scholarly journals Diabetes Mellitus in a Patient With Lafora Disease: Possible Links With Pancreatic β-Cell Dysfunction and Insulin Resistance

2019 ◽  
Vol 6 ◽  
Author(s):  
Ramona C. Nicolescu ◽  
Sara Al-Khawaga ◽  
Berge A. Minassian ◽  
Khalid Hussain
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Pancreatic Β Cell ◽  
Lafora Disease ◽  
Β Cell ◽  
Cell Dysfunction

scholarly journals Risk Factors for Type 2 Diabetes Mellitus Preceded by β-Cell Dysfunction, Insulin Resistance, or Both in Older Adults

2013 ◽  
Vol 177 (12) ◽  
pp. 1418-1429 ◽  
Author(s):  
Fumiaki Imamura ◽  
Kenneth J. Mukamal ◽  
James B. Meigs ◽  
José A. Luchsinger ◽  
Joachim H. Ix ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Older Adults ◽  
Type 2 Diabetes Mellitus ◽  
Β Cell ◽  
Cell Dysfunction

scholarly journals Elevated Medium-Chain Acylcarnitines Are Associated With Gestational Diabetes Mellitus and Early Progression to Type 2 Diabetes and Induce Pancreatic β-Cell Dysfunction

Diabetes ◽  
2018 ◽  
Vol 67 (5) ◽  
pp. 885-897 ◽  
Author(s):  
Battsetseg Batchuluun ◽  
Dana Al Rijjal ◽  
Kacey J. Prentice ◽  
Judith A. Eversley ◽  
Elena Burdett ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Medium Chain ◽  
Cell Dysfunction ◽  
Early Progression

scholarly journals Interorgan Crosstalk Contributing to β-Cell Dysfunction

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Katsuya Tanabe ◽  
Kikuko Amo-Shiinoki ◽  
Masayuki Hatanaka ◽  
Yukio Tanizawa
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Current Knowledge ◽  
Cell Mass ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Circulating Levels ◽  
Insulin Secretory Capacity ◽  
Secretory Capacity

Type 2 diabetes mellitus (T2DM) results from pancreatic β-cell failure in the setting of insulin resistance. In the early stages of this disease, pancreatic β-cells meet increased insulin demand by both enhancing insulin-secretory capacity and increasing β-cell mass. As the disease progresses, β-cells fail to maintain these compensatory responses. This involves both extrinsic signals and mediators intrinsic to β-cells, which adversely affect β-cells by impairing insulin secretion, decreasing proliferative capacities, and ultimately causing apoptosis. In recent years, it has increasingly been recognized that changes in circulating levels of various factors from other organs play roles in β-cell dysfunction and cellular loss. In this review, we discuss current knowledge of interorgan communications underlying β-cell failure during the progression of T2DM.

Fatty acids and glucolipotoxicity in the pathogenesis of Type 2 diabetes

2008 ◽  
Vol 36 (3) ◽  
pp. 348-352 ◽  
Author(s):  
Miriam Cnop
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Cell Loss ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

The prevalence of Type 2 diabetes is increasing dramatically as a result of the obesity epidemic, and poses a major health and socio-economic burden. Type 2 diabetes develops in individuals who fail to compensate for insulin resistance by increasing pancreatic insulin secretion. This insulin deficiency results from pancreatic β-cell dysfunction and death. Western diets rich in saturated fats cause obesity and insulin resistance, and increase levels of circulating NEFAs [non-esterified (‘free’) fatty acids]. In addition, they contribute to β-cell failure in genetically predisposed individuals. NEFAs cause β-cell apoptosis and may thus contribute to progressive β-cell loss in Type 2 diabetes. The molecular pathways and regulators involved in NEFA-mediated β-cell dysfunction and apoptosis are beginning to be understood. We have identified ER (endoplasmic reticulum) stress as one of the molecular mechanisms implicated in NEFA-induced β-cell apoptosis. ER stress was also proposed as a mechanism linking high-fat-diet-induced obesity with insulin resistance. This cellular stress response may thus be a common molecular pathway for the two main causes of Type 2 diabetes, namely insulin resistance and β-cell loss. A better understanding of the molecular mechanisms contributing to pancreatic β-cell loss will pave the way for the development of novel and targeted approaches to prevent Type 2 diabetes.

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