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The aim of this experiment was to evaluate the effects of ventromedial hypothalamus lesions on the thermogenic changes that follow food intake. Four groups of six Sprague-Dawley male rats were used. Under anesthesia with pentobarbital, the animals in the first and second groups received lesions at the ventromedial hypothalamus, and animals in the third and fourth groups received sham lesions. Body weight and food intake were monitored daily until the experimental procedure began. Twenty days after lesion, oxygen consumption, firing rate of sympathetic nerves to interscapular brown adipose tissue (IBAT), and IBAT temperature were monitored for 45 min both before and after 5 g food intake in 24 h fasted rats from the first and third groups. The same variables were measured in the animals of the second and fourth groups 50 days after receiving the lesions. Lesion placements were histologically verified. The results showed that lesions produced hyperphagia and obesity. Firing rate of nerves to IBAT, IBAT temperature, and oxygen consumption increased after food intake in sham-lesioned rats. This increase was significantly reduced by the lesion at both the 20- and 50-day time points. These findings indicate that the ventromedial hypothalamus controls postingestional activation of sympathetic discharge to IBAT. The reduction of postingestional thermogenesis could be involved in the development of obesity induced by lesion of the ventromedial hypothalamus.

Conditioned taste aversion was induced in rats by pairing saccharin with intraperitoneal LiCl injection. Animals injected with NaCl served as controls. After evaluating the preference levels for saccharin in rats of both groups, the animals were anesthetized with urethane and the duration of EEG desynchronization, firing rate of sympathetic nerves innervating interscapular brown adipose tissue (BAT), and temperature of the same tissues were recorded, before and after oral stimulation with saccharin or water. The EEG desynchronization was longer in conditioned rats after stimulation with saccharin. Firing rate of sympathetic nerves was higher in conditioned rats after presentation of saccharin. BAT temperature, decreased in conditioned rats after saccharin stimulus, was unchanged in the three other conditions. In a second experiment temperature and firing rate of sympathetic nerves of BAT were recorded after oral presentation of water or saccharin in rats treated as in the first experiment and injected with the alpha 1-adrenergic blocker prazosin. As in the first experiment, saccharin presentation in conditioned animals enhanced the neural sympathetic activity, whereas differently from the first experiment it increased BAT temperature. No changes were found in the same measurements in the three other conditions. The drop in interscapular BAT temperature found in the first experiment, an unexpected finding, probably depends on the use of lithium as unconditioned stimulus, because LiCl interacting with adrenergic receptors changes the two-phase response, normally seen in interscapular BAT after increased sympathetic activity, in a single-phase response.

Postprandial thermogenesis is under the control of the autonomic nervous system and alimentary conditioned stimuli change sympathetic and parasympathetic activity. Here we studied the effect of conditioned taste aversion on postprandial thermogenesis in rats. Two groups of animals were used, rats of the first group were controls, these were placed on a standard diet and, for some days, on two other different diets: one thiamine-free and the other thiamine-rich. Each diet had a different taste. The treated animals belonged to the second group, these were fed with the same three diets but for different lengths of times: thiamine-free diet for the first 5 wk afterwards, with thiamine-rich diet for 3 wk, and finally with laboratory standard diet for a few days. After a preference test with the three familiar diets, oxygen consumption rate and brown adipose tissue temperature were evaluated three times in both groups after ingestion of a test meal, each time with one of the three different diets. The preference test was unvaried for the three different familiar foods in controls, while the treated animals showed a lower preference for thiamine-free food than for the other two. Treated rats had a significantly higher increase in O2 consumption rate than controls. In this group intake of thiamine-free food induced a significantly lower increase in O2 consumption than the other two. The increase in brown adipose tissue temperature was also higher in treated than in control animals but in treated rats this was lower after intake of thiamine-free food than after the intake of the other two.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of a hypothalamic ventromedial area lesion on energy balance were tested in exercising rats and in sedentary rats to add further information about the type of obesity developed after ventromedial lesion. Four groups of six male Sprague-Dawley rats were used. Group 1: sham-lesioned and sedentary rats, which were utilized as control rats (C); group 2: sham-lesioned and exercising rats (E); group 3: lesioned and sedentary rats (L); group 4: lesioned and exercising rats (LE). The exercise consisted of daily swimming for 30 min. Resting oxygen consumption, food intake, and body weight were measured before any treatment and 3 weeks after the lesion or/and the exercise period. The results showed that the oxygen consumption increased in the E and LE groups but not in the C and L groups. Food intake increased more in E and LE groups than in L group. The increases in body weight were higher in L and LE than in the E and C groups. These findings suggest that exercise modifies resting oxygen consumption and food intake in lesioned rats, but does not influence the degree of obesity. Thus, the ventromedial syndrome can be considered a type of obesity not completely unregulated.

The effects of electrolytic lesions in the hypothalamus paraventricular nucleus were studied in adult male and female Sprague-Dawley rats, fed different diets, consisting of either palatable human food plus chow (cafeteria diet) or chow alone. The results showed that both cafeteria diet and lesions induced an increase in energy intake and weight gain in rats of both sexes. Oxygen consumption rate and colonic temperature were significantly decreased by lesions, while cafeteria diet increased the same parameters only in intact animals. The lesion decreased weight, protein and DNA, and temperature of brown adipose tissue, while cafeteria diet increased the values considered in brown adipose tissue of sham-injured rats, but not in lesioned animals. The response to norepinephrine administration was significantly greater in intact rats and those fed cafeteria diet. The results suggest that the larger body weight gain observed in lesioned rats, particularly evident in rats fed cafeteria diet, is partly due to the disappearance of diet-induced thermogenesis that depends on the reduced mass and functional activity of brown adipose tissue.

Oxygen consumption, colonic and interscapular brown adipose tissue temperature were evaluated in four groups of male and four groups of female rats both before and after lesions in different brain regions, and following beta-blocker propranolol administration. Recovery of body weight with varying difficulties in reaching food was also recorded in the injured animals. Groups consisted of rats with bilateral lesions in the entopeduncular nucleus (group EN), rats with bilateral lesions in the globus pallidus (group GP), rats with lateral hypothalamic lesions in the left side and entopeduncular lesion in the right side (group EN-LH), and rats with bilateral lesions in the lateral hypothalamus (group LH). Colonic and brown adipose tissue temperature and oxygen consumption were significantly increased after lesions in rats of groups EN, LH and EN-LH, but not in animals of the GP groups. Similarly, propranolol administration blocked the rise in heat production only in EN, LH and EN-LH animals. No differences were found between sexes. The survival rate was the same in all groups. GP rats recovered body weight earlier than animals injured in the other regions. The difficulty in reaching food was an important factor only in rats damaged in the EN. The results suggest that lateral hypothalamus and entopeduncular nucleus share a common regulatory function of the energy metabolism, while EN lesions induce a motor deficit in addition.

Rats with unilateral or bilateral electrolytic lesions in the globus pallidus (GP) became aphagic and adipsic. Aphagia and adipsia lasted 2-3 days in rats with unilateral lesion, but were more persistent in animals with bilateral lesions. EEG arousal induced by nociceptive stimuli applied to the side of the body contralateral to the unilateral pallidal lesion was of shorter duration than that induced by ipsilateral stimulation; no difference was found between rats injured in left or right (GP). Total exploratory activity of rats with symmetrical or asymmetrical lesions, exposed to a novel environment for ten min, was not different from that of the control group, but the exploratory activity measured in a 60 sec block showed trends in the two injured groups being different than those in the controls. Rats with unilateral right or bilateral lesions showed a lower level of neophobia for saccharin than controls. Acquisition of conditioned taste aversion was similar in lesioned rats and controls, but extinction of the conditioned taste aversion was slower in the intact than in the injured animals.