Adiponectin and its gene variants as risk factors for insulin resistance, the metabolic syndrome and cardiovascular disease

被引:121
作者
Gable, D. R.
Hurel, S. J.
Humphries, S. E.
机构
[1] Royal Free & UCL Med Sch, Rayne Inst, British Heart Fdn Labs, Ctr Cardiovasc Genet, London WC1E 6JF, England
[2] UCLH NHS Fdn Trust, Dept Endocrinol & Diabet, London NW1 2PQ, England
关键词
adiponectin; single nucleotide polymorphism; metabolic syndrome; type 2 diabetes mellitus; cardiovascular disease;
D O I
10.1016/j.atherosclerosis.2006.02.010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The increasing prevalence of obesity and metabolic syndrome/insulin resistance has attracted considerable interest due to their identification as risk factors for cardiovascular disease and, hence, targets for cardiovascular disease prevention. This review focuses on adiponectin, the most profusely secreted protein from adipose tissue, which itself is being increasingly recognised as an important and very active endocrine organ, secreting a wide range of biologically active substances known as adipokines or adipocytokines. Adiponectin has been demonstrated to have insulin sensitising effects, and secretion of adiponectin is reduced as adipose tissue mass increases. Adiponectin has also been demonstrated to have anti-inflammatory and anti-atherogenic properties, and is independently associated with cardiovascular disease. The evidence that suggests adiponectin plays a role in the relationship between obesity and insulin resistance, and also insulin resistance and cardiovascular disease, is examined. Variation in the adiponectin gene is one tool to determine whether this relationship is causal. The association of identified variants with human disease, specifically obesity and its consequences, type 2 diabetes and cardiovascular disease is reviewed. This data may enable patients at greater risk of the adverse effects of obesity to be identified and, as such, benefit from more targeted therapy of its consequences. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:231 / 244
页数:14
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