Open AccessChronic alcohol consumption potentiates the development of diabetes through pancreatic β-cell dysfunction
Author(s) -
Ji Yeon Kim,
Dae Yeon Lee,
Yoo Jeong Lee,
Keon Jae Park,
Kyu Hee Kim,
Jae Woo Kim,
WonHo Kim
Publication year - 2015
Publication title -
world journal of biological chemistry
Language(s) - English
Resource type - Journals
ISSN - 1949-8454
DOI - 10.4331/wjbc.v6.i1.1
Subject(s) - diabetes mellitus , medicine , type 2 diabetes , ethanol , insulin resistance , insulin , alcohol consumption , metabolic syndrome , endocrinology , alcohol , bioinformatics , biology , biochemistry
Chronic ethanol consumption is well established as a major risk factor for type-2 diabetes (T2D), which is evidenced by impaired glucose metabolism and insulin resistance. However, the relationships between alcohol consumption and the development of T2D remain controversial. In particular, the direct effects of ethanol consumption on proliferation of pancreatic β-cell and the exact mechanisms associated with ethanol-mediated β-cell dysfunction and apoptosis remain elusive. Although alcoholism and alcohol consumption are prevalent and represent crucial public health problems worldwide, many people believe that low-to-moderate ethanol consumption may protect against T2D and cardiovascular diseases. However, the J- or U-shaped curves obtained from cross-sectional and large prospective studies have not fully explained the relationship between alcohol consumption and T2D. This review provides evidence for the harmful effects of chronic ethanol consumption on the progressive development of T2D, particularly with respect to pancreatic β-cell mass and function in association with insulin synthesis and secretion. This review also discusses a conceptual framework for how ethanol-produced peroxynitrite contributes to pancreatic β-cell dysfunction and metabolic syndrome.