| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Neurology and Neurosciences, New Jersey Medical School, Newark, New Jersey, United States; Pharmacology, Merck Research Laboratories, Rahway, New Jersey, United States
2 Neurology Service, Department of Veterans Affairs Medical Center, East Orange, New Jersey, United States; Neurology and Neurosciences, New Jersey Medical School, Newark, New Jersey, United States
3 Center for Advanced Food Technology, Cook College, Rutgers University, New Brunswick, New Jersey, United States
* To whom correspondence should be addressed. E-mail: levin{at}umdnj.edu.
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.
This article has been cited by other articles:
|
|
 |
|
  L. Kang, N. M. Sanders, A. A. Dunn-Meynell, L. D. Gaspers, V. H. Routh, A. P. Thomas, and B. E. Levin Prior hypoglycemia enhances glucose responsiveness in some ventromedial hypothalamic glucosensing neurons Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2008; 294(3): R784 - R792. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Ferezou-Viala, A.-F. Roy, C. Serougne, D. Gripois, M. Parquet, V. Bailleux, A. Gertler, B. Delplanque, J. Djiane, M. Riottot, et al. Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2007; 293(3): R1056 - R1062. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. N. Gorski, A. A. Dunn-Meynell, and B. E. Levin Maternal obesity increases hypothalamic leptin receptor expression and sensitivity in juvenile obesity-prone rats Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2007; 292(5): R1782 - R1791. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. D. Taylor and L. Poston Developmental programming of obesity in mammals Exp Physiol, March 1, 2007; 92(2): 287 - 298. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
