Abstract |
The mechanism of insulin resistance in obesity was examined in ten obese (BMI 33 +/- 1 kg/m2) and nine lean (BMI 22 +/- 1 kg/m2) Caucasian women during a hyperglycemic-hyperinsulinemic clamp using 13C and 31P nuclear magnetic resonance (NMR) spectroscopy to measure rates of muscle glycogen synthesis and intramuscular glucose-6-phosphate (G-6-P) concentrations. Under similar steady-state plasma concentrations of glucose (approximately 11 mmol/l) and insulin (approximately 340 pmol/l), rates of muscle glycogen synthesis were reduced approximately 70% in the obese subjects (52 +/- 8 micromol/[l muscle-min]) as compared with the rates in the lean subjects (176 +/- 22 micromol/[l muscle-min]; P < 0.0001). Basal concentrations of intramuscular G-6-P were similar in the obese and lean subjects; but during the clamp, G-6-P failed to increase in the obese group (deltaG-6-P obese 0.044 +/- 0.011 vs. lean 0.117 +/- 0.011 mmol/l muscle; P < 0.001), reflecting decreased muscle glucose transport and/or phosphorylation activity. We conclude that insulin resistance in obesity can be mostly attributed to impairment of insulin-stimulated muscle glycogen synthesis due to a defect in glucose transport and/or phosphorylation activity.
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Authors | K F Petersen, R Hendler, T Price, G Perseghin, D L Rothman, N Held, J M Amatruda, G I Shulman |
Journal | Diabetes
(Diabetes)
Vol. 47
Issue 3
Pg. 381-6
(Mar 1998)
ISSN: 0012-1797 [Print] United States |
PMID | 9519743
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
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Topics |
- Adult
- Cohort Studies
- Female
- Glucose
(metabolism)
- Glucose Clamp Technique
- Glycogen
(metabolism)
- Humans
- Insulin Resistance
(physiology)
- Magnetic Resonance Spectroscopy
- Obesity
(blood, metabolism, physiopathology)
- White People
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