Long-term effects of insulin in weanling rats with dorsomedial hypothalamic hypophagia: Food intake,efficiency of food utilization,body weight and composition

Twenty-five day-old Sprague-Dawley rats received electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated rats served as controls. Two weeks after the operation the DMNL rats showed reduced (p<0.001) body weight and food intake but normal body composition (Lee Index) and efficiency of food utilization (EFU). During the following 32 days subcutaneous administration twice daily of intermediary-acting insulin in increasing doses (mean daily dose 2.64 IU/kg) caused highly significant increases in food intake in both groups. Injection for the subsequent 14 days of higher doses of insulin (mean daily dose 5.64 IU/kg) caused dramatic increase in both food intake and Lee Index and equalized the rate of weight gain with that of the controls. However, in absolute terms the DMNL rats remained consistently hypophagic and weighed significantly less than the controls. Both DMNL rats and controls showed the same EFU during both periods of insulin administration. On discontinuation of hormone treatment during the subsequent 20 days, food intake and body weight gains returned to pretreatment values and the insulin-induced increased Lee Index returned into the low-normal range. However, EFU was significantly (p<0.05) decreased during this period. At sacrifice, plasma glucose, glycerol, free fatty acids and total protein and carcass lipid and protein were normal in the DMNL rats. Absolute and relative (per 100 g body weight and per metabolic size) weight of epididymal fat pads, pituitaries, adrenals and kidneys were normal in the DMNL rats but testes weight per 100 g body weight was higher (p<0.05) in the DMNL rats. Although DMN lesions may remove some glucose-sensitive elements within the hypothalamus, the animals are still capable of responding to the food intake and weight-promoting properties of insulin, as do intact animals.     

Further evidence for the existence of an "organismic" set point in rats with dorsomedial hypothalamic nucleus lesions (DMNL rats): normal catch-up growth

The present study was performed to assess the capacity of rats with dorsomedial hypothalamic nucleus lesions (DMNL rats) and sham-operated controls (CON) for catch-up growth following body weight (b.wt.) reduction prior to DMNL (and sham-lesion) production. Male SD rats (45 days, 157 +/- 1.3 g) were maintained for 11 days ad lib (ADLIB) after arrival and then divided into two groups. One group continued to feed ADLIB, the other group was fed half of the ration eaten by ADLIB rats for 32 days. At this point each group was divided into two subgroups. One subgroup received DMNL, the other subgroup consisted of CON. From then on all rats were fed ADLIB [except for one group of CON that was pair-fed to the ADLIB DMNL rats (PF-CON)] for 37 days (69th day of experiment) and then killed. DMNL rats lesioned at normal b.wt. (ADLIB DMNL) showed a precipitous drop in food intake, b.wt. and efficiency of food utilization (EFU). In striking contrast, rats that had received DMNL after b.wt. restriction (REST DMNL) and were then refed ADLIB showed a dramatic rise in food intake, b.wt., change in b.wt. and EFU, the latter being almost twice that of the ADLIB DMNL. Notably, the PF-CON weighed less than the ADLIB CON and utilized food poorer than ADLIB CON, REST CON and ADLIB DMNL. Liver weight (both absolute and relative (per kg 3/4 b.wt.) was reduced in DMNL irrespective of dietary treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Failure to demonstrate early metabolic changes in weanling growth-retarded hypophagic rats with lesions in the dorsomedial hypothalamic nuclei

Experiment 1: Weanling male rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated animals served as controls. Rats were killed four hours and three and seven days postoperatively (post-op). Plasma was obtained and epididymal fat pads, diaphragm and liver aliquots were harvested and the in vitro incorporation of U-14C-glucose into CO2, glycogen, lipid and saponifiable fatty acids (FAs) were measured. Body weight, carcass lipid and food intake were significantly lower in DMNL rats than in controls. The only significant lesion-induced metabolic changes were hypoglycemia and greater tracer incorporation into epididymal fat pad lipid and diaphragm glycogen. Both DMNL rats and controls showed similar time courses of tracer incorporation into epididymal CO2 and FAs, diaphragm lipid and liver CO2, glycogen, lipid and FAs. Lesioned rats also showed more pronounced decreases of tracer incorporation from day 0 to day 3 in epididymal glycogen and lipid and diaphragm CO2 and glycogen. These data make it appear unlikely that very early deficits in glucose metabolism are the cause of the growth retardation seen in long-term studies with DMNL rats. The data also demonstrate considerable locus specificity, since weanling rats with ventromedial hypothalamic lesions (VMNL rats) in similar short-term studies have shown dramatic alterations in the above parameters. Experiment 2: Weanling DMNL rats and sham-operated rats were injected via tail vein with tritiated water one hour post-op. One hour after the injection they were decapitated. There were no significant differences between DMNL rats and controls in mumoles tritiated water incorporated into total liver, grams liver tissue, mg liver glycogen and ml or mg plasma glucose.(ABSTRACT TRUNCATED AT 250 WORDS)     

Food intake and utilization in lateral hypothalamically lesioned rats

The daily food intake of rats with lateral hypothalamic (LH) lesions was monitored in two experiments. Confirming earlier reports, LH-lesioned animals were found to ingest nearly the same amount of food per day as nonlesioned controls even though their body weights remained substantially below those of the controls. In view of this result, an experiment was conducted to compare the efficiency of food utilization of LH-lesioned and control animals at different body weights. First, the daily food intakes of seven LH-lesioned rats and seven nonlesioned controls were determined. The body weights of these animals were then lowered by restricting food intake in four successive weekly periods to 85%, 70%, 55% and 40% of their ad lib level. Finally, all animals were refed for one week at their prerestriction levels of food intake reduced in proportion to the intervening loss in metabolic mass (body weight_kg^0.75). At each level of caloric restriction, the weight losses observed in the LH-lesioned and control animals were equivalent. Likewise, though given only prerestriction amounts (indexed to their reduced metabolic mass), LH-lesioned and nonlesioned animals both gained weight rapidly and at equivalent rates during refeeding. Thus, LH-lesioned animals appear to utilize food in a normal fashion and, as do controls, adapt to weight loss by increasing their efficiency of food utilizazion. In the case of LH-lesioned animals, however, such adjustments occur around a reduced level of maintained body weight, or set-point.     

Failure to demonstrate disruption of ultradian growth hormone rhythm and insulin secretion by dorsomedial hypothalamic nucleus lesions that cause reduced body weight,linear growth and food intake

Summary Weanling male rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated animals served as controls. At the end of a 39-day postoperative period DMNL rats were lighter and shorter than controls and also exhibited significant hyopophagia. Their efficiency of food utilization (weight gained for the amount of food eaten) was normal, however. Subsequent determination of plasma growth hormone (GH) and insulin (IRI) levels every 15 min for 6-h periods from freely moving chronically cannulated rats showed no differences in pulsatile patterns and peaks of GH nor in plasma IRI levels between DMNL rats and controls. There was also no significant difference between mean 6-H GH and IRI concentrations between the two groups. The reduced body weight, length and food intake are apparently unrelated to the normal GH and IRI secretory patterns. In conjunction with previous data indicating normal somatomedin activity and normal responses to various homeostatic challenges, the data make a strong case for the argument that DMNL rats are not growth-retarded. Rather, they are normal animals that are scaled-down to a smaller size with maintenance of normal homeostatic capacity. This has been hypothesized to be due to the existence in these animals of an organismic set point.     

Increased efficiency of food utilization following weight loss

The efficiency of food utilization following a period of restricted caloric intake was examined under controlled feeding conditions. By restricting caloric intake, the body weight of two groups of rats was reduced to either 92 or 81% of that of an unrestricted control group. For one week, all animals were then fed daily an amount of food equal to their prerestriction intake, adjusted for the intervening change in metabolic mass ($\text{FI}\text{BW}{}_{\mathrm{kg}}{}^{0.75}\text{=}\text{K}$). During this period of realimentation, the control animals gained an average of 1.6 g body weight while ingesting 156.1 g of food. The two restricted groups gained 21.4 g on 154.2 g food and 29.6 g on 140.4 g food, respectively. This inverse relationship between weight gain and food intake provides evidence that underweight animals utilize food more efficiently than do undeprived control animals.     

Weanling ventromedial hypothalamic syndrome. bone geometry and biomechanics

The effect of growth-retarding, obesifying lesions in the ventromedial hypothalamic nucleus (VMN) on bone geometry and biomechanics was investigated in male weanling rats. The animals received bilateral, symmetrical, electrolytic lesions (VMNL rats) shortly after weanling (age 27 days); sham-operated rats served as controls (SCON). The rats were maintained for 42 postoperative days and then terminated. Body weight, nose-tail length, food intake, carcass water, and lean body mass were all significantly (p < 0.001) reduced in the VMNL group compared to SCON rats. Carcass fat, lipogenic efficiency (carcass fat % laid down/mean food intake) (both p < 0.001) and epididymal fat pad weight (p < 0.01) were significantly increased in VMNL versus SCON. Femur length, anteroposterior diameter (both p < 0.001), and mediolateral femur diameter (p < 0.01) were significantly reduced in VMNL versus SCON rats, but torque and angle of torque were comparable among the groups. VMNL rats femora also showed a significant greater maximum shear stress compared to the control animals. The reduced parameters in the VMNL rats are in good agreement with the previously demonstrated reduced plasma and pituitary growth hormone levels found in this hypothalamus preparation.     

Somatic, endocrine and metabolic changes in controls pair-fed for six weeks to rats with dorsomedial hypothalamic nucleus lesions (DMNL rats)

One group of weanling male Sprague-Dawley rats received lesions in the dorsomedial hypothalamic nuclei (DMNL rats), whereas two additional groups of rats were sham-operated (CON). One of these CON groups was allowed to feed ad lib (CON-ADLIB) while the other CON group was pair-fed for 6 weeks to the DMNL rats (CON-PF). Despite eating the same amount of food as DMNL rats. CON-PF animals had consistently lower body weights and also utilized food energy more poorly than DMNL rats. The CON-PF group also had smaller kidneys and less percent liver protein but more epididymal fat pad percent protein than DMNL rats. Whereas plasma glucose concentrations were comparable among the three groups, insulin levels were significantly higher, and free fatty acid levels lower in CON-PF than in DMNL rats. The CON-PF group incorporated less glucose-U-C14 carbon into liver glycogen but more of the tracer into liver lipid than the DMNL group. Glucose carbon was also incorporated more avidly into epididymal fat pad lipid by CON-PF than by DMNL rats. The data not only confirm previous findings in DMNL rats but in addition show that the neurologically intact rats fed the same amount of food that is eaten spontaneously by DMNL rats show somatic and metabolic alterations that suggest that they cannot cope with this low amount of substrate. The normalcy of the DMNL rats, compared to ad lib-fed sham-operated controls, in all metabolic parameters suggests that the low food intake is indeed "normal" for this preparation and may be the reflection of an "organismic" set point.     

Effect of diet consistency, taste and calories on food intake of weanling rats with dorsomedial hypothalamic lesions

Male weanling Sprague-Dawley rats with dorsomedial hypothalamic lesions (DMNL rats) primarily destroying the dorosomedial hypothalamic nuclei (DMN) showed significant hypophagia on lab chow chunks compared to sham-operated controls. When given a choice between lab chow in the form of chunks or powder, both controls and DMNL rats ate similar amounts of lab chow powder while DMNL rats ate less lab chow chunks. Total caloric consumption was the same as on chunks alone. When returned to lab chow chunks as the only source of calories, the pattern and magnitude of intake was again depressed for the DMNL rats. When offered a choice between Ginger Snaps cookies in chunk form versus powder, DMNL rats remained hypophagic in terms of chunk consumption while the intake from powder was similar in both controls and DMNL rats. When offered a choice between chunks of lab chow and Ginger Snaps, DMNL rats were again hypophagic on lab chow chunks, ate the same as the controls of the cookies, and the total caloric intake was of the same magnitude and pattern as observed in previous tests. The data suggest, but do not conclusively show, that DMNL rats are not hypophagic because they have an aversion to chewing hard food and that, when offered a diet similar in hardness to lab chow chunks i.e., hard cookies, will prefer the less tasty but nutritionally complete lab chow. They are apparently capable of choosing a diet for complete nutrition and, as previously reported, can meter calories competently.     

Naloxone suppression of food and water intake and cholecystokinin reduction of feeding is attenuated 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 micrograms/kg) given at the onset of the dark cycle significantly suppressed the food intake of the SCON group but had no significant 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 that DMN may play a role in cholecystokinin-induced satiety.     

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.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of insulin in rats with lesions of the dorsomedial hypothalamic nucleus.

Four hours after insulin injection Dorsomedial Hypothalamic Nuclei (DMN) lesioned rats consumed an amount of food that was comparable to that eaten by injected sham-operated animals. However, the DMN lesioned rats are not as initially responsive to the food intake stimulating properties of insulin as are the controls. A second study showed ad lib fed and fasted lesioned animals displayed a lower plasma glucose concentration after insulin challenge than did respectively treated controls. This suggests the initial insulin-induced feeding of the lesioned rats was blunted when compared to the controls even in the face of lower plasma glucose levels. Although a previous investigation revealed that DMN lesions destroy glucoreceptor tissue, the present data shows that DMN lesioned rats will increase their food intake in the face of insulin challenge, albeit their initial feeding response to insulin challenge is somewhat blunted. Finally, the present study confirms a previous report in that DMN lesioned rats can competently meter their 24 hour calorie intake.     

The dorsomedial hypothalamic nucleus and its role in ingestive behavior and body weight regulation: lessons learned from lesioning studies

This review article discusses the well-established role of the dorsomedial hypothalamic nucleus (DMN) in feeding, drinking and body weight (BW) regulation. DMN lesions (L) in both weanling and mature rats of both sexes produce hypophagia, hypodipsia and reduced ponderal and linear growth in the presence of normal body composition. The growth reduction is not due to a deficient secretion of growth hormone, insulin-like growth factor-1, thyroxine, triiodothyronine or insulin. DMNL rats actively defend their lower BW (BW settling point) by becoming either hyper- or hypophagic, depending on the experimental manipulation, thereby defending both lean and fat mass. They also regulate their 24-h caloric intake, but they may overeat during the first hour of refeeding following a fast, possibly due to a reduced ability to monitor blood glucose or to respond to cholecystokinin (CCK). 2-Deoxy-D-glucose (2DG) increases c-fos expression in orexin-A neurons in the DMN, and DMNL eliminated the orexigenic effect of 2DG. DMNL rats on high-fat diets do not get as obese as controls, which may be due to a reduction of DMN neuropeptide Y (NPY). Rats lacking DMN CCK-A receptors are obese and have increased expression of NPY in the DMN, supporting earlier data that CCK may act at the DMN to suppress food intake. Excitotoxin studies showed that loss of DMN cell somata, and not fibers of passage, is important in the development of the DMNL syndrome. The DMN is a site where opioids increase food intake and knife-cut studies have shown that fibers traveling to/from the DMN are important in this response. An interaction of glucose and opioids in DMN may also be involved in the control of food intake. DMN knife cuts interrupting fibers in the posterior and ventral directions additively produce the hypophagia and reduced linear and ponderal growth observed after DMNL. Ventral cuts may interrupt important connections with the arcuate nucleus. Lateral and posterior DMN cuts additively produce the hypodipsic effect seen after DMNL, but DMNL rats respond normally to all water-regulatory challenges, i.e., the hypophagia is not due to a primary hypodipsia. The DMN has been shown to be involved in the rat's feeding response to an imbalanced amino acid diet. These data show the DMN has an important role in many processes that control both food intake and BW regulation.     

Strain differences in drinking in inbred mice during ad libitum feeding and food deprivation

Water intakes were measured in 7 mouse strains under 3 conditions of food availability: (a) ad lib feeding, (b) $\text{1}\text{3}\text{-}\text{normal}$ food intake, and (c) total food deprivation. Under ad lib feeding strains were ranked according to magnitude of water intake. These ranks were similar, but not identical, when absolute water intakes (ml) and relative (ml/100 g body wt) water intakes were measured. Statistically reliable, positive correlations were found between food intake and body weight, water intake and food intake, and water intake and body weight. Under the $\text{1}\text{3}\text{-}\text{food}$ condition, mean water intakes decreased significantly from ad lib feeding conditions in the BALB/cJ, A/J and C57BL/6J strains, did not change significantly in the SWR/J, CBA/J and DBA/2J strains and increased (food-deprivation polydipsia) in the C3H/HeJ strains. Results in 2 replications of total food deprivation parallelled those of $\text{1}\text{3}$ normal intake except that in the former condition DBA/2J mice showed a significant decrease in water intake. Food-deprivation polydipsia was seen in some individual SWR/J and CBA/J mice, as well as in the C3H/HeJ strain but was very rare in the other four strains.     

Increased drinking of a nonpreferred NaCl solution during food deprivation in the C3H-HeJ mouse

When food was given ad lib, C3H/HeJ mice showed a progressive decrease in NaCl solution intake as the concentration increased from 0.5–2.5% under single tube or double tube conditions. Under the latter condition, 1.5% NaCl intake volumes were approximately 20% of water intake volumes. However, when restricted to $\text{1}\text{3}$ normal food intake, the mice showed significant increase in the intake of 1.5% NaCl and several animals consumed more salt solution than water. Salt intakes declined to predeprivation levels upon return to free feeding. Since feeding of a sodium deficient diet produced no alteration in intake of 1.5% NaCl, the increase during food deprivation was attributed to hypovolemia rather than hyponatremia.     

Rapid eye movement stage of sleep participates in the generation of the nocturnal meal pattern in the rat

Twenty-four hour cycles of food intake were continuously recorded in eight male rats on a $\text{12}\text{12}$ hr light/dark schedule during baseline conditions and rapid eye movement sleep deprivation. The results suggest that food intake in the rat is controlled by two different mechanisms, one serving control of immediate caloric demands during the dark part of the LD cycle and the other, activated prior to the beginning of the inactive light hours, being responsible for the intake of a few large meals covering the total energy requirement for this time period. The correct timing of the consumption of these large meals with respect to the LD cycle seems to be dependent on undisturbed rapid eye movement sleep.     

Disruption of diurnal feeding and weight gain cycles in weanling rats by ventromedial and dorsomedial hypothalamic lesions

At the age of 28 days, male Sprague-Dawley rats received bilateral electrolytic lesions in the ventromedial (VMN) and dorsomedial (DMN) hypothalamic nuclei, repectively. Sham-operated rats served as controls. Food intake and body weight gains were measured for 13 days at the beginning of the light period (0800–2000 hr) and prior to the start of the dark period (2000-0800 hr). Both types of hypothalamic lesions caused a disruption of the naturally occurring diurnal feeding and weight gaining cycles. In accordance with previous data, the VMN rats remained normophagic and made normal weight gains while DMN animals were hypophagic and gained weight subnormally; linear growth was reduced in both types of lesioned animals, but only the VMN rats became obese. The data suggest the existence in the medial hypothalamus of an area that is involved in feeding and weight gaining cycles. From the standpoint of overall-caloric intake, this area consists of two types of neuronal assemblies that differ fuctionally as profoundly as they are anatomically separate.     

Tail pinch-induced eating does generalize to a nonpreferred but familiar food.

Mild tail pinch has been reported to induce many of the same behaviors as electrical stimulation of the brain. In this study a 4 min tail pinch induced significant eating of either canned dog food or rat chow. In contrast to eating produced by brain stimulation, which does not generalize along the appropriate stimulus dimension of food objects, removal of the tail pinch-induced eaters' preferred food resulted in their eating another nonpreferred, but familiar food. With only the nonpreferred food available, intake of animals who preferred rat chow increased and intake of animals who preferred dog food decreased compared to their respective controls, although no initial differences existed. When both foods were again available, $\text{13}\text{18}$ animals retained their initial preference while $\text{5}\text{18}$ showed no preference. No animals reversed their preference. Tail pinch-induced eating may be more similar to normal eating than that produced by electrical brain stimulation.     

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.     

Growth and metabolic changes in weanling rats with lesions in the dorsomedial hypothalamic nuclei

Summary When compared with sham-operated ad libitum-fed controls, weanling rats with lesions primarily destroying the dorsomedial hypothalamic nuclei (DMNL rats) showed reduced ponderal and linear growth and food intake, normal carcass fat but increased carcass protein. Among the metabolic parameters measured, DMNL rats showed only decreased incorporation of palmitate into epididymal fat pad phospholipid and triglyceride. When sham-operated controls were pair-fed with DMNL rats, they showed growth changes almost identical with those observed in lesioned rats. However, their carcass protein was lower than both that of the lesioned rats and the ad libitum-fed controls. Metabolically, the sham-operated, pair-fed controls showed decreased incorporation of palmitate into triglyceride of epididymal fat pads and decreased oxidation of glucose and increased incorporation into total lipid of the diaphragm. When previous data on growth hormone, insulin, triglyceride and cholesterol are compared with the present findings it is suggested that dorsomedial lesions cause a subcaloric-type dwarfism that does not involve adenohypophyseal secretions and their target organs affecting growth.This investigation was supported by USPHS Grants HD 03331, AM 14418, NIH, a Veterans Administration Grant and a Veterans Administration Clinical Investigatorship (JKG).