The immediate physiological effects of lateral hypothalamic lesions in rats

Abstract

The purpose of this experiment was to determine serum glucose and free fatty acid levels, free fatty acid mobilization rates, and carcass composition after lesions in the rat lateral hypothalamic area (LHA). It was anticipated that the experiment would determine whether there are metabolic effects of LHA lesions which are independent of the lesion-produced hypophagia. The hypothesis was offered that, since the ventromedial hypothalamus (VMH) purportedly inhibits the LHA, the measures would vary inversely with those found after VMH lesions. From the hypothesis, increases in serum glucose levels and free fatty acid mobilization rates as well as a decrease in body fat were expected in animals with LHA lesions when compared with pair-fed controls. Sixty rats were equally divided into groups which were administered small LHA lesions, given sham lesions but the same amount of food eaten by animals with lesions, or given sham lesions and free access to food. Food intake was controlled by modifying the rats' home cages so when the animal pushed a panel it received a uniform-sized food pellet. At 1, 3, or 5 days after surgery, the animals were sacrificed and measures of serum free fatty acid and glucose levels, free fatty acid mobilization rates, and the amounts of body fat, water, and residue were taken. From 4 days prior to surgery until sacrifice, food and water intake and body weight were recorded daily. There were no differences among the groups in any of the biochemical measures. The LHA group, however, lost more weight the first day after surgery than did the sham group whose food intake the LHA group controlled. The difference in weight was found by carcass analysis to be attributed to a loss in fat and not to the retention of water, although the LHA animals drank less water than their controls. By day 3 after surgery, there was no appreciable change in either weight loss for the LHA or their yoked controls, and by day 5 after surgery, there appeared the suggestion of a deficit of body water in the LHA animals. There were virtually no metabolic effects detectable from the measures selected for the experiment, although a change in metabolic effect may be responsible for the transitory excessive fat loss in LHA animals at day 1. It was concluded that small LHA lesions which produce temporary aphagia and loss of body weight in rats produce minor and transitory, if any, direct metabolic changes. If LHA lesions produce direct metabolic effects as do VMH lesions, it may require the larger lesions which produce chronic aphagia. If the changes in metabolism as a result of LHA lesions are as minor as this study suggested, then it is hypothesized that the VMH does not control food intake through modulation of the LHA. The VMH and LHA may exert their control over food intake through separate channels.