Diet palatability modulates sham feeding in VMH-lesion and normal rats: Implications for finickiness and evaluation of sham-feeding data.

Examined the capacity for taste cues to modulate the food intake of 24 ventromedial hypothalamic (VMH) and normal Long-Evans rats. Ss were implanted with a chronically indwelling gastric cannula and sham fed (cannula open) or normally fed (cannula closed) liquid diets varying in sucrose content. VMH Ss were maintained at control body-weight levels. For both groups, the discrepancy in consumption between sham and normal feeding situations depended on the sweetness of the diet. The implications of this finding for studies using sham feeding to assess putative feeding control signals are discussed. VMH lesions exaggerated the sensory control of food intake. Under sham-feeding conditions, increases in the sweetness of the diet led to disproportionately large increments of food intake in VMH Ss relative to controls. Data support the existence of a finickiness component in the VMH syndrome and allude to the nature of the physiological disturbance underlying this behavior change. (36 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)     

Reactivity of normal and VMH-lesion rats to quinine-adulterated foods: Negative evidence for negative finickiness.

Conducted 2 experiments with ventromedial hypothalamic (VMH) and normal rats to examine (1) whether the anorexic properties of quinine depend on quinine's sensory properties or on its postingestive effects, and (2) whether VMH rats overrespond to quinine adulteration. These issues were examined by comparing the feeding adjustments to quinine by VMH and normal male Long-Evans rats in a sham-feeding situation and under normal feeding circumstances, on Ss' initial exposure to this drug. In Exp I, 17 Ss received VMH lesions or sham lesions before being sham fed with various concentrations of quinine. In Exp II, 18 lesioned or sham-lesioned Ss were fed unadulterated food for 12 days, followed by a meal adulterated with quinine, 2 days of pure mash, and 1 day of quinine. Quinine caused significant depression of food intake in Ss. Little evidence exists for a conclusion that VMH rats are more reactive than normals to quinine-adulterated foods. Results suggest that major food intake perturbations of VMH rats are in response to hedonically positive dietary manipulations. (31 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)     

Food motivation and body weight levels in hypothalamic hyperphagic rats: A dual lipostat model of hunger and appetite.

Compared the food and water motivations of 26 normal and 29 hyperphagic female Carworth CFE rats using barpressing performance on continuous reinforcement, VI, and fixed-ratio schedules. Under conditions of food or water deprivation, hyperphagic Ss displayed normal barpressing rates for food or water when their body weights were limited to preoperative or control levels but subnormal barpressing rates when they were tested at obese body-weight levels. Under nondeprived conditions, dynamic hyperphagic Ss barpressed more than controls for a palatable milk diet, while obese hyperphagic Ss worked at control levels for this diet. The findings suggest a dual lipostat model of hunger and appetite to explain feeding and body weight regulations in normal and hypothalamic hyperphagic animals. (62 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)     

Influence of age and hepatic branch vagotomy on the night/day distribution of food intake in rats

The aim of the present study was to investigate the influence of age and hepatic branch vagotomy on the night/day distribution of food intake in male rats. Food intake of young (age: 2 months) and aged (age: 13.5 months) hepatic branch vagotomized (HBV) and sham-vagotomized (SV) rats was measured at intervals of 6 h during the 12 h dark and the 12 h light phase. The results show that in rats the night/day ratio of food intake decreases with age and is not affected by hepatic branch vagotomy. However, the time-course of spontaneous diurnal food intake was influenced by hepatic branch vagotomy. The change in the night/day distribution of food intake might be due to age-related changes in the nucleus suprachiasmaticus of the hypothalamus.     

Genetic versus hypothalamic obesity: Studies of intake and dietary manipulations in rats.

Studied feeding behavior in 4 experiments with a total of 86 Zucker rats. Ad-lib food and water intakes were significantly greater for the genetically obese rats (fatties) than for their nonobese littermates. The ratio of water intake per gram of food intake was not different for the 2 groups. The ability to regulate caloric intake was then tested in 4 groups of rats: genetically obese, ventromedial hypothalamic lesioned (VMH) obese, sham operated, and normal controls. In response to caloric dilution and quinine adulteration the genetically obese Ss behaved more like normal Ss than like VMH-lesioned Ss. Sensitivity to quinine increased with age in the Zucker fatty. The fact that Ss with genetic obesity and Ss with hypothalamic obesity displayed different behaviors suggests that obesity is not merely a unitary disorder. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of ventromedial hypothalamic lesions on hunger-motivated behavior in rats.

Previous studies show that lesions of the ventromedial hypothalamus (VMH) paradoxically increase food intake and decrease hunger motivation in the rat. In a series of experiments designed to examine this paradox, independent groups of VMH-lesioned, female hooded rats (N = 48) were tested on a VI schedule or were run in a straight alley to a food reward. Rate of food ingestion was also measured for all Ss. Performance of the VMH and control groups was compared at identical deprivation conditions defined in terms of preoperative base-line weights (80, 90, 100, and 110%). All test measures showed a significantly higher level of performance for VMH-lesioned Ss at the least severe deprivation conditions. Results suggest that the previously reported VMH paradox originated, in part, from inappropriate testing procedures and between-group comparisons. (20 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Conditioned taste aversion in lean and obese rats with ventromedial hypothalamic knife cuts.

Assessed the development of a conditioned taste aversion (CTA) in 60 female Sprague-Dawley rats made hyperphagic with parasagittal knife cuts in the ventromedial hypothalamus (VMH). Ss were water deprived and presented with a .1% saccharin solution paired with injections of either LiCl or NaCl. In Exp I, VMH Ss tested at a nonobese weight level did not differ from sham-operated controls in acquisition and extinction of the CTA. In Exp II, moderately obese VMH Ss displayed a stronger CTA than did sham-operated controls as evidenced by slower extinction. A 2nd group of obese VMH Ss given an amount of LiCl equivalent to that given to the controls also displayed retarded extinction of the CTA. Results reflect an obesity-induced suppression in appetitive motivation. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Regulation of energy balance in two models of reversible obesity in the rat.

Reports on 2 experiments with 114 adult male Sprague-Dawley rats. Ss were made obese either by tube feeding varying fractions (34, 47, 68, or 75%) of their normal food intake or by offering them a varied and palatable diet (cafeteria diet). After 17–30 days of these regimens, the treatments were withdrawn, and Ss were allowed free access to the normal stock diet. Tube-fed Ss precisely adjusted voluntary food intake to compensate for the energy delivered by tube but nevertheless became obese as a result of an increased metabolic efficiency. Cafeteria-fed Ss were hyperphagic and became obese without any apparent change in metabolic efficiency. Recovery from obesity was more rapid in cafeteria Ss and was due to a pronounced increase in heat production as well as concomitant hypophagia. Ss previously made obese by tube feeding exhibited hypophagia and returned to normal weight without any change in heat production. The relevance of these results to the concept of lipostasis and the relative roles of energy intake and expenditure in the regulation of energy balance are discussed. (17 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Estrus- and ovariectomy-induced body weight changes: Evidence for two estrogenic mechanisms.

Estrogenic modulation of body weight in female rats is usually thought to result indirectly from estrogenic modulation of food intake. However, present data from 5 experiments with 79 female albino rats suggest that estrogens influence body weight by at least 2 mechanisms, 1 of which is independent of changes in food intake. When Ss were ovariectomized (Ovx) and food intake was limited to preoperative levels, Ovx Ss nonetheless gained large amounts of body weight. Although Ovx Ss gained more weight than controls on the same amount of food, during 33 hrs of food deprivation Ovx and control Ss lost weight at the same rate, indicating that the prefasting metabolic rates of the 2 groups were similar. During the 1st 40 days after surgery, the ano-nasal lengths of Ovx Ss increased twice as fast as that of intact Ss, which suggests a mechanism for the gradual increase in weight induced by Ovx. The weights of intact Ss followed a regular 4-day cycle during ad lib feeding, but when the estrus-associated decrease in food intake was prevented, the cyclic weight changes were altered. Thus estrogens appear to regulate body weight by modulation of food intake and modulation of ano-nasal growth or other metabolic processes. (22 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)     

Effects of chronic intrahypothalamic infusion of insulin on food intake and diurnal meal patterning in the rat.

In Experiment 1, rats were chronically infused with insulin (2.7, 27, or 270 ng/hr) or 0.9% saline into the ventromedial (VMH), medial perifornical (PF), or lateral (LH) hypothalamus. VMH infusions of insulin caused a significant, dose-dependent decrease in food intake and body weight; PF infusion of insulin was less effective, but significant; whereas LH infusions of insulin were ineffective. In Experiment 2, rats were chronically infused with insulin (0.54 ng/hr) or 0.9% saline into the VMH, paraventricular (PVN), or posterior (PN) hypothalamic nucleus. Subjects that received VMH or PN infusions of insulin failed to regain weight lost as a result of surgery even 2 weeks after infusion; subjects that received PVN infusions of insulin regained their preoperative weights faster than did controls. All of the groups that received insulin significantly increased their daytime food intake during the infusion period and decreased their night food intake slightly; 24-hr food intake remained unchanged. (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)     

Hyperphagia in rats with experimental diabetes mellitus: A response to a decreased supply of utilizable fuels.

In 2 experiments with male Sprague-Dawley rats, alloxan-diabetic rats were hyperphagic when fed diets containing little fat, but they ate normal amounts of food when given diets rich in fat. Normal Ss increased food intake to the same degree when the caloric density of their diet was decreased by reducing the content of fats or carbohydrates in isocaloric amounts. Diabetic Ss did not respond substantially to changes in caloric density of their diet which were produced by altering the content of dietary carbohydrates, but they systematically increased food intake as the amount of fat in their diet was reduced. Diabetic Ss ate normal amounts of a high-fat diet despite continued loss of nutrients in urine and persisting impairments in glucose utilization, fat storage, and liver glycogen deposition. Findings suggest that hyperphagia in experimental diabetes mellitus is a compensatory response to a lack of utilizable fat fuels rather than the result of a metabolic disturbance per se. (33 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of models on food intake of obese and non-obese female college students.

Compared the effects of a model on the food intake of obese and nonobese females. 20 obese and 20 nonobese female Ss were paired with an experimental confederate who was either obese or nonobese. Analysis of the amount of food eaten revealed an interaction between weight status and type of confederate: obese Ss ate significantly more in the presence of an obese confederate. By contrast, nonobese Ss ate a similar amount in both conditions. There was a significant difference between the amount Ss ate and the amount they reported they had eaten, due largely to the fact that obese Ss underestimated the amount of food they had eaten. (French summary) (13 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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)     

Feeding behavior in the rat with isolated medial hypothalamus

After complete, unilateral, frontolateral, dorsal isolation of the medial hypothalamus, VMH included, or fornix section above the hypothalamus, total food consumption and diurnal pattern of food intake were followed 85 days postoperatively. It is suggested that the saftety signals are generated not only in VMH nucleus, but in a VMH-retrochiasmatic region located anteriorly to the VMH.     

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)