scholarly journals SREBP1c-PAX4 Axis Mediates Pancreatic β-Cell Compensatory Responses Upon Metabolic Stress

Diabetes ◽  
2018 ◽  
Vol 68 (1) ◽  
pp. 81-94 ◽  
Author(s):  
Gung Lee ◽  
Hagoon Jang ◽  
Ye Young Kim ◽  
Sung Sik Choe ◽  
Jinuk Kong ◽  
...  
Keyword(s):  
Metabolic Stress ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Compensatory Responses

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 JUND regulates pancreatic β cell survival during metabolic stress

2019 ◽  
Vol 25 ◽  
pp. 95-106 ◽  
Author(s):  
Austin L. Good ◽  
Corey E. Cannon ◽  
Matthew W. Haemmerle ◽  
Juxiang Yang ◽  
Diana E. Stanescu ◽  
...  
Keyword(s):  
Cell Survival ◽  
Metabolic Stress ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals NADPH Oxidase (NOX) Targeting in Diabetes: A Special Emphasis on Pancreatic β-Cell Dysfunction

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1573
Author(s):  
Suma Elumalai ◽  
Udayakumar Karunakaran ◽  
Jun-Sung Moon ◽  
Kyu-Chang Won
Keyword(s):  
Nadph Oxidase ◽  
Cell Function ◽  
Negative Impact ◽  
Redox Homeostasis ◽  
Metabolic Stress ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Therapeutic Benefits

In type 2 diabetes, metabolic stress has a negative impact on pancreatic β-cell function and survival (T2D). Although the pathogenesis of metabolic stress is complex, an imbalance in redox homeostasis causes abnormal tissue damage and β-cell death due to low endogenous antioxidant expression levels in β-cells. Under diabetogenic conditions, the susceptibility of β-cells to oxidative damage by NADPH oxidase has been related to contributing to β-cell dysfunction. Here, we consider recent insights into how the redox response becomes deregulated under diabetic conditions by NADPH oxidase, as well as the therapeutic benefits of NOX inhibitors, which may provide clues for understanding the pathomechanisms and developing strategies aimed at the treatment or prevention of metabolic stress associated with β-cell failure.

scholarly journals Nutrient-Induced Metabolic Stress, Adaptation, Detoxification, and Toxicity in the Pancreatic β-Cell

Diabetes ◽  
2020 ◽  
Vol 69 (3) ◽  
pp. 279-290 ◽  
Author(s):  
Marc Prentki ◽  
Marie-Line Peyot ◽  
Pellegrino Masiello ◽  
S.R. Murthy Madiraju
Keyword(s):  
Metabolic Stress ◽  
Stress Adaptation ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals Deletion of β-Arrestin2 in Mice Limited Pancreatic β-Cell Expansion under Metabolic Stress through Activation of the JNK Pathway

2016 ◽  
Vol 22 (1) ◽  
pp. 74-84
Author(s):  
Ziwei Lin ◽  
Yu Zhao ◽  
Lige Song ◽  
Kaida Mu ◽  
Mingliang Zhang ◽  
...  
Keyword(s):  
Cell Expansion ◽  
Metabolic Stress ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Jnk Pathway

Adipokines as key players in β cell function and failure

2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo
Keyword(s):  
Metabolic Diseases ◽  
Cell Function ◽  
Whole Body ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Axis ◽  
Β Cell Function ◽  
Prevalence Of Obesity ◽  
Specific Factors ◽  
Whole Body Metabolism

Abstract The growing prevalence of obesity and its related metabolic diseases, mainly Type 2 diabetes (T2D), has increased the interest in adipose tissue (AT) and its role as a principal metabolic orchestrator. Two decades of research have now shown that ATs act as an endocrine organ, secreting soluble factors termed adipocytokines or adipokines. These adipokines play crucial roles in whole-body metabolism with different mechanisms of action largely dependent on the tissue or cell type they are acting on. The pancreatic β cell, a key regulator of glucose metabolism due to its ability to produce and secrete insulin, has been identified as a target for several adipokines. This review will focus on how adipokines affect pancreatic β cell function and their impact on pancreatic β cell survival in disease contexts such as diabetes. Initially, the “classic” adipokines will be discussed, followed by novel secreted adipocyte-specific factors that show therapeutic promise in regulating the adipose–pancreatic β cell axis.

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.

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