Abstract
The increasing incidence of obesity in developed nations is an ever-growing challenge to health care, promoting diabetes and other diseases. The hormone leptin, which is derived from adipose tissue, regulates feeding and energy expenditure. Most forms of obesity are associated with diminished responsiveness to the appetite-suppressing effects of leptin. Here we review the mechanisms by which leptin activates intracellular signals, the roles of these signals in leptin action in vivo, and mechanisms that may attenuate leptin signaling, limiting its action in obese individuals. We highlight data regarding the expression of SOCS3 (a potential mediator of leptin resistance) in the arcuate nucleus of the hypothalamus.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Adipose Tissue / metabolism*
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Animals
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Appetite Regulation / physiology*
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Energy Metabolism / physiology*
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Humans
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Hypothalamus / metabolism
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Hypothalamus / physiopathology
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Leptin / metabolism*
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Obesity / metabolism
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Obesity / physiopathology*
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / metabolism*
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Receptors, Leptin
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Repressor Proteins / metabolism
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Signal Transduction / physiology
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Suppressor of Cytokine Signaling 3 Protein
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Suppressor of Cytokine Signaling Proteins
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Transcription Factors / metabolism
Substances
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LEPR protein, human
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Leptin
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Receptors, Cell Surface
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Receptors, Leptin
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Repressor Proteins
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SOCS3 protein, human
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Suppressor of Cytokine Signaling 3 Protein
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Suppressor of Cytokine Signaling Proteins
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Transcription Factors