期刊
DIABETES-METABOLISM RESEARCH AND REVIEWS
卷 24, 期 7, 页码 554-562出版社
WILEY
DOI: 10.1002/dmrr.883
关键词
adiponectin; adiponectin receptors; Akt; AMPK; glucose transport; insulin resistance; type 2 diabetes
资金
- Finnish Cultural Foundation
- Finnish Diabetes Research Foundation
- Finnish Foundation for Cardiovascular Research
- Maud Kuistila Foundation
- Novo Nordisk Foundation
- Paulo Foundation
- Sigrid Juselius Foundation
- Helsinki University Central Hospital (EVO-funding)
- Swedish Research Council
- Swedish Diabetes Association
- Foundation for Scientific Studies of Diabetology
- Strategic Research Foundation (INGVAR II)
- Commission of the European Communities [LSHM-CT-2004-005272 EXGENESIS, LSHMCT-2004-512013 EUGENE2]
Background Adiponectin acts as an insulin sensitizer in rodent models. The direct effect of adiponectin in intact type 2 diabetic muscle is unknown. We examined whether adiponectin stimulates glucose transport in isolated skeletal muscle strips from type 2 diabetic men. Methods We obtained open muscle biopsies from 12 men with type 2 diabetes (56 +/- 1 years, 30.5 +/- 1.1 kg/m(2)), and from 15 non-diabetic men (59 +/- 1 years, 28.0 +/- 1.0 kg/m(2)). Skeletal muscle strips were isolated and exposed to globular adiponectin (2.5 mu g/mL), insulin (120 nM) and/or AICAR (1 mM) in vitro for 1 h. Glucose transport was analysed by accumulation of intracellular 3-O-methyl [H-3] glucose, phosphorylation of Akt-Ser(473) and Akt-Thr(308) was determined using phosphospecific antibodies, and adiponectin receptor 1 and 2 content was measured using specific antibodies. Results Globular adiponectin increased glucose transport rate by 1.3-fold (P < 0.01) in type 2 diabetic, but not in non-diabetic muscle. Insulin-stimulated glucose transport rate was unaltered by exposure to globular adiponectin in either group. AICAR increased glucose transport and enhanced insulin-stimulated glucose transport in type 2 diabetic and non-diabetic muscles. Insulin-stimulated phosphorylation of Akt-Ser(473) or Akt-Thr(308) was comparable in type 2 diabetic and non-diabetic muscles and unaltered by the, addition of globular adiponectin in either group. Adiponectin receptor expression was similar in skeletal muscle from type 2 diabetic and non-diabetic men. Conclusions Globular adiponectin directly increases glucose transport in skeletal muscle from type 2 diabetic patients. This may occur via Akt-independent signalling routes. Copyright (c) 2008 John Wiley & Sons, Ltd.
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