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1 Psychiatry, University of Cincinnati, Cincinnati, OH, USA
2 Neurology Svc., Veterans Administration Medical Center, E. Orange, NJ, USA; Neurology and Neurosciences, New Jersey Medical School, Newark, NJ, USA
* To whom correspondence should be addressed. E-mail: levin{at}umdnj.edu.
Rats prone to develop diet-induced obesity (DIO) have reduced central sensitivity to many metabolic and hormonal signals involved in energy homeostasis. High fat diets produce similar defects in diet-resistant (DR) rats. To test the hypothesis that genotype and diet exposure would similarly affect central insulin signaling, we assessed the anorectic effects of 8mU third ventricular (iv3t) insulin before and after 4wk intake of a 31% fat, high energy (HE) diet intake in outbred (OutB) rats. Rats were retrospectively designated as DR or DIO by their low or high weight gains on HE diet. Prior to HE diet, iv3t insulin reduced 4h and 24h chow intake by 53% and 69% in DR rats but by only 17% and 27% in DIO rats, respectively. Also, the anorectic response to iv3t insulin in OutB rats was inversely correlated (r=0.72, P=0.002) with subsequent 4wk weight gain on HE diet. Similarly, in selectively bred (SB) chow-fed DR rats, 8mU iv3t insulin reduced 4h and 24h intake by 21% and 22%, but had no significant effect in SB DIO rats. Four week HE diet intake reduced 4h and 24h insulin-induced anorexia by 45% in OutB DR rats and completely abolished it in SB DR rats. Reduced insulin responsiveness was unassociated with differences in arcuate nucleus insulin receptor mRNA expression between DIO and DR rats or between rats fed chow or HE diet. These data suggest that DIO rats have a pre-existing reduction in central insulin signaling which might contribute to their becoming obese on HE diet. However, since HE diet reduced central insulin sensitivity in DR rats but did not make them obese, it is likely that other brain areas are involved in insulin's anorectic action or that other pathways contribute to the development and maintenance of obesity.
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