This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Obesity is a worldwide health concern, being a major contributor to the increased incidence of coronary heart disease and type II diabetes. In 1998, 18% of the adults in the United States were defined as being obese, with twice that number being overweight. Even more disturbing is the dramatic increase in obesity and type II diabetes among children. The central goal of this proposal is to use microarray analysis to investigate global changes in metabolic pathways as well as identify novel genes that may be involved in permanent changes in body weight and glucose homeostasis caused by early postnatal nutritional manipulations. For these studies we utilized three models: 1) control group: these animals are raised in litters of eight and represent normal growth and adiposity; 2) chronic postnatal overfed: these animals are raised in litters of 3 and develop early onset obesity and diabetes; and 3) chronic postnatal underfed: these animals are raised in litters of 14 and maintain a lean phenotype into adulthood, but develop diabetes. Both of these experimental models have been shown to have long-term abnormalities in metabolic balance, even when fed a healthy diet. These animals are being studied at several postnatal (P) ages, P11, P15, P21 and P60. Microarray analysis using Affymetrix chips (26,000 genes) is being used to analyze samples from the liver, white adipose tissue, skeletal muscle, stomach, and several brain areas important for the control of energy homeostasis. The data generated from these chips will provide the important insight into the molecular consequences of poor nutrition during important developmental stages. Identifying these molecular abnormalities will enable us to investigate similar metabolic systems in our nonhuman primate developmental models.
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