Dorsomedial Hypothalamic Lesions Research Articles

Body weight set point studies in weanling rats with dorsomedial hypothalamic lesions (DMNL rats)

In order to further characterize a previously postulated “organismic” set point, weanling DMNL and control (CON) rats were maintained on lab chow ad lib (AL) for 55 post-operative days. Subsequently, some DMNL and CON rats were food-restricted (REST) to 80% of the food intake of their AL-fed counterparts for 24 days. At this point, representative rats from each group were killed by decapitation and the remaining animals were re-fed AL and killed 7 and 22 days thereafter. At the end of REST, both DMNL and CON showed significant weight loss, which was greater in CON than in DMNL rats. After 7 days of refeeding, DMNL rats normalized their body weights but re-fed CON still weighed less than AL-fed CON 22 days after refeeding. Food intake in formerly REST groups overshot on refeeding for 7 days, but this was significant only in DMNL rats. Notably, during this time formerly REST-DMNL ate as much as AL-fed CON. Efficiency of food utilization was normal in DMNL during AL feeding and became reduced on REST as it did in REST-CON. Notably, on refeeding formerly REST-DMNL rats overshot that of AL-fed DMNL rats by the same magnitude as previously REST-CON overshot the values of AL-fed CON. After 22 days of refeeding, this overshoot was still evident in DMNL but not in CON. At the end of the REST period, plasma insulin and glucose were similar in AL-fed DMNL and AL-fed CON. They were significantly and comparably reduced in both REST-DMNL and REST-CON compared to the AL-fed DMNL and AL-fed CON. On refeeding these changes normalized within seven days. At the end of REST, plasma free fatty acid concentrations were higher in REST-DMNL and RESTCON than in AL-fed DMNL and AL-fed CON. After seven days of refeeding they normalized only in formerly RESTCON. Plasma glycerol and total protein were normal throughout all groups, as was carcass protein. Carcass fat was equivalently reduced in both DMNL and CON at the end of REST and normalized 7 days after refeeding. AL-DMNL had the same carcass fat as AL-CON and REST-DMNL had the same carcass fat as REST-CON. In conjunction with previously reported normal anabolic hormone levels the data suggest that DMNL rats are not growth-retarded but are merely scaled down in size without compromise of their homeostatic competence. We take this as strong evidence for the existence of an “organismic” set point.

Effect of palatable diet on growth, caloric intake and endocrine-metabolic profile in weanling rats with dorsomedial hypothalamic lesions

Weanling male Sprague-Dawley rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated rats served as controls. All animals were fed lab chow for 15 postoperative days. At that time they were subdivided into two groups each. One DMNL and one control group continued to be fed lab chow until the termination of the experiment on postoperative day 116. A second DMNL and control group were fed a high-fat diet and 32% sucrose solution (HF/SS diet). All DMNL rats showed reduced body weight and linear growth, but the HF/SS diet depressed these parameters further below the levels of the chow-fed groups. Both DMNL and control rats fed HF/SS had more carcass fat, heavier epididymal fat pads, more carcass fat per calories eaten, higher plasma levels of glucose, glycerol and free fatty acids but lower insulin levels than chow-fed DMNL rats and controls. This occurred in the face of lower body weights and caloric intake. Neither growth hormone nor insulin showed lesion effects. Rats with DMNL exhibited the same inverse relationship between plasma insulin and free fatty acids as controls. The data indicate that DMNL rats respond to the HF/SS diet essentially like sham-operated controls, i.e., they develop dietary obesity. Although they do show some small deficits, their lipogenic capacity is actually significantly greater than that of HF/SS-diet fed controls.

Meal patterns of rats with dorsomedial hypothalamic nuclei lesions or sham operations

Rats with bilateral dorsomedial hypothalamic electrolytic lesions (DMNL rats) are hypophagic, hypodipsic and have reduced linear and ponderal growth when compared to sham operated controls (SCON). Nevertheless, previous studies have shown that DMNL rats eat and drink adequate amounts for their size and have normal body composition. In the present study we investigated meal parameters: meal size, and frequency (both light and dark period), total intake and meal size per metabolic size (body weight 0.75). Compared to SCON, DMNL rats at twelve days post surgery weighed less, were shorter, but had a normal body composition as determined by the Lee Index, and were hypophagic (grams eaten/day). The animals were placed into individual, self-contained feeding modules and given powdered chow. After familiarization to the modules, meal parameters were recorded continuously by a computer for an eight day period. While dark phase meal frequency did not differ significantly between groups, the lesioned rats took more meals during the light period. Over the eight-day measurement period DMNL rats were hypophagic compared to SCON in absolute terms. However, when total intake and meal size were normalized to metabolic size, these two parameters did not differ significantly between groups. Upon refeeding, after a one-day fast, the initial meal size of the normally hypophagic DMNL rats exceeded that of SCON. Rats with DMNL have previously been shown to have deficits in some hypothesized short-term food intake control mechanism (e.g., cholecystokinin, glucose sensing). Thus overeating by the lesioned rats after a fast could possibly result from a specific short term control deficit. Nevertheless, under ad lib conditions, except for a slight diurnal disruption in meal frequency, meal parameters were normal in the DMNL rats.

Somatic, metabolic and endocrine correlates of set point recovery in food-restricted and ad lib-fed weanling rats with dorsomedial hypothalamic lesions

Male Sprague-Dawley rats received either electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats) or sham-operations (CON), and were fed lab chow ad lib for 41 post-operative (POP) days. Subsequently one lesioned (DNML-AL) and one control group (CON-AL) continued to receive lab chow ad lib until the end of the experiment (POP day 78). A second lesioned (DMNL-RE) and control group (CON-RE) were given 80% of the amount of food eaten by their ad lib-fed counterparts for 28 days. At this time several rats from each group were killed. The remaining animals were then given lab chow ad lib for nine days and then also killed. Both DMNL-RE and CON-RE recovered their lowered body weight, food intake and feeding efficiency and showed the same pattern and relative magnitude as their ad lib-fed counterparts. Similarly, carcass lipid, epididymal fat pad lipid, incorporation of glucose-U-C14 into fat pad saponifiable lipid, total lipid, total glycogen (DPM/protein), liver protein, incorporation of glucose into liver CO2 and concentrations of plasma glucose, glycerol, triglycerides and free fatty acids normalized on refeeding to the same extent and in the same pattern in DMNL-RE as in CON-RE. In contrast to previous studies, plasma insulin was lower in DMNL-AL than in CON-AL but DMNL-RE and CON-RE had similar levels on refeeding. Also on refeeding, both DMNL-RE and CON-RE showed the same enhanced glucose incorporation into liver total lipid. The data show that DMNL rats, although smaller in size and hypophagic in absolute terms, recovered lost body weight--at least under our relative mild reduction of 80% of their ad lib-fed controls--with the same competence and in the same time interval as sham-operated controls. It is quite possible that a more severe restriction of body weight would have uncovered some deficits in DMNL rats, however. Under the constraints of the present experimental arrangement, the data strengthen previous evidence for the existence in DMNL rats of an "organismic" set point that makes for a "scaled-down" but homeostatically normal animal.

Somatic, metabolic and endocrine correlates of set point recovery in food-restricted and ad lib-fed weanling rats with dorsomedial hypothalamic lesions

Somatic, metabolic and endocrine correlates of set point recovery in food-restricted and ad lib-fed weanling rats with dorsomedial hypothalamic lesions

Plasma hormone levels in growth-retarded rats with dorsomedial hypothalamic lesions

Rats with lesions in the dorsomedial hypothalamic nuclei (DMNL rats) are hypophagic and growth-retarded. Since previous work had shown normal plasma growth hormone and insulin levels in DMNL rats we investigated the diurnal patterns of these and other hormones involved in growth. Trial 1: Rats received electrolytic DMNL or sham operations (SCON). The DMNL rats exhibited no differences from SCON rats in plasma triiodothyronine (T3), growth hormone (GH), insulin and somatomedin (SM) concentrations, Trial 2: kainic acid, a neurotoxin, was used for lesion production. Again, DMNL rats showed no deficiencies in plasma levels of T3, GH or insulin. Trial 3: In this experiment, diurnal hormone profiles were assessed. The GH profile and mean 24-hour secretion of both DMNL and SCON groups did not differ significantly. Both groups exhibited a diurnal release of T3, with the DMNL rats showing slightly higher levels. Plasma insulin rose after dark, i.e., at the onset of feeding, in SCON but not in DMNL rats; the later have a previously reported disrupted feeding rhythm. Glucose patterns were in keeping with insulin profiles. Controls showed a normal plasma corticosterone rhythm whereas DMNL rats had an altered pattern. The data suggest that deficiencies in the principal anabolic and growth-promoting hormones cannot be responsible for the retarded growth of DMNL rats.

Normal pancreatic and intestinal enzymes in hypophagic growth-retarded rats that received dorsomedial hypothalamic lesions shortly after weaning

Male weanling Sprague-Dawley rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats). Sham-operated rats served as controls. After being fed lab chow for two postoperative weeks, the animals were divided into four groups. One group of DMNL rats and controls received a high-caloric diet (high-fat diet, chocolate chip cookies, 32% sucrose solution, potato chips and marshmallows), whereas another group of DMNL rats and controls continued to receive lab chow. The experiment was terminated on the 185th postoperative day. In accordance with previous findings, DMNL rats, irrespective of diet, were lighter and shorter than controls. In addition, DMNL rats fed junk food were lighter than DMNL rats fed lab chow, and junk-fed controls weighed as much as chow-fed controls. Both DMNL rats and controls fed junk food were also shorter and showed higher carcass fat than their chow-fed counterparts. Also, DMNL rats fed junk food had less carcass fat than junk-fed sham-operated controls, whereas in accordance with previous findings, there was no difference between chow-fed DMNL rats and chow-fed sham-operated controls. Irrespective of diet, DMNL rats ate less calories than their respective sham-operated controls. Both absolute and percent pancreas weight and protein pancreas weight and protein/pancreas were unaffected in DMNL rate but were reduced in both junk-fed groups in comparison with their chow-fed counterparts. Both concentrations and contents of pancreatic trypsinogen, amylase and lipase were unaffected in DMNL rats but total activities of all three enzymes were dramatically reduced in the junk-fed compared with the chow-fed DMNL rats. Total activities of trypsinogen and amylase but not lipase were also reduced. Duodenal mucosal weight, total protein and specific activities of enterokinase, leucine amino peptidase and maltase were uninfluenced by lesions and diet alike. In the jejunum, specific activity of enterokinase was dramatically reduced in junk-fed versus chow-fed DMNL rats; the same obtained for junk-fed vs. chow-fed sham-operated control groups. Jejunal lactase, sucrose and maltase were not affected by DMN lesions but both DMNL rats and sham-operated controls fed junk foods showed lower specific activities than their chow-fed counterparts. The data indicate that production of DMN lesions in weanling rats, although followed by dramatic alterations in ponderal and linear growth and food intake, causes little, if any, changes in a number of pancreatic and small intestinal parameters, including enzymes. The only significant changes are those related to diet effects. These findings suggest that the DMNL rat responds to dietary factors like its sham-operated control and suggest that changes in digestive function cannot be invoked as possible causes of growth retardation and food intake in the weanling DMNL rat.

Suppression of feeding by cholecystokinin but not bombesin is attenuated in dorsomedial hypothalamic nuclei lesioned rats

Rats with dorsomedial hypothalamic lesions (DMN-L) or sham operations were injected IP with saline or the satiety peptide cholecystokinin (CCK) at 3.0 and 6.0 μg/kg at the onset of the dark phase. Food consumption was then measured 15, 30 and 60 min later. Compared to saline baseline intake. CCK suppressed feeding during the first 30 min following injection in the sham operated group but not in the DMN-L group. Bombesin (BBS), another satiety peptide was also injected (4.0 and 8.0 μg/kg) into the two groups. BBS produced significant and comparable suppression of feeding in both DMN-L and sham operated rats. In a third trial a large dose of CCK (12.0 μg/kg) was injected into the two groups as described above. The CCK suppressed feeding for 60 min in the control group. CCK also attenuated feeding in the DMN-L group, but for only 30 min. However, even this suppression was reduced compared to the control group. The data suggest that the DMN may play a role in CCK induced satiety.

Naloxone suppression of food and water intake and cholecystokinin reduction of feeding is attentuated in weanling rats with dorsomedial hypothalamic lesions

In Experiment 1, sham operated (SCON) and dorsomedial hypothalamic nuclei (DMN) lesioned (L) rats were given saline or naloxone (0.1, 1.0 or 2.0 mg/kg) just prior to the onset of the dark cycle, lights out. Compared to saline injections, naloxone at all doses suppressed the cumulative food intake of the SCON during the second and third hr of measurement. Naloxone was without significant effect on the food intake of DMNL rats. Similar results were obtained in Experiment 2, except that naloxone at 2.0 mg/kg significantly suppressed the DMNL rats' food intake by the fourth hr of measurement. Cumulative water intake of both groups was significantly suppressed by naloxone in both experiments but its effects appeared to be attenuated in the DMNL group. In a preliminary trial cholecystokinin octapeptide (3.0 and 6.0 μg/kg) given at the onset of the dark cycle significantly suppressed the food intake of the SCON group but had on signficant effect on the DMNL rats. The possibility exists that the reduced food intake and lower body weight of DMNL rats may partially result from damage to an opioid system. The data also tentatively suggest the DMN may play a role in cholecystokinin-induced satiety.

Aphagia and adipsia after kainic acid lesioning of the dorsomedial hypothalamic area.

Unlike rats which have electrolytic dorsomedial hypothalamic area lesions and are hypophagic and hypodipsic, the rats of the present study with dorsomedial hypothalamic area, kainic acid lesions (KAL) were postoperatively aphagic and adipsic. Subsequently, KAL rats rejected chow or a high-fat diet but ate a 30% sucrose-chow diet. Similarly the KAL rats were adipsic but drank a 30% sucrose solution. Slowly most of the KAL rats began to eat chow and drink tap water but remained hypophagic and hypodipsic. When tested for glucoprivic-induced feeding using 2-deoxy-D-glucose (200 or 400 mg/kg) the KAL rats, in contrast to the sham-operated controls, did not increase their food intake. During water deprivation the recovered KAL rats that would drink tap water ate, and following it they responded with an adequate increase in water consumption. During food deprivation the KAL rats, whether eating chow or sucrose-chow diet, drank, and subsequently the normally hypophagic rats actually ate more than the controls. Although the growth rate (linear and ponderal) of KAL rats was reduced compared with that of the controls, their body composition by indirect measurement was normal. The present data indicate that most of the dorsomedial hypothalamic syndrome results from damage to DMHA neurons and not to fibers of passage.

Body energy balance and food intake: a neuroendocrine regulatory mechanism.

Body energy balance and food intake: a neuroendocrine regulatory mechanism.

Water regulation in weanling hypodipsic dorsomedial hypothalamic-lesioned rats.

Weanling rats with dorsomedial hypothalamic nuclei lesions (DMN-L) are hypodipsic and hypophagic when compared to sham-operated rats. When tested for interdependence of food and water intake (WI) the DMN-L rats drank in the absence of food and ate in the absence of water. The data suggest DMN-L rats are not prandial drinkers. On testing for intracellular thirst (5.8 or 5.4% NaCl, 1 ml/100 g body wt), extracellular thirst [polyethylene glycol (PG), 25% wt/vol, 0.5 ml/35 g body wt], or a combination of both thirsts, the DMN-L rats responded as well or better than the control animals when the test data were expressed as a percentage of the rat's base-line WI. Both groups were more responsive to PG when tested in the light phase. When injected with angiotensin II (200 micrograms/100 g body wt) both groups responded similarly. Therefore, whereas the DMN-L rats were hypodipsic in comparison to controls, they respond as well or better than control animals when classical thirst testing procedures are utilized. It is suggested that DMN-L may have "reset" WI similarly to the previously proposed reset for body weight and food intake.

Response of Growth-Retarded, Hypophagic-Hypodipsic Rats with Dorsomedial Hypothalamic Lesions to a Diet in Liquid and Powder Forms

Weanling rats with dorsomedial hypothalamic lesions (DMNL rats) and sham-operated controls exhibited significantly reduced food intake and ponderal and linear growth during an 11-day post-operative period on lab chow. For 28 days, a synthetic liquid diet (Liquid) was fed to one DMNL and one control group; a second DMNL and control group received the same diet in a powder form (Powder). DMNL rats remained hypophagic on either diet but DMNL and control rats fed Liquid ate significantly more than their counterparts fed Powder. Total fluid intake pattern was identical to caloric intake. For 27 days all groups again received lab chow. They reverted to the caloric intake pattern shown during the 11-day post-operative period. Body weight gains paralleled the caloric and fluid intake patterns except that during the synthetic diet period the Liquid-fed controls outgained all other groups and that there was no difference between DMNL rats on Liquid and Powder. At sacrifice, plasma glucose, glycerol, free fatty acids and total protein were similar in all groups but carcass protein was higher in the DMNL rats formerly fed Liquid. DMNL rats behave in accordance with extensive previous data that led to the formulation of a “resetting” hypothesis.hypothalamic lesions energy intake set point linear growth dietary hydration plasma substrates

Dorsomedial hypothalamic hypophagia: Self-selection of diets and macronutrients, efficiency of food utilization, “stress eating”, response to high-protein diet and circulating substrate concentrations

Compared to sham-operated controls, male weanling rats with bilateral dorsomedial hypothalamic lesions (DMNL rats) showed hypophagia, reduced ponderal and linear growth, normal body composition and decreased efficiency of food utilization (EFU) two weeks after the hypothalamic operation. Subsequently, all animals were given a choice between three equicaloric diets with different macronutrient content for a period of 31 days. DMNL rats selected significantly less high-fat (HFD) and high-protein (HPD) diet than controls, but in percent of total intake, they selected only less from the HPD. DMNL rats consumed less of all three macronutrients than the controls, but in percent of total calories consumed, their intake was comparable to that of the controls; the EFU during this period was normal. Tail pinch (TP) stress did not result in hyperphagia, nor in a macronutrient choice different from the non-TP rats. However, TP caused reduced EFU and linear growth irrespective of hypothalamic damage, suggesting a stress response. During the 25-day availability of a HPD (43.2%), both DMNL rats and controls ate amounts of macronutrients comparable to the self-selection experiment. Although the DMNL rats were hypophagic in comparison with the controls, they ate more protein than in the self-selection experiment because of the higher protein content of the diet. Thus, DMNL rats will eat more protein when other macronutrients are limited. In both fed and 48h-fasted rats, there was no significant alteration in plasma glucose, glycerol, and total protein that could be related to the DMN lesions. It is concluded that the DMNL rat, despite its dramatically reduced size and energy intake, has not lost the capacity to select macronutrients for normal growth and health within the framework of its reduced somatic-metabolic potential.

Dorsomedial hypothalamic lesions at weaning and ovariectomy after maturity: Somatic and metabolic changes

Weanling Sprague-Dawley rats received lesions in the dorsomedial hypothalamic nuclei or sham operations. Analysis of variance revealed a significant lesion-induced depression of body weight (BW) and food intake (FI). After sexual maturity, bilateral ovariectomy (OVX) and/or sham-ovariectomy (S-OVX) were performed in each of the above groups. OVX produced a significant increase in BW in both lesioned and non-lesioned rats without changes in food intake. Following DMN lesions efficiency of food utilization (EFU) was greater than normal and OVX caused a further significant increase, irrespective of hypothalamic manipulation. DMN lesions, as previously shown, were followed by a reduction in linear growth; subsequent OVX exerted a growth-promoting effect in both DMN-lesioned and sham-lesioned rats. However, OVX did not alter plasma growth hormone or insulin levels. When calculated on the basis of per gram tissue protein, DMN lesions significantly diminshed the incorporation of glucose into lipids of diaphragm and fat pad, but not of liver. DMN lesions had no effect on the incorporation of glucose into glycogen of diaphragm, fat pad or liver. OVX did not produce significant changes in lipogenesis from glucose or incorporation of glucose into glycogen in either sham-lesioned OVX or DMN-lesioned OVX rats. The data support the concept that increased weight gain following OVX can be attributed to factors other than increased food intake. They also support previous findings that DMN lesions lower the BW “settling point” (i.e., both lean body mass and fat commensurately). The data also suggest that the DMNL rat is responsive to various manipulations—in this case OVX—of the adipose tissue mass “settling point”.

Ingestive behavior in adult rats with dorsomedial hypothalamic lesions

Large lesions in the dorsomedial hypothalamus (DMH) resulted in transient hypophagia that produced a significant weight loss. Energy intake per g of body weight returned to normal levels within 2 weeks after surgery but the body weight loss incurred during the immediate postoperative period was not compensated in 3 months of observation. The experimental animals responded poorly, if at all, to 2-deoxy-D-glucose induced cellular glucoprivation but ate normally after 2 doses of insulin and compensated appropriately for 24 hours of food deprivation. Rats with DMH lesions also displayed persisting hypodipsia (even when the animals' reduced body weights were taken into account) but responded normally, or nearly so, to water deprivation (with and without food), cellular dehydration, or extracellular hypovolemia. (Rats with DMH lesions drank slightly less than controls on most of these tests even when their chronically lowered body weights were taken into account but the impairment was small and, in most instances, not statistically reliable.)

Somatic and metabolic responses of mature female rats with dietary obesity to dorsomedial hypothalamic lesions: Effects of diet palatability

Caloric intake, body weight, obesity status (Lee Index) and incorporation of U-14 C-glucose into liver and retroperitoneal fat pad glycogen and lipid were studied in mature female rats that had received bilateral lesions or sham-operations in the dorsomedial hypothalamic nuclei (DMN) after dietary obesity was well established. Their diet consisted of a high-fat-sucrose chow mix, chocolate chip cookies and a drinking fluid of 32% sucrose in tap water. Comparable groups of DMN lesioned rats (DMNL rats) and sham-operated controls were maintained on lab chow pellets and tap water. Prior to the hypothalamic operation, the animals on the high-caloric regimen consumed significantly more calories than the rats on lab chow and also attained commensurately higher body weights and obesity indices. The bulk of the calories consumed during this time was derived from the cookies. Following DMNL, the animals maintained on lab chow became hypophagic and had lower body weights than the sham-operated rats, as has been previously reported. In rats on the high-caloric regimen, DMNL resulted in hyperphagia in comparison to all other groups. The greatest percentage of the calories during this time was derived from the high-fat-sucrose chow mix and sugar water. Correspondingly, DMNL rats on the high-caloric regimen had higher body weights and obesity indices than all other groups. At sacrifice, both a diet and lesion effect were noted in an elevated incorporation of U 14-C glucose in both fat pad and liver lipid and glycogen. The data are interpreted to mean that (1) when a highly palatable, high-caloric diet is available, DMNL do not exert their usual hypophagic and weight-lowering effects; (2) DMNL and control rats show excessive caloric intake when both groups are fed a highly palatable, high-caloric diet in comparison to their chow-fed counterparts. However, DMNL rats fed high-caloric diet also consume significantly more than controls fed this diet; (3) This excessive caloric intake of the DMNL rats possibly predisposes these animals to exaggerated lipogenesis in liver and adipose tissue; (4) the sham-operated controls on the high-caloric regimen also show greater lipogenesis but at a level intermediate between the chow-fed controls and the DMNL rats on the high-caloric diet.

Characterization of tissue enzyme activities in rats with dorsomedial hypothalamic lesions and their sham-operated controls

The dorsomedial hypothalamic lesions (DMNL) resulted in a depression in food intake and linear and ponderal growth. The present study was designed to examine basic enzymatic adaptations to the lesions produced in the dorsomedial hypothalamus. Liver glucose-6-PO 4 dehydrogenase, citrate cleavage enzyme and malic enzyme were depressed in DMNL rats. These observations suggest a depression in fatty acid synthesis in liver tissue; however, no change in the enzyme fatty acid synthetase was observed. Adipose tissue enzymes involved in the conversion of dietary carbohydrate to fatty acid were not significantly altered in the DMN syndrome. Subtle changes in enzyme activity may be responsible for the development of the DMN syndrome. The mechanisms of the induced changes in enzyme activity remain to be elucidated.

Tail‐pinch‐induced hyperphagia in weanling rats with dorsomedial hypothalamic lesions

AbstractDorsomedial hypothalamic lesions (DMNL) were produced in 26‐day‐old and 44‐day‐old male rats. Sham‐operated rats served as controls. Tail‐pinching (TP) was performed for five minutes at a time over two periods: the first TP period of six sessions each from post‐operative day 1 to day 17 and the second TP period of eight sessions from post‐operative day 18 to day 35. Three equicloric diets, high‐carbohydrate, high‐fat, and high‐protein, were presented ad libitum in pellet form during the TP sessions. Lab chow was available ad libitum in the home cages. Rats with DMNL at age 26 days did not show TP‐induced hyperphagia and HCD preference compared to the controls until the second TP period. In rats lesioned at age 44 days, TP‐induced hyperphagia and HCD‐preference (compared with controls) became evident immediately after the operation. In the home cages (lab chow), DMNL rats showed a decline in food intake from the first to the second TP period, while the sham‐operated controls showed an increase. TP‐induced hyperphagia in the rat with DMNL does not appear to be caused by some arousal‐related process as has been shown for the rat with lateral hypothalamic lesions. Lesions in the nigrostriatal system have been reported to attenuate TP‐induced feeding, while the present study indicates that lesions in the DMN enhance it. This suggests that fibers in the central nervous system may be involved in facilitation or inhibition of TP‐induced eating.

Feed efficiency in growth-retarded rats with ventromedial and dorsomedial hypothalamic lesions produced shortly after weaning

Weanling male rats received electrolytic lesions (L) in the ventromedial (VMN) and dorsomedial (DMN) hypothalamic nuclei; sham-operated rats served as controls. The animals were maintained for various periods up to 50 postoperative days on lab chow under standard conditions. In a short-term study, food intake and body weights were measured daily and body weight gain was divided by the food eaten to obtain the efficiency of food utilization. Also, gains in metabolic size ( kg 3 4 ) were divided by food eaten. Both manipulations showed that DMNL rats, except for the first two postoperative days, utilized food normally. The same changes were obtained for weanling VMNL rats, except that they did not show a decline in utilization during the first two postoperative days. Computation of efficiency of food utilization for both VMNL and DMNL rats over postoperative durations ranging from 7 to 50 days showed that among 12 out of 14 experiments DMNL rats utilized food as well as controls. Out of 8 experiments, rats with VMNL utilized food better for weight gained than controls in one and poorer than controls also in one experiment; in reference to metabolic size they utilized food normally. The foregoing data, gathered from 225 DMNL, 64 VMNL and 181 control rats show quite convincingly that food utilization in both types of experimental animals is unimpaired despite profound reductions in ponderal and linear growth and food intake in the DMNL rat and reduced circulating growth hormone levels in the VMNL rat.