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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Obesity-prone rats have preexisting defects in their counterregulatory response to insulin-induced hypoglycemia

¹University of Pennsylvania School of Nursing, Philadelphia, Pennsylvania 19104-6096; ²Neurology Service, Veterans Affairs Medical Center, East Orange 07018-1095; and ³Department of Neurology and Neurosciences, New Jersey Medical School, Newark, New Jersey 07103

Submitted 12 May 2004 ; accepted in final form 27 July 2004

Rats that develop diet-induced obesity (DIO) on a 31% fat [high-energy (HE)] diet have defective sensing and responding to altered glucose levels compared with diet-resistant (DR) rats. Thus we postulated that they would also have defective counterregulatory responses (CRR) to insulin-induced hypoglycemia (IIH). Chow-fed selectively bred DIO and DR rats underwent three sequential 60-min bouts of IIH separated by 48 h. Glucose levels fell comparably, but DIO rats had 22–29% lower plasma epinephrine (Epi) levels during the first two bouts than DR rats. By the third trial, despite comparable Epi levels, DIO rats had lower 30-min glucose levels and rebounded less than DR rats 85 min after intravenous glucose. Although DIO rats gained more carcass and fat weight after 4 wk on an HE diet than DR rats, they were unaffected by prior IIH. Compared with controls, DR rats with prior IIH and HE diet had higher arcuate nucleus neuropeptide Y (50%) and proopiomelanocortin (POMC; 37%) mRNA and an inverse correlation (r = 0.85; P = 0.004) between POMC expression and body weight gain on the HE diet. These data suggest that DIO rats have a preexisting defect in their CRR to IIH but that IIH does not affect the expression of their hypothalamic neuropeptides or weight gain as it does in DR rats.

diet-induced obesity; epinephrine; norepinephrine; neuropeptide Y; proopiomelanocortin; hypoglycemia-associated autonomic failure

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