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Editorial
. 2014 Jun;28(6):785-9.
doi: 10.1210/me.2014-1140.

Editorial: Molecular Obesity Research: Lessons Learned?

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Free PMC article
Editorial

Editorial: Molecular Obesity Research: Lessons Learned?

Rexford S Ahima. Mol Endocrinol. .
Free PMC article

Figures

Figure 1.
Figure 1.
Parabiosis experiments in mice. Seminal studies by Coleman showed that parabiosis (cross-circulation) of ob/ob and normal WT mice resulted in weight loss in ob/ob mice. In contrast, parabiosis of db/db and WT resulted in weight loss in WT. Parabiosis of db/db and ob/ob mice resulted in weight loss in ob/ob mice. It was therefore postulated that the ob locus produces a circulating factor that inhibits food intake, and the db locus encodes the receptor for the circulating satiety factor.
Figure 2.
Figure 2.
Hypothalamic neuronal targets of leptin. Leptin inhibits feeding and increases energy expenditure by directly suppressing neuropeptide Y (NPY) and increasing proopiomelanocortin (POMC). Neurons in the arcuate nucleus expressing these peptides project to the paraventricular nucleus and lateral hypothalamic area, resulting in increases in CRH and TRH and reductions in melanin-concentrating hormone (MCH) and orexins. The net effect of leptin is to suppress appetite, reduce weight, and enhance fatty acid oxidation and insulin sensitivity in peripheral organs. AGRP, Agouti-related peptide; LRb, long leptin receptor; MC4R, melanocortin 4 receptor; MSH, melanin-stimulating hormone; TG, triglycerides.

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