Thermogenesis In Rats Research Articles

Efferent projection from the preoptic area for the control of non-shivering thermogenesis in rats.

1. To investigate the characteristics of efferent projections from the preoptic area for the control of non-shivering thermogenesis, we tested the effects of thermal or chemical stimulation, and transections of the preoptic area on the activity of interscapular brown adipose tissue in cold-acclimated and non-acclimated anaesthetized rats. 2. Electrical stimulation of the ventromedial hypothalamic nucleus (VMH) elicited non-shivering thermogenesis in the brown adipose tissue (BAT); warming the preoptic area to 41.5 C completely suppressed the thermogenic response. 3. Injections of d, l-homocysteic acid (DLH; 0.5 mM, 0.3 microliter) into the preoptic area also significantly attenuated BAT thermogenesis, whereas injections of control vehicle had no effect. 4. Transections of the whole hypothalamus in the coronal plane at the level of the paraventricular nucleus induced rapid and large rises in BAT and rectal temperatures. This response was not blocked by pretreatment with indomethacin. The high rectal and BAT temperatures were sustained more than 1 h, till the end of the experiment. Bilateral knife cuts that included the medial forebrain bundle but not the paraventricular nuclei elicited similar rises in BAT and rectal temperatures. Medial knife cuts had no effect. 5. These results suggest that warm-sensitive neurones in the preoptic area contribute a larger efferent signal for non-shivering thermogenesis than do cold-sensitive neurones, and that the preoptic area contributes a tonic inhibitory input to loci involved with non-shivering thermogenesis. This efferent inhibitory signal passes via lateral, but not medial, hypothalamic pathways.

Energy balance and thermogenesis in rats consuming nonstarch polysaccharides of various fermentabilities

BackgroundThe equivalents of dietary protein, fat, and available carbohydrate as fuels for maintenance (kJ apparent metabolizable energy/kJ maintenance requirement) are known from classical experiments and are similar across species; that for nonstarch polysaccharide (NSP) is undetermined. ObjectiveOur objectives were to determine the energy equivalent of NSP and the thermic responses to NSP. DesignIn a randomized block design, 120 rats were treated in groups of 10 for 28 d with a basal diet (control) supplemented with starch and 10 different NSP treatments in amounts between 38 and 92 g/kg basal diet. Cellulose and starch were references. Thermic responses, deduced from body-composition changes and modeling of energy disposition, and energy and substrate excretion were determined. ResultsNSP had fermentabilities between 0.01 and 0.93 g/g intake. Fermentability, partial digestible energy, and net metabolizable energy values of NSP were closely related. Generally, 51% of apparent metabolizable energy from NSP (fermentable gross energy) met maintenance requirements. Diet (energy)- induced thermogenesis (DIT) was evident from whole diets. Fermentable NSP supplied net metabolizable energy and caused DIT. After DIT and fermentation were accounted for, NSPinduced thermogenesis was generally –2 ± 4% (x – ± SEM) of gross NSP energy, except for an outlying pectic preparation, which was 33% (P< 0.1). ConclusionsThe energy equivalent of NSP was 196 (100/51) kJ/kJ, compared with 128, 105, and 100 for protein, fat, and glucose, respectively, from the classical experiments. With the exception of pectic NSP, NSP does not induce thermogenesis in excess of that associated with DIT and fermentation.

Sex-associated differences in cold-induced UCP1 synthesis in rodent brown adipose tissue.

The effects of acute and chronic acclimation to cold on uncoupling protein 1 (UCP1) levels, as well as on GDP-binding to mitochondria, cytochrome c oxidase activity and mitochondrial protein concentration in brown adipose tissue (BAT) of intact male and female rats have been analyzed. Results reveal that females rats are more sensitive to cold because their threshold temperature for the thermogenic response is set at a higher value (around 22 degreesC) than that of males (around 18 degreesC), hence leading to differences in BAT UCP1 levels between the sexes at different environmental temperatures. In vitro experiments showed that steroid hormones, beta-estradiol, estrone and progesterone, can reduce norepinephrine-induced UCP1 synthesis in brown adipocytes differentiated in primary culture. Thus the different sex-associated response of cold-induced thermogenesis in rats does not appear to be explained by a direct action of sex steroids upon the adipocyte, implying that other factors in the thermogenic regulatory system must be involved.

Adaptive changes in the thermogenesis of rats by cold acclimation and deacclimation.

Male Wistar rats, aged 6 weeks, were maintained at 25 degreesC for 9 to 11 weeks (W group), at 10 degreesC for 9 to 11 weeks (C group), and at 25 degreesC for 2 weeks after exposure to 10 degreesC for 9 weeks (D group). Thermogenesis at 10 degreesC was significantly greater than at 25 degreesC. Thermogenesis per body mass in the C group was greater than in the W and D groups. The RQ value at 10 degreesC was greater than at 25 degreesC in the W group, whereas the opposite was observed in the C and D groups. It is suggested that a large part of enhanced thermogenesis, caused by cold acclimation for 9 weeks, is lost because of a decreased secretion of calorigenic hormones, in spite of a slight decrease in BAT mass, during deacclimation for 2 weeks.

Functional identification of rat atypical beta-adrenoceptors by the first beta 3-selective antagonists, aryloxypropanolaminotetralins.

1. We have assessed the relative abilities of compounds belonging to the new aryloxypropanolaminotetralin (APAT) class and of the reference beta-adrenoceptor-blocking agent, alprenolol, to antagonize functional responses in vitro and in vivo involving atypical (beta 3) or conventional (beta 1 and beta 2) beta-adrenoceptors. 2. The range of pA2 values for three representative APATs against inhibition of spontaneous motility in the rat isolated colon by the selective beta 3-adrenoceptor agonist, SR 58611A (8.1-8.8), was well above similarly calculated values for non-competitive antagonism of guinea-pig trachea relaxation by salbutamol (beta 2, 6.5-6.9) and the atrial chronotropic response by isoprenaline (beta 1, 6.7-7.3). Alprenolol, however, was substantially more potent in antagonizing atrial (pA2, 8.2) and tracheal (pA2, 8.9) responses than SR 58611A mediated inhibition of colonic motility (pA2, 6.8). 3. Several APAT isomers with different configurations at the chiral carbons, when tested on isolated organs, presented stringent stereochemical requirements for beta 3-selectivity, including high antagonist potency-ratios between active and inactive enantiomers. 4. In vivo, the inhibition of colonic motility and the thermogenic response of brown adipose tissue elicited in rats by the selective beta 3-adrenoceptor agonists SR 58611A and BRL 37344 respectively were substantially diminished by the representative APAT, SR 59230A, at oral doses (< or = 5 mg kg-1) well below those half maximally effective (ID50) for preventing beta 1-(isoprenaline tachycardia > or = 80 mg kg-1) or beta 2-(salbutamol bronchodilatation, 44 mg kg-1) mediated responses. Alprenolol, as expected, was a less potent and nonselective antagonist of the putative beta 3-responses. 5. These findings support APATs as the first potent, orally effective selective antagonists at beta 3-adrenoceptors, and provide final unambiguous evidence that beta 3-adrenoceptors underlie inhibition of colonic motility and brown adipose tissue thermogenesis in rats.

Effects of acute and chronic inhibition of nitric oxide synthase on brown adipose tissue thermogenesis.

This study was undertaken to examine the possible role of nitric oxide (NO) on brown adipose tissue (BAT) thermogenesis in rats. The chronic administration of N omega-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor) in drinking water given to rats decreased interscapular BAT (IBAT) weight as well as DNA content in a warm environment (25 +/- 1 degrees C; 2 and 4 weeks), and inhibited the cold-stimulated (5 +/- 1 degrees C; 2 weeks) increase in IBAT weight and DNA content. L-Arginine administration (4 weeks in a warm environment) increased the DNA content of IBAT. Chronic L-NAME administration (2 weeks in a warm environment) eliminated the NE-stimulated increase in in vivo oxygen consumption (VO2), caused hypothermia in acute cold exposure (0 degree C), and suppressed the NE-stimulated increase in in vitro IBAT VO2. In vitro incubation of native IBAT with L-NAME suppressed the basal and NE-stimulated increase in in vitro VO2. In vitro incubation of IBAT with methylene blue (soluble guanylate cyclase inhibitor and a scavenger of free NO) eliminated the NE-stimulated increase in in vitro IBAT VO2. These results suggest that the nitric oxide and NO-cGMP signaling systems are involved in the regulation of BAT cellularity and thermogenesis in rats.

Thermogenic responses to high-energy phosphate contents and/or hindlimb suspension in rats.

Effects of chronic depletion of high-energy phosphate compounds by feeding beta-guanidinopropionic acid (beta-GPA) with or without hindlimb suspension (HS) on body temperature were studied in rats. Lower rectal and skin temperatures were observed in rats after 10 d of HS. Suspension-related enlargement of the interscapular brown adipose tissue (BAT), associated with adrenal hypertrophy, was seen. Feeding beta-GPA also caused a hypothermia and BAT enlargement. It is suggested that the hypothermic response to HS may be due to decreased contractile activity and metabolic rate in skeletal muscles, associated with stress. It is also speculated that the changes in the thermogenesis in rats fed beta-GPA might be related to a stimulated ATP synthesis with sacrificed heat production, but not associated with stress.

Exercise-training reduces BAT thermogenesis in rats

In the energy balance equation, physical activity represents one component of energy expenditure. From various studies it appears that exercise-training does not affect clearly thermogenesis which depends on brown adipose tissue (BAT) activity. In the present work we examine how exercise-training can influence food intake and body weight regulation in relation to BAT thermogenesis. The proton conductance of the uncoupling protein of BAT was examined in male adult Wistar trained 2 h/day for 20 days and compared to that of sedentary (2 h of fasting instead of exercise) or control animals. All animals were provided with separate sources of the 3 macronutrients (protein, fat and carbohydrate) containing an identical percentage of vitamins, salt mixture and cellulose powder. At the end of training, rat were placed at 5°C during 10 days, then during 4 days at 28°C. This condition has been demonstrated to favour and amplify BAT responsiveness to moderate modifications of stimulation. The body weight of trained rats became significantly lower than that of the control and sedentary rats and this difference persisted all throughout the experiment. When placed at 5°C, all rats increased their total ingestion: control rats enhanced fat intake, while sedentary and trained rats enhanced carbohydrate ingestion. When placed at 28°C, all rats had identical total energy and that of the 3 items intakes. BAT proton conductance was about 40% lower in the trained compared with the sedentary plus the control rats. This indicated a lower BAT thermogenic activity in the trained animals. It could be concluded that exercise-training in rats induces negative energy balance; the reduced BAT activity could restrain weight loss and overeating.

Metabolic changes associated with ingestion of different macronutrients and different meal sizes in rats

Indirect calorimetry was used to investigate whole-body metabolic changes occurring during and after feeding in the rat. Measurement of respiratory exchange allowed the derivation of respiratory quotient (RQ = CO 2 produced/O 2 consumed) and energy expenditure [EE= O 2 consumed (364 + 113RQ)], giving an estimate of the energy substrate (fat, carbohydrate, or protein) being utilised and the total substrate oxidation occurring, respectively. Concurrent measurement of locomotor activity (ACT) allowed the changes in EE attributable to feeding (postprandial thermogenesis) to be generally dissociated from those attributable to activity. Experiment I examined alterations in RQ, EE, and ACT following brief (<5 min) calorically matched meals of Froot Loops (86% carbohydrate), casein (protein), lard (fat) and lab chow (mixed macronutrient) and following the ingestion of 0.1%o saccharin (which is calorically inert). Rapid (< 5mins) and sustained increases in RQ occurred following Froot Loop and lab chow meals indicating increased utilization of carbohydrates as an energy substrate. Casein caused little change in RQ, while lard caused a drop in RQ approximately 30 min following ingestion, indicating increased fat utilization following absorption of the lard meal. Saccharin caused little change in RQ, suggesting that a sweet taste is not sufficient to alter substrate utilization. Increased EE was seen following the Front Loops and lab chow meals in the absence of corresponding increases in ACT, suggesting a postprandial thermogenic effect of these meals. In Experiment 2, the metabolic changes accompanying a large (5 g) and small (0.5 g) Froot Loops meal were compared. The large meal resulting in a larger, more rapid and more sustained increase in RQ than the small meal. In addition, there was an increase in EE in the absence of corresponding increases in ACT following the large meal suggesting the presence of postprandial thermogenesis. It is concluded that both meal macronutrient content and meal size are important determinants of postprandial substrate utilization and thermogenesis in rats.

Postprandial thermogenesis and conditioned taste aversion or preference

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 O 2 consumption rate than controls. In this group intake of thiamine-free food induced a significantly lower increase in O 2 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. The higher rise in postprandial thermogenesis in treated rats and the lower response found after intake of an aversive meal is probably due to changes in the autonomic nervous and of endocrine systems.

Concerning the mechanism of increased thermogenesis in rats treated with dehydroepiandrosterone.

Dehydroepiandrosterone (DHEA) treatment of rats decreases gain of body weight without affecting food intake; simultaneously, the activities of liver malic enzyme and cytosolic glycerol-3-P dehydrogenase are increased. In the present study experiments were conducted to test the possibility that DHEA enhances thermogenesis and decreases metabolic efficiency via transhydrogenation of cytosolic NADPH into mitochondrial FADH2 with a consequent loss of energy as heat. The following results provide evidence which supports the proposed hypothesis: (a) the activities of cytosolic enzymes involved in NADPH production (malic enzyme, cytosolic isocitrate dehydrogenase, and aconitase) are increased after DHEA treatment; (b) cytosolic glycerol-3-P dehydrogenase may use both NAD+ and NADP+ as coenzymes; (c) activities of both cytosolic and mitochondrial forms of glycerol-3-P dehydrogenase are increased by DHEA treatment; (d) cytosol obtained from DHEA-treated rats synthesizes more glycerol-3-P during incubation with fructose-1,6-P2 (used as source of dihydroxyacetone phosphate) and NADP+; the addition of citrate in vitro further increases this difference; (e) mitochondria prepared from DHEA-treated rats more rapidly consume glycerol-3-P added exogenously or formed endogenously in the cytosol in the presence of fructose-1,6-P2 and NADP+.

Effects of running training on in vitro brown adipose tissue thermogenesis in rats.

Brown adipose tissue (BAT) is a major site of nonshivering thermogenesis (NST) during cold acclimation for most mammals. Repetitive nonthermal stress such as immobilization has been shown to enhance the capacity of NST as cold acclimation. In the present study, the effects of running training, another type of nonthermal stress, were investigated on in vitro thermogenesis and the cellularity of interscapular BAT in rats. The rats were subjected to treadmill running for 30 min daily at 30m/min under 8 degrees inclination for 4-5 weeks. In vitro thermogenesis was then measured in minced tissue blocks incubated in a Krebs-Ringer phosphate buffer containing glucose and albumin at 37 degrees C, using a Clark type oxygen electrode. The trained rats showed less body weight gain during the experiment. The weights of BAT and epididymal white adipose tissue were smaller in the trained rats. Noradrenaline- and glucagon-stimulated oxygen consumption were also significantly smaller in the trained rats. The tissue DNA level was greater in the trained rats, but the DNA content per tissue pad did not significantly differ. The results indicate that running training reduces BAT thermogenesis, possibly as an adaptation to conserve energy substrates for physical work.

Physiological responses of cold-stressed blue and snow phase Lesser Snow Goose goslings

A comparison of cold-stressed Lesser Snow Goose (Chen caerulescens caerulescens) goslings revealed that the metabolic rates of light-colored (snow) and dark-colored (blue) goslings did not differ when they were measured in the dark. Small differences in plumage insulation (higher in snow goslings) and core body temperature (lower in blue goslings) seemed to balance each other so that there was no difference in rates of thermogenesis between morphs. We conclude that physiological thermoregulation does not compensate for potential differential radiative heat loads between the morphs.

Influence of mild cold on the components of 24 hour thermogenesis in rats.

1. The influence of two weeks' acclimation to either 28 degrees C (thermal neutrality) or 21 degrees C (mild cold) on 24 h heat production and motor activity has been investigated in male Wistar rats. Food intake was controlled and provided as a single meal of approximately 170 kJ per day. Mathematical modelling was used to relate metabolic rate to measured movement and time of day. 2. For animals at thermal neutrality it was clear that metabolic rate increased during periods of substantial measured movement and returned to baseline during periods of minimal activity. Total heat production could therefore be divided into two components: underlying and movement-induced thermogenesis. 3. At 21 degrees C, a more complex model was needed. During periods of substantial activity, the relation between metabolic rate and movement was similar to that at 28 degrees C and total heat production could be divided into the same two components of underlying and movement-induced thermogenesis. However, during periods of prolonged inactivity, a different model was required, which included a component of extra metabolic activity, termed supplementary thermogenesis. By fitting this model to data at 28 and 21 degrees C, it was possible to partition 24 h heat production into the three possible sources of underlying, movement-induced and supplementary thermogenesis. 4. Total 24 h heat production was approximately 25% higher for rats at 21 compared with 28 degrees C (P less than 0.01) and underlying thermogenesis was approximately 20% higher for those in the mild cold (P less than 0.01). Measured movement was significantly reduced in the mild cold (P less than 0.05) although it was energetically less efficient since there was no difference in movement-induced thermogenesis, which accounted for 18 and 15% of total heat production at 28 and 21 degrees C respectively. Supplementary thermogenesis was observed only in the mild cold and it accounted for approximately 6% of 24 h heat production, while the peak value accounted for 20% of total heat production. Circadian variations in thermogenesis were also different at 28 compared with 21 degrees C. Possible mechanisms accounting for the components of underlying thermogenesis and supplementary thermogenesis are discussed.

Stimulation of the paraventricular nucleus with glutamate activates interscapular brown adipose tissue thermogenesis in rats

The paraventricular nucleus (PVN) of the hypothalamus is involved in the control of energy balance in rodents through its influences on feeding, pituitary hormone secretion and the autonomic nervous system. In the present study, selective stimulation of PVN neurons by means of local microinjection of the excitatory amino acid glutamate (100 mM, 500 mM of 1 M, in 100 nl) led to a concetration-dependent increase in interscapular brown adipose tissue (IBAT) temperature in urethane-anaesthetized rats. This effect could be prevented by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride, or the β-adrenergic receptor antagonist, propranolol, but not by hypophysectomy, implicating the involvement of the sympathetic outflow. Thermogenesis in brown adipose tissue (BAT) is an important accompaniment of overfeeding in small mammals, and previous studies have shown that signals generated in response to feeding gain access to the PVN. The present finding that direct activation of PVN neurons stimulates thermogenesis in BAT, taken together with data that the PVN receives dietary signals from the gut, support the view that PVN neurons may function in monitoring the balance between energy intake and its expenditure.

Retinohypothalamic tract stimulation activates thermogenesis in brown adipose tissue in the rat

We have shown that injecting glutamate into the hypothalamic suprachiasmatic nucleus (SCN) stimulates interscapular brown adipose tissue (IBAT) thermogenesis in rats. In the present study, electrical stimulation of the retinohypothalamic tract (RHT), a projection of retinal ganglion cell axons that course via the optic tract and terminate in the SCN, mimicked the effect of intra-SCN glutamate injection on IBAT thermogenesis. This effect could be blocked by prior injection of the local anesthetic procaine or the excitatory amino acid blockers kynurenic] acid and σ- d-glutamylaminomethyl-phosphorinic acid into the contralateral SCN, implicating the involvement of SCN glutamate receptors. The mediating this effect. On the basis of these observations and our finding of thermogenic responses to RHT stimulation or intra-SCN glutamate, we conclude that photic signals transmitted to the SCN via release of glutamate from the RHT might be capable of acutely modulating thermogenesis in IBAT.

Effects of corticotropin-releasing factor on food intake and brown adipose tissue thermogenesis in rats.

Corticotropin-releasing factor (CRF) has been administered into the third ventricle of rats in acute and chronic experiments. Following a single 5-micrograms injection of CRF, there was an acute reduction in food intake at 30 and 60 min that was no longer significant at 3 h. Guanosine 5'-diphosphate (GDP) binding to mitochondria from interscapular brown adipose tissue (IBAT) of 21-h deprived rats was significantly increased 30 min after the acute infusion of 5 micrograms of CRF. Serum corticosterone was elevated in both groups but was significantly higher in the group treated with CRF. Serum glucose was unchanged. During a 7-day infusion of CRF (4.8 micrograms/day) into the third ventricle, the treated animals showed a slight, but significant, decrease in food intake but a progressive decline in body weight of 53 g over 7 days. Mitochondrial GDP binding was increased in the ad libitum-fed rats chronically treated with CRF. Serum corticosterone levels, although significantly higher than controls, were lower than following acute administration of CRF. These data show that CRF can acutely reduce food intake and increase sympathetic activity and that chronically it reduces body weight and may increase sympathetic activity without any consistent decrease in food intake.

Nonshivering thermogenesis and brown fat in spontaneously hypertensive rats.

Oxygen consumption was measured before and during infusion of the catecholamine isoproterenol in age-matched spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rats. Mass-independent rates of oxygen consumption of anesthetized 7-week-old rats were similar in the WKY and SHR rats (11.08 +/- 0.74 and 11.33 +/- 0.82 ml O2 min-1 kg-.67, respectively). Catecholamine infusion elicited increased total oxygen consumption in both WKY and SHR animals (15.0 +/- 1.0 and 14.9 +/- 1.2 ml O2 min-1 kg-.67, respectively), and the magnitude of these increases did not significantly differ. To assess whether there were changes in the metabolic state of brown adipose tissue, the major site of catecholamine-induced thermogenesis in rats, enzymes whose activity is proportional to aerobic capacity were assayed in vitro. In both the interscapular and cervical brown fat depots, maximal citrate synthase and maximal HOAD (beta-hydroxyacyl-CoA dehydrogenase) activities were similar in SHR and WKY rats. There were also no significant differences in brown fat protein content, suggesting no differential growth of this tissue in the two rat strains. Our results indicate that the nonshivering thermogenic capacity of the hypertensive SHR rats does not differ from that of the normotensive WKY animals.

Nicotine increases thermogenesis in brown adipose tissue in rats

This study has tested the hypothesis that nicotine might increase thermogenesis in rats by activating the sympathetic nervous system which supplies brown adipose tissue. Three hours after a single injection of nicotine, both the turnover of norepinephrine and the binding of the purine nucleotide, guanosine 5′-diphosphate (GDP) to mitochondria from brown adipose tissue were significantly increased. After 11 days of treatment with nicotine, the turnover of norepinephrine and the GDP binding to mitochondria from brown adipose tissue both remained elevated but weight gain was not different. These data are consistent with the hypothesis that nicotine may have part of its effect through changes in thermogenesis involving sympathetic nervous activation of peripheral thermogenic tissues such as brown adipose tissue.

Cortical control of thermogenesis induced by lateral hypothalamic lesion and overeating.

Increased O2 consumption was found in rats after bilateral lesions of the lateral hypothalamus (LH) or during voluntary overeating. This phenomenon appears to be mediated by the sympathetic nervous system (SNS) in both conditions, since it is blocked by the beta-blocker propranolol administration. In the first experiment we showed that the brain cortex is involved in the thermogenesis induced by LH lesion and this effect is mediated by SNS, since bilateral functional decortication induced by cortical-spreading depression (CSD) impaired the increase of O2 consumption to the same extent as administration of propranolol. In the second experiment the role played by the cerebral cortex on thermogenesis in rats during voluntary overeating of "cafeteria" diet and in control rats was investigated. Cafeteria rats showed a significantly higher colonic temperature, brown adipose tissue temperature (Tbat), and rate of O2 consumption than control animals. CSD led to a significant decrease of Tbat and O2 consumption in cafeteria rats but not in controls. On the basis of the results obtained in the two experiments, the possibility that the cerebral cortex could be involved in the metabolic responses for reduction of body weight to the "set-point" is hypothesized.