Abstract
Summary
Several lines of evidence are cited in support of the hypothesis that the genetic defect in the Zucker fatty rat occurs in the central nervous system. A number of abnormalities in hypothalamic neurotransmitters and neuropeptides have been identified and have the potential to influence the level of food intake, the endocrine status and finally the capacity for lipid storage in the fatty rat. Large increases in liver and adipose lipogenic capacity can be attributed to elevated levels of food intake and to hyperinsulinemia combined with an apparent decrease in sympathetic activity. Decreased efficiency of protein utilization for muscle and bone growth may be linked to low circulatory levels of growth hormone and somatomedin combined with an elevated glucocorticoid status. These large shifts in neuroendocrine status (Fig. 2) result in an environment that favors the partitioning of exogenous energy toward lipid deposition and obesity.
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