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Type 2 diabetes mellitus is a chronic metabolic disorder associated with insulin resistance and is common in those over the age of 60, but the mechanisms that cause insulin resistance later in life have been unclear. In the May 16 Science, Kitt Falk Petersen and colleagues at Yale University School of Medicine show that an age-associated decline in mitochondrial function contributes to insulin resistance in the elderly (Science, 300:1140-1142, May 16, 2003).
Petersen et al. studied healthy, lean, elderly, and young participants matched for lean body mass and fat mass. They observed that elderly participants were markedly insulin-resistant compared with younger controls, and this resistance was attributable to reduced insulin-stimulated muscle glucose metabolism. In addition, they used nuclear magnetic resonance spectroscopy and showed that insulin resistance in the elderly was associated with increased fat accumulation in muscle and liver tissue and a 40% reduction in mitochondrial oxidative and phosphorylation activity.
"Because mitochondrial oxidative and phosphorylation activity is the major source of energy in most organs, including the brain, our data add support to the hypothesis that a decline in mitochondrial oxidative and phosphorylation energy production may also have an important role in aging," conclude the authors.
References
| 1. | | S.B. Wheatcroft, "Pathophysiological implications of insulin resistance on vascular endothelial function," Diabetic Medicine, 20:255-268, April 2003.
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| 2. | | [http://www.sciencemag.org]
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| | | K.F. Petersen et al., "Mitochondrial dysfunction in the elderly: possible role in insulin resistance," Science, 300:1140-1142, May 16, 2003. Return to citation in text:
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| 3. | | [http://info.med.yale.edu/ysm/]
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| | | Yale University School of Medicine Return to citation in text:
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