期刊
CLINICAL SCIENCE
卷 116, 期 1-2, 页码 99-111出版社
PORTLAND PRESS LTD
DOI: 10.1042/CS20080090
关键词
endoplasmic reticulum stress; inflammation; mitochondrion; obesity; pancreatic beta-cell; Type 2 diabetes
资金
- National Institutes of Health [DK062948, DK060837]
- Graetz Fund
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK062948, R01DK060837] Funding Source: NIH RePORTER
T2DM (Type 2 diabetes mellitus) has reached epidemic proportions worldwide, exerting major health consequences at an individual and public health level alike. Unfortunately, the molecular pathophysiology of diabetes remains incompletely understood, impairing progress towards more effective prevention and treatment strategies. Although the rapid increase in the prevalence of insulin resistance and T2DM over the past several decades highlights a major environmental contribution related to overnutrition, obesity and inactivity, susceptibility is likely to reflect individual differences in complex gene-environment interactions. In the present review, we focus on mediators of genetic and environmental risk for T2DM at a molecular level.
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