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L L Bernardis

Publications and source records attributed to L L Bernardis.

At least 37 records · Page 2Linked to original sources

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.

Animals↗

Metabolic-endocrine correlates of the lateral hypothalamic syndrome: the first 48 hours.

Mature (224 g) male Sprague-Dawley rats received bilateral electrolytic (1 mA for 8 sec) lesions in the lateral hypothalamic area (LHAL) or sham operations (CON). One group of CON was allowed to eat ad lib (CON-ADLIB), a second CON group was pair-fed to the LHAL rats (CON-PF). Tap water was available ad lib. Two days after the operation/sham operation all rats were killed by decapitation. Body weight, body weight change, food intake, carcass fat, liver weight, epididymal fat pad weight, in vitro incorporation of U-C14-glucose into liver total lipid, glycogen and CO2 (oxidation) (DPM, DPM/mg protein) as well as oxidation in fat pad tissue, plasma glucose and insulin were significantly reduced in LHAL and CON-PF rats compared with CON-ADLIB. Glucose carbon incorporation into epididymal fat pad lipid and glycogen were normal in LHAL and CON-PF. Liver protein and plasma free fatty acids (FFA) were both higher in LHAL and CON-PF than in CON-ADLIB groups. Thus, many of the somatic and metabolic changes that appear in the first few days after lesion production are simply due to hypophagia. However, CON-PF rats also exhibited some significant differences from the LHAL group, i.e., their plasma glucose and incorporation of glucose carbon into liver glycogen (DPM) were significantly lower than in LHAL rats; alternatively, plasma FFA levels were higher in CON-PF than in LHAL rats. Also, liver weight/100 g body weight was lower and fat pad weight/100 g body weight was higher in CON-PF than in LHAL rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Failure to demonstrate an effect of dietary fatty acid composition on body weight, body composition and parameters of lipid metabolism in mature rats.

The objectives of the present study were to examine the effects of dietary fatty acid composition on body composition and on several parameters of lipid metabolism in adipose tissue and to assess the ease of weight loss with restricted dietary intake. Rats were fed diets containing 14% fish oil, safflower oil or beef fat plus 2% corn oil. These diets were fed ad libitum for 4 wk (first phase). A number of the animals from each group were killed, and the others were fed 50% of their first-phase food intake for an additional 4 wk (second phase). The diets used in the second phase contained 3% of the above fats plus 2% corn oil. Food consumption, food efficiency and body weights were monitored. After the rats were killed, fatty acid composition of epididymal fat pads was examined. In addition, in vivo lipolysis and in vitro lipogenesis in epididymal fat pads were examined. The results indicate that dietary fatty acid composition had no effect on body weight, food consumption, in vivo lipolysis and in vitro lipogenesis in epididymal fat pads. In addition, although dietary fatty acid manipulation resulted in alteration in adipose tissue fatty acid composition, it had no effect on the rate of weight loss, body composition, in vivo lipolysis and in vitro lipogenesis in epididymal fat pads. It is concluded that dietary fatty acid composition does not play a role in body composition and in lipid metabolism in adipose tissue of mature rats.

Animals↗

Normal catch-up growth in rats severely food-restricted prior to lesions of the dorsomedial hypothalamic nucleus: the first 48 hours.

Following a brief period of ad lib (AL) feeding, 45-day-old male Sprague-Dawley rats were either fed AL or food-restricted (REST) for 21 days to 50% of the intake of the AL rats. At this time, some AL and some REST rats received electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL), whereas other AL and REST rats were sham-operated (CON). Following this, all rats were refed (REF) AL and killed two days later. At this time, DMNL-REST + REF and DMNL-AL weighed as much as CON-REST + REF and CON-AL, whereas the body weight of the DMNL-AL group began to separate from the CON-AL group; carcass lipid and protein were normal among the groups. DMNL-AL laid down more % lipid and % protein/g food eaten than CON-AL; this was not the case in the REST + REF groups. DMNL-AL were hypophagic vs. CON-AL, but DMNL-REST + REF ate as much as CON-REST + REF. Compared to DMNL-AL, DMNL-REST + REF increased their food intake more than four-fold and also utilized food energy more efficiently than DMNL-AL rats. Epididymal fat pads and kidneys were smaller in REST + REF vs. AL groups, irrespective of brain manipulation. Plasma glucose and growth hormone were normal among the groups, but plasma insulin concentrations were higher in REST + REF DMNL and CON groups vs. DMNL-AL and CON-AL, respectively. Glucose incorporation into epididymal fat pad lipid and CO2 and liver lipid was elevated in REST-REF groups vs. respective AL groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

Animals↗

Recovery of rats with dorsomedial hypothalamic nucleus lesions (DMNL rats) from body weight restriction: effect of duration of postoperative prerestriction period.

The present study was performed to see whether somatic and underlying metabolic-adaptive responses of DMNL rats and sham-operated controls (CON) to body weight restriction and subsequent refeeding could be influenced by the duration of ad lib feeding between lesion production and start of restriction. In contrast to previous studies (42 and 55 days, respectively) this time was reduced to 25 days. Restriction was similar, i.e., 27 days. DMNL rats show the same adaptive capacity in most parameters as do restricted CON. However, this response was at a lower level of absolute body weight, appropriate, so it appears, for their DMNL-induced lower body weight. In some parameters different responses were noted, however, suggesting that the time of ad lib feeding following the DMNL does indeed affect adaptive responses. Notably, this is the case in both DMNL and CON commensurately. Linear growth was reduced by restriction in the present but not in the two previous studies. Food intake showed a pronounced "overshoot" on refeeding but did not previously. Efficiency of food utilization was normal in the present study but depressed previously. A rise in plasma free fatty acids was not evident but was so in previous experiments. We concluded that, although DMNL rats respond to food restriction and recovery like similarly-treated CON, the duration of the ad lib feeding before restriction and/or the absolute age of the animals at that time, do indeed affect some parameters. This may be related to the fact that different aspects of the DMNL syndrome declare themselves in a sequential rather than a simultaneous manner.

Adipose Tissue↗

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.

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 hypophagia. 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.

Activity Cycles↗

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)

Animals↗

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 REST-CON than in AL-fed DMNL and AL-fed CON. After seven days of refeeding they normalized only in formerly REST-CON. 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.

Animals↗

Differential effect of common snack foods on caloric intake, growth and obesity in weanling male and female rats with hypothalamic obesity.

In order to see whether weanling normophagic rats with hypothalamic obesity (VMNL rats) become hyperphagic and more obese than when fed lab chow, and to see in addition whether there is a possible sex difference in whatever response is found, male and female VMNL rats were fed lab chow for 14 days after lesion production and then, for the following 42 days, they received Hostess HoHos, potato chips, marshmallows and french fries in addition to lab chow. At termination, body weights were similar among the groups, but VMNL rats were fatter and shorter than controls. Also, female VMNL rats were fatter and shorter than male VMNL rats and layed down more fat per unit of food energy. Total caloric intake was greater in controls than in VMNL rats and in males than in females. However, the females showed a decrease in intake and the males an increase over time. Males ate more lab chow and french fries than females. Lab chow was the only food that VMNL rats ate more of than controls. The VMNL rats ate less french fries, HoHos and potato chips than controls, but similar amounts of marshmallows. There was no sex difference in macronutrient intake and per cent macronutrient intake. Moreover, controls ate as much carbohydrate and less per cent carbohydrate than VMNL rats, more fat than VMNL rats, but normal per cent fat and normal protein and per cent protein. Sex X lesion interactions indicated that female VMNL rats ate more per cent carbohydrate than female controls and male VMNL rats, ate more protein than male controls. The greater degree of obesity in the females despite the lower caloric intake may be due to enhanced food energy utilization. The data also show that weanling VMNL rats do not exhibit the great preference for palatable diets that have been reported for mature rats with ventromedial hypothalamic area lesions and that the only sex difference in intake is with french fries, which have neither the highest fat nor the highest carbohydrate content of the foods tested.

Animals↗

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.

Animals↗

Differential spontaneous and stimulated in vitro release of newly synthesized or stored rGH and rPRL by pituitaries from rats with hypothalamic lesions.

These experiments were designed to examine which aspects of basal and responsive somatotroph and lactotroph synthesis and release behavior in vitro are functions of in vivo tonic hypothalamic environment. Although we cannot specifically define in vivo hypothalamic tone, we show that spontaneous rates of hormone synthesis and release in vitro, as well as release in response to a secretagogue, are influenced by altered in vivo hypothalamic tone. This work combines in vivo destruction of hypothalamic (ventromedial [VMN] or dorsomedial [DMN]) nuclei with in vitro double-label perifusion to track hormone synthesis and release of newly synthesized and stored hormone. We demonstrate that hormone synthesis rates are greater in DMN-lesioned (DMNL) or sham-operated (SHAM) animals than in VMN-lesioned (VMNL) animals and that DMNL and SHAM synthesis rates fall with time outside the hypothalamic environment. We show that basal release of newly synthesized rGH by DMNL tissue exceeds that of SHAM, while release from VMNL tissue is less than that of SHAM. Accidental placement of small bilateral lesions between and not impinging on either the DMN or VMN nuclei did not alter newly synthesized rGH release but accelerated newly synthesized rPRL release. Although basal fractional release of stored growth hormone and prolactin was the same for the three groups, potassium ion-induced release of stored hormone was similar in DMNL or SHAM tissue, but depressed in VMNL tissue. Thus, the creation of definable hypothalamic damage in a living animal produced specific modifications in in vitro pituitary synthetic/secretory behavior, presumably by reproducibly altering hypothalamic secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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.

Animals↗

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)

Adipose Tissue↗

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.

Animals↗

Pancreatic and intestinal digestive enzymes in post-weanling rats with hypothalamic obesity.

Male Sprague-Dawley rats received bilateral electrolytic lesions in the ventromedial hypothalamic nuclei (VMNL rats) at the age of 31 days; sham-lesioned rats served as controls. For 28 post-operative days all animals self-selected from three synthetic diets, each high in carbohydrate, fat and protein, respectively. Following this, half of the VMNL rats and half of the controls were switched to lab chow for 14 days. Body weights were comparable among the groups, but linear growth was greatly reduced and body fat (Lee Index) was elevated in VMNL rats, irrespective of diet. In the sham-lesioned controls, the synthetic diets reduced most parameters of exocrine pancreatic activity. In VMNL rats, in contrast, pancreatic parameters were unaffected by the synthetic diet. The data suggest that VMN lesions disinhibit the exocrine pancreas. In contrast, most parameters of intestinal activity were not influenced by VMN lesions.

Animals↗

Ventromedial and dorsomedial hypothalamic syndromes in the weanling rat: is the "center" concept really outmoded?

This report juxtaposes findings from weanling rats with precise lesions in the ventromedial (VMNL rats) to data of weanling rats with lesions in the dorsomedial (DMNL) hypothalamic nuclei. Despite the proximity of the two nuclei their destruction produces opposite effects in most cases but similar responses in other parameters. Absolute and relative food intake are normal in VMNL rats yet they become obese in the face of normal body weight gains. DMNL rats show both reduced absolute food intake and body weight but normal relative food intake and body composition. Both VMNL and DMNL cause reduced linear growth and running wheel activity. DMNL rats defend their lower body weight set point against various challenges and maintain normal body composition. Organ growth in both absolute and relative terms is reduced in VMNL rats. In DMNL rats relative organ growth is normal. Pancreatic growth, protein/pancreas and content and concentrations of several pancreatic enzymes are normal in DMNL but reduced in VMNL rats. Mean 24-hour plasma growth hormone (GH) and corticosterone (B) levels are reduced and insulin levels are greatly elevated in VMNL rats; prolactin (PRL) levels are normal. In DMNL rats, GH, B, insulin and somatomedin activity are normal but PRL is elevated. Circadian rhythms of GH, insulin and triiodothyronine are normal in DMNL rats but B levels are disrupted, as they are in VMNL rats. Glucose incorporation and oxidation in adipose tissue of VMNL rats are enhanced in VMNL rats but normal in DMNL rats. Gluconeogenesis in VMNL rats is enhanced as early as 4 hours post-operatively; in DMNL rats it is normal at this time and several weeks thereafter. Basal lipolysis in epididymal fat pads is elevated in both VMNL and DMNL rats but epinephrine-stimulated lipolysis is elevated in VMNL and decreased in DMNL rats. Both VMNL and DMNL rats show normal basal and epinephrine-stimulated lipolysis in interscapular brown adipose tissue. Several hepatic enzymes are normal in DMNL and depressed in VMNL rats. The above data suggest that the DMN and its circuitry are part of an "organismic" set point system with a "true" body weight and no fat set point, as seems to be the case in the VMNL rat.

Animal Population Groups↗