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Key enzyme in leptin-induced anorexia

Kevin D. Niswender, Gregory J. Morton, Walter H. Stearns, Christopher J. Rhodes, Martin G. Myers and Michael W. Schwartz ()
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Kevin D. Niswender: Endocrinology and Nutrition, University of Washington School of Medicine and Harborview Medical Center
Gregory J. Morton: Endocrinology and Nutrition, University of Washington School of Medicine and Harborview Medical Center
Walter H. Stearns: Joslin Diabetes Center, Harvard Medical School
Christopher J. Rhodes: Pacific Northwest Research Institute
Martin G. Myers: Joslin Diabetes Center, Harvard Medical School
Michael W. Schwartz: Endocrinology and Nutrition, University of Washington School of Medicine and Harborview Medical Center

Nature, 2001, vol. 413, issue 6858, 794-795

Abstract: Abstract Leptin is a key hormonal regulator of energy balance that acts upon hypothalamic neurons to reduce food intake, but the intracellular mechanisms involved are incompletely understood. Here we show that systemic administration of leptin in rats activates the enzyme phosphatidylinositol-3-OH kinase (PI(3)K) in the hypothalamus and that intracerebro-ventricular (i.c.v.) infusion of inhibitors of this enzyme prevents leptin-induced anorexia. Our results indicate that PI(3)K is a crucial enzyme in the signal-transduction pathway that links hypothalamic leptin to reduced food intake.

Date: 2001
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DOI: 10.1038/35101657

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