• B E Levin and E Govek.
• Neurology Service, Veterans Affairs Medical Center, East Orange 07018; and Department of Neurosciences, New Jersey Medical School, Newark, New Jersey 07103, USA.
• Am. J. Physiol. 1998 Oct 1;275(4 Pt 2):R1374-9.

AbstractMaternal obesity and genetic background can affect the development of obesity and diabetes in offspring. Here we used selected strains of rats resistant (DR) vs. susceptible to development of diet-induced obesity (DIO) on high-energy (HE) diets to assess this issue. DR and DIO dams were fed either Chow or HE diet for 4 wk. DIO HE diet-fed dams and additional DR rats fed a palatable liquid diet (Ensure) became more obese and hyperinsulinemic than the other groups. During lactation, all dams were fed their respective diets, and offspring were fed Chow from weaning to 16 wk of age. All offspring of DIO dams gained more weight and had heavier retroperitoneal fat pads and higher leptin levels than DR progeny, but offspring of the more obese DIO HE dams had heavier fat pads and higher glucose levels than DIO Chow offspring. After 4 wk on HE diet, all DIO offspring gained more weight and had heavier total adipose depots and higher insulin and leptin levels than DR offspring. Offspring of DIO HE dams also gained more weight and had heavier fat depots and higher leptin levels than DIO Chow offspring. Therefore maternal obesity and hyperinsulinemia were associated with increased obesity in those offspring already genetically predisposed to become obese.

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