Pancreatic β-cell responses to GLP-1 after near-normalization of blood glucose in patients with type 2 diabetes

2010 ◽  
Vol 160 (1-3) ◽  
pp. 175-180 ◽  
Author(s):  
Meena Asmar ◽  
Patricia V. Højberg ◽  
Carolyn F. Deacon ◽  
Kristine Hare ◽  
Jens J. Holst ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Responses

INCRETIN AND DIABETES

2011 ◽  
pp. 5-10
Author(s):  
Huu Dang Tran
Keyword(s):  
Type 2 Diabetes ◽  
Cell Proliferation ◽  
Glycaemic Control ◽  
Animal Studies ◽  
Dipeptidyl Peptidase ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Glucose Sensitivity ◽  
Cell Glucose

The incretins are peptide hormones secreted from the gut in response to food. They increase the secretion of insulin. The incretin response is reduced in patients with type 2 diabetes so drugs acting on incretins may improve glycaemic control. Incretins are metabolised by dipeptidyl peptidase, so selectively inhibiting this enzyme increases the concentration of circulating incretins. A similar effect results from giving an incretin analogue that cannot be cleaved by dipeptidyl peptidase. Studies have identified other actions including improvement in pancreatic β cell glucose sensitivity and, in animal studies, promotion of pancreatic β cell proliferation and reduction in β cell apoptosis.

scholarly journals Islet Inflammation Impairs the Pancreatic β-Cell in Type 2 Diabetes

Physiology ◽  
2009 ◽  
Vol 24 (6) ◽  
pp. 325-331 ◽  
Author(s):  
Marc Y. Donath ◽  
Marianne Böni-Schnetzler ◽  
Helga Ellingsgaard ◽  
Jan A. Ehses
Keyword(s):  
Type 2 Diabetes ◽  
Cell Mass ◽  
Metabolic Stress ◽  
Innate Immune ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Amyloid Deposits ◽  
Impaired Insulin ◽  
Islet Inflammation

Onset of Type 2 diabetes occurs when the pancreatic β-cell fails to adapt to the increased insulin demand caused by insulin resistance. Morphological and therapeutic intervention studies have uncovered an inflammatory process in islets of patients with Type 2 diabetes characterized by the presence of cytokines, immune cells, β-cell apoptosis, amyloid deposits, and fibrosis. This insulitis is due to a pathological activation of the innate immune system by metabolic stress and governed by IL-1 signaling. We propose that this insulitis contributes to the decrease in β-cell mass and the impaired insulin secretion observed in patients with Type 2 diabetes.

scholarly journals Diminished Sphingolipid Metabolism, a Hallmark of Future Type 2 Diabetes Pathogenesis, Is Linked to Pancreatic β Cell Dysfunction

iScience ◽  
2020 ◽  
Vol 23 (10) ◽  
pp. 101566
Author(s):  
Saifur R. Khan ◽  
Yousef Manialawy ◽  
Andreea Obersterescu ◽  
Brian J. Cox ◽  
Erica P. Gunderson ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Sphingolipid Metabolism ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

scholarly journals Ameliorative Effect and Mechanism of the Purified Anthraquinone-Glycoside Preparation from Rheum Palmatum L. on Type 2 Diabetes Mellitus

Molecules ◽  
2019 ◽  
Vol 24 (8) ◽  
pp. 1454 ◽  
Author(s):  
Fang-Rong Cheng ◽  
Hong-Xin Cui ◽  
Ji-Li Fang ◽  
Ke Yuan ◽  
Ying Guo
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Blood Glucose ◽  
Cell Apoptosis ◽  
Fasting Blood Glucose ◽  
Β Cell ◽  
Diabetes Mellitus Group ◽  
Rheum Palmatum

Rheum palmatum L. is a traditional Chinese medicine with various pharmacological properties, including anti-inflammatory, antibacterial, and detoxification effects. In this study, the mechanism of the hypoglycemic effect of purified anthraquinone-Glycoside from Rheum palmatum L. (PAGR) in streptozotocin (STZ) and high-fat diet induced type 2 diabetes mellitus (T2DM) in rats was investigated. The rats were randomly divided into normal (NC), T2DM, metformin (Met), low, middle (Mid), and high (Hig) does of PAGR groups. After six weeks of continuous administration of PAGR, the serum indices and tissue protein expression were determined, and the pathological changes in liver, kidney, and pancreas tissues were observed. The results showed that compared with the type 2 diabetes mellitus group, the fasting blood glucose (FBG), total cholesterol (TC), and triglyceride (TG) levels in the serum of rats in the PAGR treatment groups were significantly decreased, while superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) levels were noticeably increased. The expression of Fas ligand (FasL), cytochrome C (Cyt-c), and caspase-3 in pancreatic tissue was obviously decreased, and the pathological damage to the liver, kidney, and pancreas was improved. These indicate that PAGR can reduce oxidative stress in rats with diabetes mellitus by improving blood lipid metabolism and enhancing their antioxidant capacity, thereby regulating the mitochondrial apoptotic pathway to inhibitβ-cell apoptosis and improve β-cell function. Furthermore, it can regulate Fas/FasL-mediated apoptosis signaling pathway to inhibit β-cell apoptosis, thereby lowering blood glucose levels and improving T2DM.

scholarly journals Appropriate therapy for type 2 diabetes mellitus in view of pancreatic β-cell glucose toxicity: “the earlier, the better”

2015 ◽  
Vol 8 (2) ◽  
pp. 183-189 ◽  
Author(s):  
Hideaki Kaneto ◽  
Taka-aki Matsuoka ◽  
Tomohiko Kimura ◽  
Atsushi Obata ◽  
Masashi Shimoda ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Glucose Toxicity ◽  
Appropriate Therapy ◽  
Cell Glucose

Insulin administration may trigger pancreatic β-cell destruction in patients with type 2 diabetes

2008 ◽  
Vol 79 (2) ◽  
pp. 220-229 ◽  
Author(s):  
Mai Nakamura ◽  
Wataru Nishida ◽  
Yuya Yamada ◽  
Daisuke Chujo ◽  
Yuji Watanabe ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Pancreatic Β Cell ◽  
Insulin Administration ◽  
Β Cell ◽  
Cell Destruction

scholarly journals Associations of Glucose Control with Insulin Sensitivity and Pancreatic β-Cell Responsiveness in Newly Presenting Type 2 Diabetes

2002 ◽  
Vol 87 (1) ◽  
pp. 198-203 ◽  
Author(s):  
Ahmed I. Albarrak ◽  
Stephen D. Luzio ◽  
Ludovic J. Chassin ◽  
Rebecca A. Playle ◽  
David R. Owens ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Plasma Glucose ◽  
Glucose Control ◽  
Interindividual Variability ◽  
Postprandial Glucose ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Fasting Plasma

We examined the ability of indices of insulin sensitivity and pancreatic β-cell responsiveness to explain interindividual variability of clinical measures of glucose control in newly presenting type 2 diabetes. Subjects with newly presenting type 2 diabetes (n = 65; 53 males and 12 females; age, 54 ± 1 yr; body mass index, 30.5 ± 0.7 kg/m2; mean ± se) underwent an insulin-modified iv glucose tolerance test to determine minimal model-derived insulin sensitivity (SI), glucose effectiveness, first-phase insulin secretion, and disposition index. Subjects also underwent a standard meal tolerance test (MTT) to measure fasting/basal (M0) and postprandial (MI) pancreatic β-cell responsiveness. Stepwise linear regression used these indices to explain interindividual variability of fasting and postprandial plasma glucose and insulin concentrations and glycated hemoglobin (HbA1C). All measures of pancreatic β-cell responsiveness (M0, MI, and first-phase insulin secretion) were negatively correlated with fasting plasma glucose (P < 0.01) and positively correlated with fasting plasma insulin (FPI) and insulin responses to MTT (P < 0.05). SI demonstrated negative correlation with FPI (P < 0.001) but failed to correlate with any glucose variable. MI followed by disposition index (composite index of insulin sensitivity and pancreatic β-cell responsiveness) were most informative in explaining interindividual variability. It was possible to explain 70–80% interindividual variability of fasting plasma glucose, FPI, HbA1C, and insulin responses to MTT, and only 25–40% interindividual variability of postprandial glucose. In conclusion, postprandial insulin deficiency is the most powerful explanatory factor of deteriorating glucose control in newly presenting type 2 diabetes. Indices of insulin sensitivity and pancreatic β-cell responsiveness explain fasting glucose and HbA1C well but fail to explain postprandial glucose.

Sign in / Sign up

Export Citation Format

Share Document