examines the effects of acute and chronic exposure to succinic acid monomethyl ester (SAM) on insulin secretion, glucose metabolism and pancreatic beta cell function using the BRIN-BD11 cell line. SAM stimulated insulin release in a dose-dependent manner at both non-stimulatory (1.1mM) and stimulatory (16.7mM) glucose. The depolarizing actions of arginine also stimulated a significant increase in SAM-induced insulin release but 2-ketoisocaproic acid (KIC

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Sayers, Sophie R., Rebecca L. Beavil, Nicholas H. F. Fine, et al. "Structure-functional changes in eNAMPT at high concentrations mediate mouse and human beta cell dysfunction in type 2 diabetes." Diabetologia 63, no. 2 (2019): 313–23. http://dx.doi.org/10.1007/s00125-019-05029-y.

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Abstract Aims/hypothesis Progressive decline in functional beta cell mass is central to the development of type 2 diabetes. Elevated serum levels of extracellular nicotinamide phosphoribosyltransferase (eNAMPT) are associated with beta cell failure in type 2 diabetes and eNAMPT immuno-neutralisation improves glucose tolerance in mouse models of diabetes. Despite this, the effects of eNAMPT on functional beta cell mass are poorly elucidated, with some studies having separately reported beta cell-protective effects of eNAMPT. eNAMPT exists in structurally and functionally distinct monomeric and

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Lv, Wu, Jialin Zhang, Ao Jiao, Bowen Wang, Baomin Chen, and Jie Lin. "Resveratrol attenuates hIAPP amyloid formation and restores the insulin secretion ability in hIAPP-INS1 cell line via enhancing autophagy." Canadian Journal of Physiology and Pharmacology 97, no. 2 (2019): 82–89. http://dx.doi.org/10.1139/cjpp-2016-0686.

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It has been proved that human islet amyloid polypeptide (hIAPP), the main constituent of islet amyloid deposition, is one of the important factors that can induce type 2 diabetes or graft failure after islet transplantation. As there is no research on whether resveratrol degrading the amyloid deposition by its special chemical structure or enhancing autophagy had been published, we decided to detect the function of resveratrol in degrading the amyloid deposition in pancreatic beta cells. We established stable hIAPP-INS1 cell line via transfecting INS1 cells by lentivirus that overexpresses hIA

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Chabosseau, Pauline, Guy A. Rutter, and Steven J. Millership. "Importance of Both Imprinted Genes and Functional Heterogeneity in Pancreatic Beta Cells: Is There a Link?" International Journal of Molecular Sciences 22, no. 3 (2021): 1000. http://dx.doi.org/10.3390/ijms22031000.

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Diabetes mellitus now affects more than 400 million individuals worldwide, with significant impacts on the lives of those affected and associated socio-economic costs. Although defects in insulin secretion underlie all forms of the disease, the molecular mechanisms which drive them are still poorly understood. Subsets of specialised beta cells have, in recent years, been suggested to play critical roles in “pacing” overall islet activity. The molecular nature of these cells, the means through which their identity is established and the changes which may contribute to their functional demise an

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Ohta, Akio, Hiroyuki Kato, Katura Murayama, et al. "Effect of insulin glargine on endogenous insulin secretion and beta-cell function in Japanese type 2 diabetic patients using oral antidiabetic drugs." Endocrine Journal 61, no. 1 (2014): 13–18. http://dx.doi.org/10.1507/endocrj.ej13-0304.

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Hughes, Alice E., Andrew T. Hattersley, Sarah E. Flanagan, and Rachel M. Freathy. "Two decades since the fetal insulin hypothesis: what have we learned from genetics?" Diabetologia 64, no. 4 (2021): 717–26. http://dx.doi.org/10.1007/s00125-021-05386-7.

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AbstractIn 1998 the fetal insulin hypothesis proposed that lower birthweight and adult-onset type 2 diabetes are two phenotypes of the same genotype. Since then, advances in research investigating the role of genetics affecting insulin secretion and action have furthered knowledge of fetal insulin-mediated growth and the biology of type 2 diabetes. In this review, we discuss the historical research context from which the fetal insulin hypothesis originated and consider the position of the hypothesis in light of recent evidence. In summary, there is now ample evidence to support the idea that v

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