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DEVELOPMENTAL PHYSIOLOGY AND PREGNANCY

Postnatal environment overrides genetic and prenatal factors influencing offspring obesity and insulin resistance

¹Department of Neurology and Neurosciences, New Jersey Medical School, University of Medicine and Dentistry New Jersey, Newark, New Jersey; ²Department of Pharmacology, Merck Research Laboratories, Rahway, New Jersey; ³Neurology Service, Department of Veterans Affairs New Jersey Health Care System, East Orange, New Jersey; ⁴and Center For Advanced Food Technology Cook College, Rutgers University, New Brunswick, New Jersey

Submitted 27 February 2006 ; accepted in final form 10 April 2006

There is growing evidence that the postnatal environment can have a major impact on the development of obesity and insulin resistance in offspring. We postulated that cross-fostering obesity-prone offspring to lean, obesity-resistant dams would ameliorate their development of obesity and insulin resistance, while fostering lean offspring to genetically obese dams would lead them to develop obesity and insulin resistance as adults. We found that obesity-prone pups cross-fostered to obesity-resistant dams remained obese but did improve their insulin sensitivity as adults. In contrast, obesity-resistant pups cross-fostered to genetically obese dams showed a diet-induced increase in adiposity, reduced insulin sensitivity, and associated changes in hypothalamic neuropeptide, insulin, and leptin receptors, which might have contributed to their metabolic defects. There was a selective increase in insulin levels and differences in fatty acid composition of obese dam milk which might have contributed to the increased adiposity, insulin resistance, and hypothalamic changes in obesity-resistant cross-fostered offspring. These results demonstrate that postnatal factors can overcome both genetic predisposition and prenatal factors in determining the development of adiposity, insulin sensitivity, and the brain pathways that mediate these functions.

diet-induced obesity; hypothalamus; milk; development; plasticity; Agouti-related peptide; leptin

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