Abstract |
Defects in signaling by leptin, a hormone produced primarily by adipose tissue that informs the brain of the body's energy reserves, result in obesity in mice and humans. However, the majority of obese humans do not have abnormalities in leptin or its receptor but instead exhibit leptin resistance that could result from defects in downstream mediators of leptin action. Recently, two potential downstream mediators, agouti-related protein (Agrp) and its receptor, the melanocortin-4 receptor (Mc4r), have been identified. Agrp and Mc4r are excellent candidates for human disorders of body weight regulation and represent promising targets for pharmacological intervention in the treatment of these disorders.
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Authors | B D Wilson, M M Ollmann, G S Barsh |
Journal | Molecular medicine today
(Mol Med Today)
Vol. 5
Issue 6
Pg. 250-6
(Jun 1999)
ISSN: 1357-4310 [Print] England |
PMID | 10366820
(Publication Type: Journal Article, Review)
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Chemical References |
- AGRP protein, human
- Agouti-Related Protein
- Agrp protein, mouse
- Intercellular Signaling Peptides and Proteins
- Leptin
- Proteins
- Receptor, Melanocortin, Type 4
- Receptors, Peptide
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Topics |
- Agouti-Related Protein
- Animals
- Body Weight
(physiology)
- Humans
- Hypothalamus
(metabolism)
- Intercellular Signaling Peptides and Proteins
- Leptin
- Mice
- Mice, Transgenic
- Obesity
(physiopathology)
- Proteins
(genetics, metabolism)
- Receptor, Melanocortin, Type 4
- Receptors, Peptide
(genetics, metabolism)
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