Sham feeding in rats after ventromedial hypothalamic lesions and vagotomy.

Two studies examined sham feeding in female Sprague-Dawley rats with ventromedial hypothalamic (VMH) lesions with or without abdominal vagotomy. In Exp I, intact Ss consumed more than twice as much sweet milk during 1-hr tests of sham feeding as they did when feeding normally. Ss with VMH lesions showed exaggerated sham feeding, which was elevated almost four-fold over their already high normal feeding baseline. In Exp II, vagotomy substantially reduced sham feeding in Ss with VMH lesions. After vagotomy, VMH Ss sham fed half as much as nonvagotomized VMH Ss. Vagotomy did not, however, reduce sham feeding to control levels. Results are consistent with the hypothesis that VMH hyperphagia arise from exaggeration of orosensory responsiveness, which is, in part, a consequence of perturbed vagal function. (40 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Atropine fails to block the overconsumption of sugar solutions by hypothalamic hyperphagic rats.

Adult female Sprague-Dawley rats given bilateral parasagittal knife cuts in the medial hypothalamus (VMH group) were hyperphagic and became obese on a chow diet, compared with sham-operated controls. VMH Ss also overconsumed, relative to controls, sucrose and glucose solutions during 30-min/day tests. Pretreating VMH and control Ss with atropine methyl nitrate (1.0, 5.0, or 10.0 mg/kg) reduced their intake of the sugar solutions in 3 of 5 experiments, and in all experiments it suppressed their 24-hr chow intake. However, VMH Ss continued to drink more of the sugar solutions than the controls after all atropine treatments, and in 3 of 4 experiments their hyperphagia on the chow diet was not blocked by the atropine. Results do not support the hypothesis that vagally stimulated insulin release or other cholinergically mediated cephalic responses of digestion are essential for the expression of hypothalamic hyperphagia and finickiness. (44 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Thiamin deprivation in ventromedial hypothalamic hyperphagic rats: Anorexia, specificity of food aversion, and a dietary consideration.

In 3 studies, the anorexic consequence of thiamine deprivation was investigated in ventromedial hypothalamic (VMH) hyperphagic CD male rats under either high-fat or low-fat (HF and LF, respectively) thiamine-free diet conditions. The LF diet maintained feeding significantly longer in thiamine-deprived VMH Ss than in intact Ss, whereas the HF diet sustained feeding in thiamine-deficient intact Ss and accelerated anorexia onset in vitamin-B1-deprived VMH Ss. This effect was noted under both ad lib and pair-feeding conditions. Thiamine-deprived VMH Ss subjected to weight control developed anorexia sooner than intact Ss regardless of the diet employed. The VMH Ss fed an HF diet failed to resume feeding after thiamine readministration, which is interpreted as a permanent aversion to this diet. The relation between dietary intake and conditioned taste aversion is discussed with reference to the VMH and intact rats. (28 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Active regulation to be lean by rats with ventromedial hypothalamic lesions.

52 adult female Long-Evans rats with electrolytic or radio-frequency thermocoagulatory lesions of the ventromedial hypothalamus (VMH) lived on pellet fragments or powdered chow containing as much as 1.2% quinine sulfate or lived in Skinner boxes with 45-mg pellets delivered contingent on FRs of leverpressing up to FR 128. Body weights maintained by VMH Ss were determined by the percentage of quinine in or the contingency of reinforcement of the food on which they lived. Even when Ss lived on highly adulterated or response-contingent food and were lean, they ate more of that food when the ambient temperature was reduced and less of that food during several weeks of forced feeding of eggnog. Weight maintenance in the cold and caloric compensation during forced feeding were as precise for VMH Ss eating highly adulterated chow or Noyes pellets contingent on high FRs as for VMH Ss eating laboratory chow ad lib, even though the former Ss at the time maintained weights no greater than intact Ss and the latter Ss were grossly obese. Regulation in the cold or during forced feeding was only a little less precise for Ss with lesions than for intact Ss. It may be as characteristic of VMH Ss that they eat to become lean and remain lean as that they eat to be obese. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Vagotomy blocks hypothalamic hyperphagia in rats on a chow diet and sucrose solution, but not on a palatable mixed diet.

Adult female Sprague-Dawley rats were given ventromedial hypothalamic parasagittal knife cuts (VMH treatment) or control surgery (Con treatment), followed 10 days later by subdiaphragmatic vagotomy (Vag treatment) or sham vagotomy (Sham treatment). The hyperphagia and obesity produced by the VMH cuts to Ss on a chow diet was completely blocked by vagotomy (VMH-Vag group). Vag also inhibited the VMH Ss' overconsumption of a 20% sucrose solution during 1-hr/day and 24-hr/day tests, which contrasts with the effects of atropine treatment. However, when offered a selection of palatable foods (cookies, sweet milk, high-fat ration) in addition to chow, VMH-Vag Ss overate and gained considerably more weight than did the Con-Vag or the Con-Sham Ss. Con-Vag Ss, on the other hand, gained less weight than Con-Sham Ss on the palatable diet. Results indicate that intact subdiaphragmatic vagi are not essential for the expression of VMH hyperphagia and finickiness, and they therefore question the role of vagally mediated cephalic responses in the hypothalamic hyperphagia syndrome. On the other hand, results indicate that in brain-intact animals Vag suppresses the development of diet-induced obesity. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Multiple knife cuts between the medial and lateral hypothalamus in the rat: A reevaluation of hypothalamic feeding circuitry.

In 2 experiments single or multiple sets of bilateral knife cuts were made in a total of 73 female CFE rats just lateral to the ventromedial hypothalamus (VMH) and/or just medial to the lateral hypothalmus (LH). The lateral VMH knife cuts by themselves produced greater hyperphagia and obesity than did the medial LH cuts. The lateral VMH knife cuts also significantly increased food intake and body weight in Ss previously given bilateral cuts along the medial LH border. Findings indicate that the feeding inhibitory fibers responsible for the hyperphagia syndrome do not project from the VMH to the LH, and this calls for a reevaluation of hypothalamic circuitry. It was also discovered that sham surgery in 7 Ss had a significant suppressive effect on the hyperphagia syndrome produced by hypothalamic knife cuts. (25 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Ventromedial hypothalamic hyperphagia in the hypophysectomized weanling rat.

Previous findings that ventromedial hypothalamic (VMH) lesions in weanling rats lead to obesity only after a delay of several weeks suggests either that the VMH is (a) undeveloped and not yet functioning; or (b) capable of functioning in weanlings, but inoperative for some reason. The present study demonstrates that 17 hypophysectomized weanling rats, which otherwise eat very little and grow at a markedly reduced rate, show hyperphagia with rapid onset following VMH lesions. Results support G. Kennedy's view that the presence of high levels of growth hormone in the weanling is responsible for VMH inactivity, either by eliminating the usual metabolic satiety signals and/or via a direct effect of the hormone on the VMH. Growth hormone involvement is suggested to account for the greater ease in producing hypothalamic hyperphagia in female than in male rats. (18 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Decrease in food intake following cortical spreading depression in static obese rats with ventromedial hypothalamic lesions.

Subjected 19 male and 23 female rats with ventromedial hypothalamic (VMH) lesions or with sham lesions to cortical spreading depression (CSD) 150 days after lesioning. Lesioned Ss showed a significantly lower food intake (as percentage of intake before CSD) than sham-lesioned Ss in the 14 days after CSD, but water intake did not differ between lesioned and sham-lesioned Ss. Both groups showed a slight decline in body weight, but lesioned Ss lost significantly more weight than sham-lesioned Ss. After 14 days, body weight, food intake, and water intake had returned to pre-CSD levels in both groups. Findings indicate that Ss with VMH damage are more sensitive to the effects of CSD than are normals and suggest that CSD acts to increase the activity of the VMH and to inhibit food intake, and this increase in activity is prolonged in VMH-lesioned Ss. (22 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Benfluorex normalizes hyperglycemia and reverses hepatic insulin resistance in STZ-induced diabetic rats

We have examined the effect of chronic (20 days) oral administration of benfluorex (35 mg/kg) in a rat model of NIDDM, induced by injection of STZ 5 days after birth and characterized by frank hyperglycemia, hypoinsulinemia, and hepatic and peripheral insulin resistance. We assessed the following: 1) basal blood glucose and insulin levels, 2) glucose tolerance and glucose-induced insulin release in vivo and in vitro, and 3) basal and insulin-stimulated in vivo glucose production and glucose utilization, using the insulin-clamp technique in conjunction with isotopic measurement of glucose turnover. The in vivo insulin response of several individual tissues also was evaluated under the steady-state conditions of the clamp, using the uptake of the glucose analogue 2-deoxy-D-glucose as a relative index of glucose metabolism. In the benfluorex-treated diabetic rats, postabsorptive basal plasma glucose levels were decreased (8.1 +/- 0.2 mM compared with 10.5 +/- 0.5 mM in the pair-fed untreated diabetic rats and 6.1 +/- 0.2 mM in the benfluorex-treated nondiabetic rats), whereas the basal and glucose-stimulated intravenous glucose tolerance test plasma insulin levels were not improved. Such a lack of improvement in the glucose-induced insulin release after benfluorex treatment was confirmed under in vitro conditions (perfused pancreas). In the pair-fed untreated diabetic rats, the basal glucose production and overall glucose utilization were significantly increased, and during hyperinsulinemia both liver and peripheral tissues revealed insulin resistance. In the benfluorex-treated diabetic rats, the basal glucose production and basal overall glucose utilization were normalized. After hyperinsulinemia, glucose production was normally suppressed, whereas overall glucose utilization was not significantly improved.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vagotomy Blocks Hypothalamic Hyperphasia in Rats on a Chow Diet and Sucrose Solution, but Not on a Palatable Mixed Diet: Correction.

Reports an error in the original article by A. Sclafani, P. Aravich and M. Landman (Journal of Comparative and Physiological Psychology, 1981, Vol. 95, No. 5, 720-734). Table 3 contains several errors in the mean and standard error values for the second and third groups. The correct table is provided. (The following abstract of this article originally appeared in record 1982-09338-001): Adult female Sprague-Dawley rats were given ventromedial hypothalamic parasagittal knife cuts (VMH treatment) or control surgery (Con treatment), followed 10 days later by subdiaphragmatic vagotomy (Vag treatment) or sham vagotomy (Sham treatment). The hyperphagia and obesity produced by the VMH cuts to Ss on a chow diet was completely blocked by vagotomy (VMH-Vag group). Vag also inhibited the VMH Ss' overconsumption of a 20% sucrose solution during 1-hr/day and 24-hr/day tests, which contrasts with the effects of atropine treatment. However, when offered a selection of palatable foods (cookies, sweet milk, high-fat ration) in addition to chow, VMH-Vag Ss overate and gained considerably more weight than did the Con-Vag or the Con-Sham Ss. Con-Vag Ss, on the other hand, gained less weight than Con-Sham Ss on the palatable diet. Results indicate that intact subdiaphragmatic vagi are not essential for the expression of VMH hyperphagia and finickiness, and they therefore question the role of vagally mediated cephalic responses in the hypothalamic hyperphagia syndrome. On the other hand, results indicate that in brain-intact animals Vag suppresses the development of diet-induced obesity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Ventromedial syndrome: The rat's "finickiness" results from the obesity, not from the lesions.

6 obese, finicky female hooded rats with lesions of the hypothalamic ventromedial nucleus (VMH) and 7 sham-lesioned controls progressively lost weight on an unpalatable diet until at a critical basal level they increased their intake to prevent further loss of weight. The critical basal body weight was similar in both groups and showed no change in the controls when they were subsequently lesioned and retested. At weight levels below the critical basal level the feeding behavior of lesioned and unlesioned Ss was similar, and finickiness could be demonstrated only when body weight exceeded it. The basal level bore no relation to the plateau level of body weight reached by Ss on a free diet. Suggestions that the VMH excites as well as inhibits feeding seem untenable in view of the failure of VMH lesions to impair defense of body weight in the nonobese rat. (17 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Adrenocortical response to hypertonic saline in rats with lateral hypothalamic lesions.

Used plasma corticosterone levels to assess the response to stress induced by ip injections of hypertonic saline in 27 male albino Harlan-Sprague rats with lateral hypothalamic (LH) or sham lesions. Ss with LH lesions displayed a corticosterone response equal to that of normal Ss under basal conditions, after control injections of isotonic saline, and 20 min after injection of hypertonic saline (1.5 M, 1.0 ml/100 g of body weight). The corticosterone response of Ss with LH lesions, however, was significantly less than that of normal Ss 90 min after injection of hypertonic saline when no water was available. With access to water, normal Ss displayed substantial drinking (14.5 ml/90 min), which resulted in a reduction in plasma corticosterone concentrations to a level observed after a control injection of isotonic saline, but the little water ingested by Ss with LH lesions (2.5 ml) had no effect on the pituitary-adrenal system. It is concluded that the failure of Ss with LH lesions to drink following a hydrational challenge is not the result of an exaggerated response to stress. (17 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Seasonal weight gain is attenuated in food-restricted ground squirrels with lesions of the suprachiasmatic nuclei.

Assessed the role of seasonal hyperphagia in the genesis of prehibernation fattening 19 female golden-mantled ground squirrels (Spermophilus lateralis). Control Ss (n?=?17) were fed ad lib throughout the weight gain phase of the annual bodyweight cycle (June–October), and neurologically intact Ss (n?=?7) and Ss with brain lesions incorporating the suprachiasmatic nuclei (SCN; n?=?5) were fed amounts of food equivalent to quantities consumed prior to the bodyweight trough (May). Results indicate that part of the seasonal increase of body mass was independent of increases in food consumption; intact Ss and controls underwent similar increases in body mass and possessed equivalent amounts of abdominal white adipose tissue. Food restriction combined with SCN lesions attenuated seasonal weight gain and reduced abdominal fat mass. However, some brain-damaged Ss still evidenced weight gain. It is concluded that SCN are involved in circannual body weight rhythm generation, but their contribution to this process is not essential for continued rhythmicity in most individuals. (19 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of prefeeding on the DRL performance of rats with septal lesions.

Conducted 2 experiments with a total of 17 Long-Evans male hooded rats (8 with septal lesions and 9 unoperated controls) to study the effects of prefeeding prior to daily sessions on a DRL-20 schedule. Prefeeding reduced responses and increased reinforcement in the case of septal Ss, regardless of the level of body weight. In the case of normal Ss, prefeeding led to a decrease in responding and an increase in the number of reinforcements obtained only when the Ss were at 85% of ad lib body weight. At ad lib levels, prefeeding, although it decreased responding, also decreased the frequency of obtained reinforcements. Results suggest an impairment in normal Ss in the discrimination of response feedback by stimulation arising from stomach distention. (18 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Some characteristics of feeding during streptozotocin-induced diabetes in the rat.

Injected 24 male Sprague-Dawley albino rats with a buffer solution or 25-45 or 50-60 mg/kg of streptozotocin. 4-9 days after 50-60 mg. of streptozotocin Ss showed abbreviated intermeal intervals. There was also a lack of proportionality in intermeal interval duration to size of the preceding meal. This result probably accounts for the hyperphagia which develops at 4-6 days and increases over 2 wk. Such effects were not seen in the lst 3 days, even though the Ss were glucosuric and polydipsic within 24 hr. of streptozotocin treatment. In contrast, decreases in basal feeding rate and in meal size did begin to develop in the 1st 3 days of diabetes. It is suggested that aversion to the diet develops immediately on insulin deficiency, but that the satiety deficits and hyperphagia in chronic diabetes are secondary to considerable changes in body composition. (41 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Increased motivation in rats with ventromedial hypothalamic lesions.

25 female albino rats were implanted with chronic electrodes aimed for the ventromedial hypothalamic area (VMH), deprived to 82% of normal weight, and trained on a 2-min VI schedule for food reinforcement. After rates of response became stable, bilateral DC lesions were made, and weight was held constant. Over 10 days after lesioning, Ss with extensive VMH damage showed increases in rates of response for food. Unilateral lateral hypothalamic lesions resulted in decreases in response rates followed by recovery, regardless of VMH damage. Under more severe deprivation (48 hrs and 72 hrs), Ss with extensive VMH damage showed further increases in response rate. Results indicate that VMH lesions increased food motivation. Some factors which can produce opposite results are discussed. (38 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Conditioned insulin secretion and meal feeding in rats.

Previous researchers have reported that rats placed upon a feeding regimen such that they receive only 2 hrs of food/day (meal-fed rats) develop hyperinsulinemia at the time of the day associated with feeding, even in the absence of food. Controls fed ad lib show no such response. In the 3 experiments reported here, the 74 meal-fed Charles River rats had elevated insulin levels at only the specific time of the day associated with feeding, and the increment of insulin at that time could be eliminated with atropine. The 58 free-feeding controls, on the other hand, always had higher insulin levels than the meal-fed rats, did not have an elevation of insulin at the time of the day that the meal-fed rats normally ate, and had insulin values that were unaffected by atropine. Further experimentation showed that hyperinsulinemia could become associated with arbitrary stimuli always associated with eating for meal-fed rats. It is concluded that the hyperinsulinemia of meal-fed rats associated with their feeding time is a learned response. (19 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Metabolic and endocrine aspects of the ventromedial hypothalamic syndrome in the rat.

Subjected 8 male Long-Evans hooded rats to parasagittal knife cuts that separated the medial from the lateral hypothalamic areas; following surgery, some Ss were given free access to food while others were restricted to normal quantities. Compared with 6 sham-operated controls, the restricted-food Ss exhibited hyperinsulinemia as early as 36 hr after surgery without any change in plasma glucose levels. The blood samples of free-food Ss which had become obese, showed hyperinsulinemia, mild hyperglycemia, and elevated levels of free fatty acids. These results suggest that the interruption of mediolateral hypothalamic connections produces hyperinsulinemia directly, and that further increases in insulin, glucose, and free fatty acid levels are caused by overeating. The surgical cuts produced an increase in aggressive behavior but no change in the circulating levels of testosterone. (41 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Enhancement and suppression of self-stimulation after ventromedial hypothalamic lesions.

Investigated the effects of lesions in the ventromedial hypothalamus (VMH) upon self-stimulation in 25 male hooded Long-Evans rats. Ss trained to press a bar for lateral hypothalamic (LH) stimulation showed an enhancement of responding during the 1st 24 hrs after VMH lesioning, followed by a suppression of responding for several days. The degree of response suppression, but not enhancement, was correlated with an increase in food intake. In Ss trained to shuttle for LH stimulation, only the suppression effect was observed after VMH lesions. Barpressing for dorsal tegmental stimulation was not affected by the lesions. Results suggest that LH stimulation activates at least 2 groups of neurons: one group is specifically involved in barpressing and the other is involved equally in barpressing and shuttling. (French summary) (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Food-deprivation-induced behavioral arousal: Mediation by hypothalamus and amygdala.

Conducted 5 experiments, using a total of 238 male albino Sprague-Dawley rats. Electrolytic lesions of the basomedial hypothalamus eliminated food-deprivation-induced stabilimeter activity in Ss that were prevented from becoming obese. Knife cuts lateral to the basomedial area (separating the medial and lateral hypothalamus) potentiated this activity, as did transections posterior to the basomedial region. Anterior transections (between anterior and medial hypothalamus), however, eliminated the effect. Lesions of the stria terminalis and amygdala likewise abolished deprivation-induced locomotor activity, but elevated ad lib activity to a level comparable with that after deprivation in intact Ss. Ss with combined basomedial-stria terminalis lesions behaved like Ss with basomedial lesions. Results suggest that food-deprivation-induced locomotor activity in stabilimeter cages was due to a disinhibition of the basomedial hypothalamus by the amygdala via the stria terminalis. (79 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)