| dc.description.abstract | The purpose of this investigation was to determine the relationships between food consumption, finickiness, serum glucose, serum free fatty acids (FFA), FFA mobilization attributable to epinephrine, and carcass fat in ventromedial hypothalamic (VMH) lesioned rats as a function of weeks following surgery. A brief review of the literature concerning the above variables revealed inconsistent conclusions as to the interrelations between these variables following VMH lesions. The investigation consisted of two experiments each involving normal and VMH-lesioned rats. Experiment I consisted of measuring food, water, and quinine consumption, and finickiness, the difference score between a subject's water and quinine intake, at 1, 4, 7, and 10 weeks following surgery. Measures taken in Experiment II were serum glucose, serum FFA, FFA mobilization attributable to epinephrine- stimulation, and carcass fat at 1, 4, 7, and 10 weeks following surgery. In Experiment I all consumption measures of the lesioned Ss were at normal levels at Week 1, at their highest levels at Week 4, and progressively decreased during Weeks 7 and 10 to control levels. Measures of finickiness also began at control levels but thereafter increased across weeks. In Experiment II the lesioned Ss demonstrated, during the first week, normal serum FFA levels which increased thereafter, very low initial serum glucose levels which increased to normal values across weeks, a consistent decrement in FFA mobilization attributable to epinephrine, and a significant increase in amount of carcass fat at week 1 which continued to increase across weeks. It was concluded that (1) changes in metabolism resulted directly from the brain lesion and preceded changes in food consumption and motivation, (2) changes in food consumption and motivation were not immediate direct effects of the lesion, but resulted from more primary metabolic changes, (3) changes in food consumption preceded changes in finickiness, (4) food consumption and finickiness were affected by different mechanisms, and (5) finickiness appeared to be determined by some correlate of the increased body weight resulting from the metabolic changes and hyperphagia. A proposed mechanism to explain the data of the present experiment was discussed. Briefly, it was based on the assumption that VMH lesions resulted in increased insulin levels which stimulated the formation of fat from glucose. It also assumed that adipose cells decreased their lipogenic capacity as they became engorged with fat, thus decreasing their demand for glucose which in turn resulted in decreased food consumption. | |
