Hypophagic Rats Research Articles

Effect of stress on feeding behavior in rats: individual differences

Abstract The experiment was conducted to study individual differences in stress-induced changes of food intake in rats and to examine concomitant changes of non-eating behaviors. Eating and non-eating behaviors were measured during five consecutive test sessions under stressful noise (95 dB white noise, n =18) and control conditions (60 dB white noise, n =18). Two thirds of the stressed rats were classified as normophagic, one third showed hypophagic responses. Hypophagic rats spent less time eating and more time grooming and resting than normophagic and control rats. Hypophagic rats also showed an increased tendency of scanning movements during eating and an increased tendency to leave the food area. Their eating speed was significantly lower than that of the normophagic rats. Hypophagic rats were characterized by a heightened reactivity to stressors which may have counteracted the adaptation to the stressful feeding situation. Results point to a role of biological factors for individual differences in stress-induced changes of eating.

Nitric oxide reduces hypophagia induced by threonine free diet in the rat

Food intake and concentrations of glutamic (GLU) and aspartic (ASP) acids in the nucleus accumbens were monitored in male Sprague–Dawley rats fed a threonine free diet. These variables were measured before and after an intracerebroventricular injection of 20 nmole nitroprusside (NP), a non-enzymatic nitric oxide donor. The same variables were also monitored in: (a) rats fed a threonine free diet and injected with saline; (b) animals fed a standard diet and injected with nitroprusside; (c) rats fed a standard diet and injected with saline. The results showed that the threonine-free diet reduced food intake and GLU and ASP concentrations in the accumbens. NP reduced the hypophagia, but it did not change GLU and ASP levels in rats fed the threonine-free diet. In animals fed the standard diet, NP increased GLU and ASP concentration, and food intake. No change was found in the animals with saline injection. These findings suggest that nitric oxide reduces the hypophagia in the rats fed a threonine-free diet. The lack of increase in GLU and ASP concentration in the nucleus accumbens of the hypophagic rats indicates that NP acts on hypophagia independently by GLU and ASP.

Hypophagic rats with dorsomedial hypothalamic lesions produce lighter and smaller pups with a lower survival rate at weaning than offspring of sham-operated controls

Weanling and mature rats with dorsomedial hypothalamic nucleus lesions (DMNL rats) show reduced ponderal and linear growth and hypophagia and hypodipsia in the presence of normal body composition and anabolic hormone levels. The present study was conducted to assess their reproductive/parenting capacity and some offspring parameters. Four groups were used: DMNL mothers and fathers, DMNL mothers and control (SCON) fathers, SCON mothers and DMNL fathers, and SCON mothers and SCON fathers. The constituent rats of each group were bred to yield between 14 and 22 litters. The smallest litter size, litter weight, mean pup weight, percent of live-born and percent of weaned pups and greatest percentage of still-born pups were recorded when both parents were DMNL rats. The latter parents also cannibalized the majority of litters. The above parameters improved when only one parent was a DMNL rat, but this was still significantly below the offspring of SCON × SCON parents. The DMN is not part of the classical hypophysiotropic area (HTA), but earlier findings indicate hyperprolactinemia in DMNL rats. Therefore, the lesion-induced hypophagia during gestation and the postpartum neuroendocrine profile of the DMNL mothers may be the cause of the observed litter deficiencies and poor survival.

The effect of diet consistency on food intake of anorectic tumor‐bearing rats

Delayed gastric emptying has been shown to occur in cancer patients complaining of anorexia and early satiety. Given that liquids are emptied from the stomach faster than solid food, the present study was undertaken to determine if diet consistency would affect food intake of hypophagic rats implanted with the Walker 256 carcinosarcoma. By Day 15 of tumor-growth, caloric intake of tumor-bearing animals was 20% less than controls. The caloric intake of tumor-bearing animals fed a liquid diet was not significantly different from animals fed a solid diet. Furthermore, a delay in gastric emptying was not seen in this animal model of tumor-induced anorexia.

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 CO 2, 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 CO 2 and FAs, diaphragm lipid and liver CO 2, 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 CO 2 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 μmoles tritiated water incorporated into total liver, grams liver tissue, mg liver glycogen and ml or mg plasma glucose. These data suggest normal glucogenesis in DMNL rats one hour after lesion production and made it unlikely that the growth retardation in DMNL rats is related to an early defect in this aspect of protein metabolism. By contrast, weanling VMNL rats show enhanced gluconeogenesis four hours after lesion production.

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

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

Blood metabolites and feeding during postinsulin hypophagia

Physiological changes accompanying a period of voluntary hypophagia in male Sprague-Dawley rats after insulin-induced hyperphagia and body weight gain were investigated. Postinsulin hypophagia was manifested as a reduction in meal duration diurnally and nocturnally (Geary et al., Behav. Neural Biol. 31: 435-442, 1981). Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats, suggesting a postabsorptive mechanism controlled the hypophagia. Basal blood glucose and plasma nonesterified fatty acids, 3-hydroxybutyrate, glycerol, and some amino acids were elevated during hypophagia, while liver glycogen content was reduced. Hypophagic rats' arteriovenous blood glucose differences and glucose oxidation rates, however, were not different from controls. After nutrient repletion blood glucose and plasma glycerol remained elevated in hypophagic rats in comparison to controls, while differences in other plasma metabolites were reduced. Liver glycogen accumulated faster in hypophagic rats. These data were related to the lipostatic and other hypotheses how energy balance status affects hunger and satiety.

Obesity in exercising, hypophagic rats treated with monosodium glutamate

Two experiments employing 32 female and 28 male rats, respectively, were performed in order to assess the effects of monosodium glutamate (MSG) on locomotor activity levels, as well as the consequences of such activity on the known obesity that follows MSG injections. In both sexes activity levels of MSG-treated animals were not significantly different from those of controls. Obesity developed in both sexes despite normal activity levels and hypophagia. Vaginal smears and autopsy data indicated that the female reproductive system was severely disturbed while no apparent anomalies were noted in the males. Skeletal growth arrest was evident in both sexes at 130 days of age. The data are interpreted in the context of the hypopituitarism of the MSG animal. A sexual dimorphism in both MSG and intact animals was noted as regards the food intake-activity interaction: spontaneously active females ate significantly more than nonactive females, while there was no such difference in males.

Energy metabolism of tube-fed hypophysectomized rats bearing hypothalamic lesions.

ARTICLESEnergy metabolism of tube-fed hypophysectomized rats bearing hypothalamic lesionsPW HanPW HanPublished Online:01 Dec 1968https://doi.org/10.1152/ajplegacy.1968.215.6.1343MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByHypothalamic control of energy expenditure and thermogenesis17 March 2022 | Experimental & Molecular Medicine, Vol. 54, No. 4Silencing of estrogen receptor α in the ventromedial nucleus of hypothalamus leads to metabolic syndrome13 February 2007 | Proceedings of the National Academy of Sciences, Vol. 104, No. 7The rise, fall, and resurrection of the ventromedial hypothalamus in the regulation of feeding behavior and body weightPhysiology & Behavior, Vol. 87, No. 2Obesity1 January 2011The effects of chronic ventromedial hypothalamic stimulation on weight gain in ratsPhysiology & Behavior, Vol. 50, No. 6Adipose Cellularity in Gallus domesticus: Investigations to Control Body Composition in Growing ChickensThe Journal of Nutrition, Vol. 121, No. 9The nervous system and adipose tissueClinics in Dermatology, Vol. 7, No. 4Central control of brown adipose tissue28 February 2007 | Proceedings of the Nutrition Society, Vol. 48, No. 2Fetal hypothalamic brain grafts reduce the obesity produced by ventromedial hypothalamic lesionsBrain Research, Vol. 424, No. 2Neural activity in hypothalamic and genetic obesity28 February 2007 | Proceedings of the Nutrition Society, Vol. 46, No. 1Central Nervous System Control of Nutrient Homeostasis1 January 2011Hyperphagia: A Necessary Precondition to Obesity?Appetite, Vol. 6, No. 2The role of brown adipose tissue thermogenesis in energy balanceDieting: Ideology Versus PhysiologyPsychiatric Clinics of North America, Vol. 7, No. 2Changes in body weight and food-related behaviour induced by destruction of the ventral or dorsal noradrenergic bundle in the ratNeuroscience, Vol. 10, No. 4The interaction of psychological and metabolic factors in the control of eating and obesityScandinavian Journal of Psychology, Vol. 23, No. s1The role of vagally-mediated hyperinsulinemia in hypothalamic obesityNeuroscience & Biobehavioral Reviews, Vol. 6, No. 2Reduced sympathetic nervous system activity in rats with ventromedial hypothalamic lesionsLife Sciences, Vol. 30, No. 11Metabolic aspects of obesityMolecular Aspects of Medicine, Vol. 5, No. 5Intragastric pair feeding fails to prevent VMH obesity or hyperinsulinemiaJ. E. Cox, and T. L. Powley1 May 1981 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 240, No. 5Heat-induced saliva secretion and thermoregulation in female rats with ventromedial hypothalamic lesionsPhysiology & Behavior, Vol. 26, No. 5Effects of ventromedial hypothalamic lesions on adipose tissue of weanling male rats1 March 1981 | Diabetologia, Vol. 20, No. S1Efficiency of food utilization during body weight gain in dormice (Glis glis)Physiology & Behavior, Vol. 24, No. 6Stress-induced eating: Fact, fiction or misunderstanding?Appetite, Vol. 1, No. 2Hypophysectomy blocks the weight gain and obesity produced by goldthioglucose lesionsBehavioral and Neural Biology, Vol. 28, No. 3Hypothalamic hyperphagia prevented by damage to brain dopamine-containing neuronsPhysiology & Behavior, Vol. 22, No. 4Obesity in exercising, hypophagic rats treated with monosodium glutamatePhysiology & Behavior, Vol. 19, No. 6Independence of food intake and obesity following ventromedial hypothalamic lesions in the ratPhysiology & Behavior, Vol. 13, No. 6Anorexia nervosa and the regulation of intake: a review9 July 2009 | Psychological Medicine, Vol. 4, No. 3Effect of damage to the ventromedial hypothalamic nuclei on the state of the pancreatic islets in rats on a restricted dietBulletin of Experimental Biology and Medicine, Vol. 77, No. 4Protein metabolism in rats with ventromedial hypothalamic lesionsMetabolism, Vol. 22, No. 11In vivo and in vitro metabolism in hypothalamic obesityDiabetologia, Vol. 8, No. 3Gastric Capacity and Energy Absorption in the Force-fed RatThe Journal of Nutrition, Vol. 101, No. 5The effect of hypothalamic lesion in the sand rat maintained on a high fat diet1 April 1971 | Diabetologia, Vol. 7, No. 2Adipose tissue metabolism of weanling rats after destruction of ventromedial hypothalamic nuclei: Effect of hypophysectomy and growth hormoneMetabolism, Vol. 19, No. 11 More from this issue > Volume 215Issue 6December 1968Pages 1343-1350 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.215.6.1343PubMed4972668History Published online 1 December 1968 Published in print 1 December 1968 Metrics

The relationship of energy expenditure and spontaneous activity to the aphagia of rats with lesions in the lateral hypothalamus.

1. Lesions in the lateral hypothalamus of rats always produced an immediate increase in total energy expenditure. The increase was maintained for 24 hr or longer only in rats that became and remained aphagic. Rats that showed no recovery from the aphagia and were maintained by tube feeding showed a second, larger increase in metabolic rate after about 7 days.2. The increase in total energy expenditure was associated, initially, with almost continuous motor activity. With continued aphagia an abnormally differentiated pattern of activity appeared at the same time as the second increase in metabolic rate, and the compartment of energy attributable to activity remained high (34% as compared with 23% in normal rats). These changes were accompanied by a recovery of an instrumental response for food (lever pressing), of interest in offered foods and of grooming activity.3. Metabolic abnormality not attributable to activity was indicated by increased creatinine excretion of aphagic but not of hypophagic rats.4. Rats that recovered spontaneous feeding after aphagia returned towards a normal differentiated pattern of activity, with bursts of activity separated by periods of rest, but showed residual abnormality in creatinine excretion.5. The intimate association between increase of energy expenditure, abnormality of motor activity and the aphagia produced by lateral hypothalamic lesions is consistent with the hypothesis that motor incoordination or disorganization is a cause of the aphagia.

Genetic, traumatic and environmental factors in the etiology of obesity.

ArticlesGenetic, Traumatic and Environmental Factors in the Etiology of ObesityJean MayerJean MayerPublished Online:01 Oct 1953https://doi.org/10.1152/physrev.1953.33.4.472MoreSectionsPDF (6 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByWhat models eat6 June 2018 | Nature Medicine, Vol. 24, No. 6The “Journal of Functional Morphology and Kinesiology” Journal Club Series: Highlights on Recent Papers in Physical Activity and Sedentary Behavior9 April 2018 | Journal of Functional Morphology and Kinesiology, Vol. 3, No. 2Cognitive behavior therapy for eating disorders versus normalization of eating behaviorPhysiology & Behavior, Vol. 174Psychobiological mechanisms in food choiceObesity Medications and the Treatment of Type 2 DiabetesDiabetes Technology & Therapeutics, Vol. 1, No. 3Correction of the sterility defect in homozygous obese female mice by treatment with the human recombinant leptin1 March 1996 | Nature Genetics, Vol. 12, No. 3Comparison of the metabolic and behavioral disturbances following paraventricular- and ventromedial-hypothalamic lesionsBrain Research Bulletin, Vol. 14, No. 6Islet organ, blood glucose and glucose tolerance of lean and obese Mongolian gerbilsCell and Tissue Research, Vol. 220, No. 3Role of gonadal hormones in diet selection and food utilization in female ratsPhysiology & Behavior, Vol. 24, No. 2An hypothesis on the control of food intake in fishAquaculture, Vol. 17, No. 3Regional and subcellular distribution of gold in brain of gold thioglucose obese mouseBrain Research Bulletin, Vol. 3, No. 3Obesity in exercising, hypophagic rats treated with monosodium glutamatePhysiology & Behavior, Vol. 19, No. 6Increased feeding in response to bilateral injection of insulin antibodies in the VMHPhysiology & Behavior, Vol. 19, No. 2Laboratory animals exhibiting obesity and diabetes syndromesMetabolism, Vol. 26, No. 1Plasma insulin and the time pattern of feeding in the ratPhysiology & Behavior, Vol. 18, No. 1Involvement of the medial hypothalamus and the septal area in the control of food intake and body weight in geesePharmacology Biochemistry and Behavior, Vol. 5, No. 6Metabolic factors in the control of energy storesMetabolism, Vol. 24, No. 1The effect of intrahypothalamic administration of sodium pentobarbital on eating behaviour and feed intake in chickensPhysiology & Behavior, Vol. 10, No. 1Analysis of diabetic hyperphagia and polydipsiaPhysiology & Behavior, Vol. 9, No. 5A central site for the hyperglycemic action of 2-deoxy-D-glucose in mouse and ratLife Sciences, Vol. 10, No. 18Treatment of obesity with special reference to seven severely obese patientsJournal of Psychosomatic Research, Vol. 14, No. 3Premorbid factors in adult disorders of weight, with particular reference to primary anorexia nervosa (weight phobia). A literature reviewJournal of Psychosomatic Research, Vol. 14, No. 1Plasma insulin content in relation to blood glucose level and meal pattern in the normal and hypothalamic hyperphagic ratPhysiology & Behavior, Vol. 5, No. 2Bloodglucose and FFA levels in relation to the meal pattern in the normal rat and the ventromedial hypothalamic lesioned ratPhysiology & Behavior, Vol. 4, No. 2Food intake: Regulation by plasma amino acid patternLife Sciences, Vol. 8, No. 2Some etiological factors in obesity1 April 1966 | Journal of the American Oil Chemists' Society, Vol. 43, No. 4Single neurone activity of hypothalamic feeding centres: Effect of local heatingBrain Research, Vol. 1, No. 3Prevention of Obesity in Childhood2 July 2016 | Clinical Pediatrics, Vol. 2, No. 7Electrical activity of the hypothalamic ‘feeding centres’ under the effect of changes in blood chemistryElectroencephalography and Clinical Neurophysiology, Vol. 13, No. 1THE CAUSES AND CURE OF OBESITYThe Lancet, Vol. 274, No. 7112The measurement of success in weight reductionJournal of Chronic Diseases, Vol. 10, No. 5ObesityThe American Journal of Medicine, Vol. 19, No. 1METABOLISM IN OBESITYThe Lancet, Vol. 263, No. 6803TRAINING OF DISTRICT NURSESThe Lancet, Vol. 263, No. 6803MYCOBACTINThe Lancet, Vol. 263, No. 6803 More from this issue > Volume 33Issue 4October 1953Pages 472-508 https://doi.org/10.1152/physrev.1953.33.4.472PubMed13100066History Published online 1 October 1953 Published in print 1 October 1953 Metrics

MECHANISM OF THE DEVELOPMENT OF OBESITY IN ANIMALS WITH HYPOTHALAMIC LESIONS

MECHANISM OF THE DEVELOPMENT OF OBESITY IN ANIMALS WITH HYPOTHALAMIC LESIONS