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Am J Physiol Regul Integr Comp Physiol (January 11, 2007). doi:10.1152/ajpregu.00749.2006
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Submitted on October 25, 2006
Accepted on January 5, 2007

Maternal obesity increases hypothalamic leptin receptor expression and sensitivity in juvenile obesity-prone rats

Judith N Gorski1, Ambrose A. Dunn-Meynell2, and Barry E. Levin2*

1 Neurology and Neurosciences, New Jersey Medical School, Newark, New Jersey, United States; Pharmacology, Merck Research Laboratories, Rahway, New Jersey, United States
2 Neurology and Neurosciences, New Jersey Medical School, Newark, New Jersey, United States; Neurological Service (127C), VA Medical Center, East Orange,, New Jersey, United States

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

In rats selectively bred to develop diet-induced obesity (DIO) or to be diet-resistant (DR), DIO maternal obesity selectively enhances the development of obesity and insulin resistance in their adult offspring. We postulated that the interaction between genetic predisposition and factors in the maternal environment alter the development of hypothalamic peptide systems involved in energy homeostasis regulation. Maternal obesity in the current studies led to increased body and fat pad weights and higher leptin and insulin levels in postnatal day 16 offspring of both DIO and DR dams. However, by 6wk of age, most of these intergroup differences disappeared and offspring of obese DIO dams had unexpected increases in arcuate nucleus leptin receptor mRNA, peripheral insulin sensitivity, diet- and leptin-induced brown adipose temperature increase and 24h anorectic response as compared to offspring of lean DIO, but not lean DR dams. On the other hand, while offspring of obese DIO dams did have the highest ventromedial nucleus melanocortin-4 receptor expression, their anorectic and brown adipose thermogenic responses to the melanocortin agonist, MTII, did not differ from those of offspring of lean DR or DIO dams. Thus, during their rapid growth phase, juvenile offspring of obese DIO dams have alterations in their hypothalamic systems regulating energy homeostasis which ameliorates their genetic and perinatally-determined predisposition towards leptin resistance. Since they later go onto become more obese, it is possible that interventions during this time period might prevent the subsequent development of obesity.




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