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Am J Physiol Endocrinol Metab (July 15, 2003). doi:10.1152/ajpendo.00186.2003
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Submitted on April 25, 2003
Accepted on July 8, 2003

Abnormalities of Leptin and Ghrelin Regulation in Obesity-prone Juvenile Rats

Barry E. Levin1*, Ambrose A. Dunn-Meynell1, Matt R. Ricci2, and David E. Cummings3

1 Department of Neurology Service, Veterans Affairs Medical Center, E. Orange, NJ, USA; Department of Neurosciences, New Jersey Medical School, Newark, NJ, USA
2 Research Diets, Inc., New Brunswick, NJ, USA
3 Endocrine Division, Department of Medicine, University of Washington, Seattle, WA, USA

* To whom correspondence should be addressed. E-mail: levin{at}umdnj.edu.

Rats selectively bred to develop diet-induced obesity (DIO) spontaneously gain more body weight between 5-7wk of age than do those bred to be diet-resistant (DR). Here, chow-fed DIO rats ate 9% more and gained 19% more body weight from 5-6wk of age than did DR rats but had comparable leptin and insulin levels. However, 6wk old DIO rats had 29% lower plasma ghrelin levels at dark onset but equivalent levels 6h later, compared to DR rats. When subsequently fed a high energy (HE; 31% fat) diet for 10d, DIO rats ate 70% more, gained more body and adipose depot weight, had higher leptin and insulin levels and had 22% lower feed efficiency than DR rats fed HE diet. In DIO rats on HE diet, leptin levels increased significantly at 3d followed by increased insulin levels at 7d. These altered DIO leptin and ghrelin responses were associated with 10% lower leptin receptor (Ob-Rb) mRNA expression in the arcuate (ARC), dorsomedial (DMN) and ventromedial hypothalamic nuclei and 13% and 15% lower ghrelin receptor (GHS-R) mRNA expression in the ARC and DMN than DR rats. These data suggest that increased ghrelin signaling is not a proximate cause of DIO, whereas reduced leptin sensitivity might play a causal role.




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