Why the study?
Do obesity, T2DM, and genetic predisposition to T2DM impair insulin-stimulated muscle glucose transport and phosphorylation compared to lean controls?
Population
Lean and obese nondiabetic subjects, lean and obese type 2 diabetic subjects, and normal glucose-tolerant…
Comparison
Euglycemic insulin clamp (40 mU.m.min) with… vs Lean controls
Design
Cross-sectional
Follow-up
135 minutes (acute experimental procedure)
Authors
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Links obesity, T2DM, and genetic risk to muscle insulin resistance; leaves open relative contributions of transport versus phosphorylation defects.
Do obesity, T2DM, and genetic predisposition to T2DM impair insulin-stimulated muscle glucose transport and phosphorylation compared to lean controls?
Obese nondiabetic, lean T2DM, and offspring of T2DM parents manifest moderate-to-severe muscle insulin resistance characterized by decreased insulin-stimulated glucose transport and phosphorylation, with the defect in phosphorylation likely exceeding that of transport.
Pendergrass et al. (2006) studied this question.
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