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- Title
Globular adiponectin stimulates glucose transport in type 2 diabetic muscle.
- Authors
Kuoppamaa, Heidi; Skrobuk, Paulina; Sihvo, Maarit; Hiukka, Anne; Chibalin, Alexander V.; Zierath, Juleen R.; Koistinen, Heikki A.
- Abstract
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/m2), and from 15 non-diabetic men (59 ± 1 years, 28.0 ± 1.0 kg/m2). Skeletal muscle strips were isolated and exposed to globular adiponectin (2.5 µg/mL), insulin (120 n M) and/or AICAR (1 m M) in vitro for 1 h. Glucose transport was analysed by accumulation of intracellular 3- O-methyl [3H] glucose, phosphorylation of Akt-Ser473 and Akt-Thr308 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-Ser473 or Akt-Thr308 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 © 2008 John Wiley & Sons, Ltd.
- Publication
Diabetes/Metabolism Research & Reviews, 2008, Vol 24, Issue 7, p554
- ISSN
1520-7552
- Publication type
Article
- DOI
10.1002/dmrr.883