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. 2002 May;109(10):1345-50.
doi: 10.1172/JCI15001.

Leptin reverses insulin resistance and hepatic steatosis in patients with severe lipodystrophy

Kitt Falk Petersen  1 , Elif Arioglu Oral, Sylvie Dufour, Douglas Befroy, Charlotte Ariyan, Chunli Yu, Gary W Cline, Alex M DePaoli, Simeon I Taylor, Phillip Gorden, Gerald I Shulman
Affiliations

Leptin reverses insulin resistance and hepatic steatosis in patients with severe lipodystrophy

Kitt Falk Petersen et al. J Clin Invest. 2002 May.

Abstract

Lipodystrophy is a rare disorder that is characterized by selective loss of subcutaneous and visceral fat and is associated with hypertriglyceridemia, hepatomegaly, and disordered glucose metabolism. It has recently been shown that chronic leptin treatment ameliorates these abnormalities. Here we show that chronic leptin treatment improves insulin-stimulated hepatic and peripheral glucose metabolism in severely insulin-resistant lipodystrophic patients. This improvement in insulin action was associated with a marked reduction in hepatic and muscle triglyceride content. These data suggest that leptin may represent an important new therapy to reverse the severe hepatic and muscle insulin resistance and associated hepatic steatosis in patients with lipodystrophy.

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Figures

Figure 1
Figure 1
Basal rates of glucose production and percent suppression of hepatic glucose production in subjects during hyperinsulinemic-euglycemic clamp.
Figure 2
Figure 2
Rates of glucose infusion and whole-body glucose metabolism during the hyperinsulinemic-euglycemic clamp study.
Figure 3
Figure 3
Basal rates of glycerol turnover.
Figure 4
Figure 4
Effect of recombinant leptin treatment on glucose infusion rates and percent suppression of glucose production in lipodystrophic subjects during the hyperinsulinemic-euglycemic clamp study.
Figure 5
Figure 5
Effect of recombinant leptin treatment on muscle and hepatic triglyceride content (relative to baseline) in lipodystrophic subjects. Inset above: Effect of recombinant leptin treatment on intramyocellular triglyceride content and muscle fatty acyl CoA concentrations in a lipodystrophic subject (NIH-6).
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References

    1. Rossini AA, et al. Metabolic and endocrine studies in a case of lipoatrophic diabetes. Metabolism. 1977;26:637–650. - PubMed
    1. Reitman ML, Arioglu E, Gavrilova O, Taylor SI. Lipoatrophy revisited. Trends Endocrinol Metab. 2000;11:410–416. - PubMed
    1. Arioglu E, et al. Efficacy and safety of troglitazone in the treatment of lipodystrophy syndromes. Ann Intern Med. 2000;133:263–274. - PubMed
    1. Shimomura I, Hammer RE, Ikemoto S, Brown MS, Goldstein JL. Leptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystrophy. Nature. 1999;401:73–76. - PubMed
    1. Oral EA, et al. Efficacy and safety of leptin replacement in lipodystrophy. N Engl J Med. 2002;346:570–578. - PubMed

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