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PubMed1988

Clonidine hyperphagia: neuroanatomic substrates and specific function.

Recent studies have indicated that the alpha 2-noradrenergic agonist clonidine (CLON), when peripherally and centrally administered, potentiates feeding in satiated rats in a manner similar to that observed following injection of norepinephrine (NE) into the hypothalamic paraventricular nucleus (PVN). The present experiments examined the effects of CLON on meal patterns and macronutrient selection and compared these findings to earlier NE-stimulated feeding studies. Administration of CLON (25 nmoles), directly into the PVN (n = 5), similar to PVN injected NE, produced an increase in meal size (190%) and feeding duration (164%), with no change in meal frequency. Additional tests were conducted in rats with PVN electrolytic or 6-hydroxydopamine lesions. In Sham rats (n = 16) peripheral CLON (0.05 mg/kg), like NE, produced an increase in food intake and particularly potentiated carbohydrate ingestion. Discrete electrolytic lesions of the PVN (n = 5) abolished this CLON-induced feeding and carbohydrate preference, suggesting that the PVN may be a primary site for CLON-stimulated hyperphagia. Neurotoxin lesions of the PVN (n = 17), which reduced PVN NE levels by 75%, failed to alter peripheral CLON-induced feeding. This and other evidence indicates that this agonist may be acting via postsynaptic alpha 2 receptors in the PVN to potentiate carbohydrate intake, rather than via presynaptic release of NE from nerve endings in the PVN.

Animals↗
PubMed1984

Chronic norepinephrine injection into the hypothalamic paraventricular nucleus produces hyperphagia and increased body weight in the rat.

A single injection of norepinephrine (NE) into the paraventricular nucleus (PVN) is known to elicit a feeding response in the satiated rat. Through repeated NE injections, the present study set out to determine whether chronic noradrenergic stimulation of the PVN is effective in producing changes in total daily food intake, as well as in body weight gain. The results indicate that repeated injections of NE (20 nmoles/injection given 4 times/day) cause a stimulation of eating with each injection and consequently produce a significant increase in total daily food intake. This stimulatory effect on feeding behavior occurs under food-restricted conditions, where food is available only at times (in the daytime) when NE is injected, and also under food-satiated conditions were food is available essentially ad lib. This hyperphagia results in a gradual increase in body weight which develops over the course of a 5-day sequence of repeated NE injections. There is some evidence to suggest that the overeating produced by NE throughout the day may be attributed specifically to an increase in meal size rather than to a change in meal frequency. This evidence suggests that medial hypothalamic NE, particularly within the PVN, may play a role in long-term feeding behavior and body weight regulation.

Animals↗
PubMed1986

8-OH-DPAT-induced hyperphagia: its neural basis and possible therapeutic relevance.

The pharmacological and neurochemical bases of hyperphagia induced by the serotonin agonist 8-OH-DPAT were examined. In addition, the possible therapeutic potential of 8-OH-DPAT and related drugs in the treatment of anorexic pathology was assessed in an animal model of anorexia (as induced by acute immobilization stress). In normal rats 8-OH-DPAT elicited feeding after peripheral injection and after intracerebral application to the brainstem raphé nuclei. Feeding elicited by peripheral injection of the drug was attenuated by pretreatment with the serotonin synthesis inhibitor para-chlorophenylalanine. Following a hyperphagic dose of 8-OH-DPAT, brain serotonin metabolism was reduced, particularly in midbrain and pons-medulla. Our interpretation of these data is that 8-OH-DPAT elicits feeding via an agonist action on serotonin autoreceptors in the raphé nuclei. These receptors are probably of the 5-HT1A subtype as 8-OH-DPAT has a high affinity for this receptor and other putative 5-HT1A agonist (i.e. buspirone, TVX Q 7821) also elicit feeding. In contrast, putative 5-HT1B agonists (i.e. RU-24969 and quipazine) decrease feeding and cause anorexia. 8-OH-DPAT and other 5-HT1A agonists attenuated the anorexia and body weight loss caused by immobilization stress. Therefore, it seems possible that 5-HT1A agonists may be clinically useful in the treatment of anorexia.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1975

Delayed hyperphagia and increased body length after hypothalamic knife cuts in weanling rats.

Four-week-old female rats received parasagittal hypothalamic knife cuts. Polydipsia began right surgery, but hyperphagia, obesity, and excessive nose-anal length did not begin until after the rats were 7-8 wk. old. The delayed onset appears to await some maturational event that is required for the expression of hypothalamic obesity. It appears likely that puberty is the critical maturational event.

Animals↗
PubMed1977

Hyperphagia and obesity produced by parasagittal and coronal hypothalamic knife cuts: further evidence for a longitudinal feeding inhibitory pathway.

Hyperphagia and obesity are produced both by parasagittal knife cuts through the medial hypothalamus and by coronal knife cuts through the posterior hypothalamus. The results of this study indicate that the two types of cuts produce their overeating effect by severing the same neural pathway. Experiment 1 demonstrated that unilateral parasagittal knife cuts combined with contralateral coronal cuts in either the posterior hypothalamus or the midbrain significantly increase food intake and body weight. Experiment 2 revealed that bilateral parasagittal cuts and bilateral coronal cuts in the hypothalamus produce qualitatively similar effects on food intake, diurnal ingestive pattern, finickiness, and amphetamine anorexia. The two types of cuts differentially altered water intake, however. In Experiment 3, coronal cuts in the posterior hypothalamus, like parasagittal cuts in the medial hypothalamus, were found to increase the food intake and body weight of rats previously given bilateral parasagittal transections through the lateral perifornical region. The neuroanatomy and neurochemistry of the longitudinal feeding inhibitory pathway suggested by these results are discussed.

Amphetamine↗
PubMed1978

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

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 rats 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 rats 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 rats 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. These findings suggest that hyperphagia in experimental diabetes mellitus is a compensatory response to a lack of utiliziable fat fuels rather than the result of a metabolic disturbance per se.

Animals↗
PubMed1980

Nocturnal hyperphagia in the rat is characterized by decreased postprandial satiety.

Rats eat more at night than during the day. This work investigated whether this nocturnal hyperphagia is characterized by increased hunger, decreased postprandial satiety, or both. Rats were presented with liquid food after 3-hr food deprivation at the midpoint of the night or day phase of a 12:12 hr light/dark cycle. Quinine adulteration of food produced equal percentage suppression of first meal size (MS) and of 60-min intakes in the night and the day. This suggests that rats are equally hungry after 3-hr food deprivation in the night and the day. In contrast to apparently equal hunger, rats were less satiated by ingested food after 3 hr of food deprivation at night than during the day. This conclusion is based on the observations that the postprandial intermeal interval (IMI) was significantly shorter at night and that the satiety ratio (IMI/MS) was smaller at night. This nocturnal decrease in the satiating potency of ingested food was demonstrated for two specific preabsorptive satiety mechanisms: (a) the pregastric satiety mechanism(s) stimulated by sham feeding and (b) cholecystokinin, the putative satiety hormone released by food contacting the mucosal surface of the upper small intestine. All the results suggest that the diurnal variation of food intake in rats is primarily the result of diurnal variation in the potency of postprandial satiety mechanisms.

Animals↗
PubMed1984

Effects of denervating brown adipose tissue on the responses to cold, hyperphagia and noradrenaline treatment in the rat.

Surgical denervation of the five sympathetic nerves supplying one lobe of the interscapular brown fat of control rats caused small reductions in mass, protein content and the activity of the thermogenic mitochondrial proton conductance pathway (assessed from guanosine-5'-diphosphate (GDP) binding) when compared to the intact lobe. Denervation did not affect the acute 100% increase in mitochondrial GDP binding capacity seen after a single injection of noradrenaline. Cold-adaptation (4 degrees C for 7 days) or over-feeding (cafeteria diet for 10 days) caused marked increases in the mass, protein content and specific mitochondrial GDP binding in intact brown adipose tissue, but these changes were totally prevented by surgical denervation. These data indicate that the hypertrophy and the increased thermogenic capacity of brown fat induced by cold-adaptation or hyperphagia depend entirely upon the sympathetic innervation of the tissue.

Adaptation, Physiological↗
PubMed1976

Hyperphagia and increased growth in rats after intraventricular injection of 5,7-dihydroxytryptamine.

Juvenile male rats given intracerebroventricular injections of 5,7-dihydroxytryptamine, following treatment with desmethylimipramine, maintained body weight gains of 5 to 6 grams per day into adulthood and grew much larger than control rats. Biochemical analyses of brain tissue obtained 50 to 140 days after the injections revealed 60 to 86% depletions of telencephalic 5-hydroxytryptamine, with catecholamine levels unchanged. Hyperphagia did not develop despite comparable losses of 5-hydroxytryptamine when the pretreatment was withheld, perhaps because substantial depletions of norepinephrine occurred as well.

Animals↗
PubMed1976

Hyperphagia and obesity following serotonin depletion by intraventricular p-chlorophenylalanine.

Loss of brain serotonin was associated with overeating and increased body weight. Rats injected with p-chlorophenylalanine intraventricularly began overeating after 3 days and continued to display marked hyperphagia, primarily in the daytime, accompanied by increased body weight for 1 to 2 weeks. The effect was related to drug dose and to the degree and duration of serotonin depletion. Norepinephrine and dopamine levels were not significantly affected. It is concluded that p-chlorophenylalanine disinhibits feeding, as it does a number of other behaviors, by depleting serotonin. This suggests that hypothalamic lesions or dietary deficiencies which selectively and sufficiently deplete serotonin would lead to overeating.

Animals↗
PubMed1974

Hyperphagia in intestinal disease.

Six patients with hyperphagia (ingestion of 5-11 000 Kcals/day) associated with severe malabsorption and steatorrhoea are described. The cause of the malabsorption was coeliac disease in three patients, Crohn's disease with ileal resection in two, and carcinoma of the pancreas in one patient. There was no evidence of neurological or endocrine disease (apart from mild diabetes mellitus in the patient with carcinoma of the pancreas) but three patients suffered from severe depression. This association may be commoner than previously realized and be revealed in patients with steatorrhoea of unexplained severity by careful dietary assessment. Its detection has therapeutic implications since restriction of caloric and fat intake decreased steatorrhoea without weight loss in several of the patients described.

Adult↗
PubMed1980

Development of obesity in Zucker obese (fafa) rat in absence of hyperphagia.

The free-feeding, genetically obese rat is hyperphagic, hyperinsulinemic, and hypertriglyceridemic and has increased fat cell size and number compared to its lean littermate. These experiments demonstrate that, when fafa rats are prevented from expressing hyperphagia throughout life, the complete obese "syndrome" still develops. Furthermore, life-long food restriction does not prevent increased lipoprotein lipase in the fafa rat. The data support the concept that a peripheral metabolic adaptation, probably in lipid metabolism, results in preferential shunting of dietary substrate in the restricted obese rats to adipose tissue with concomitant decreases in other tissues.

Adipose Tissue↗
PubMed1980

Hypothalamic hyperphagia and obesity in rats with jejunoileal bypass.

Jejunoileal bypass or sham surgery was performed in adult female rats followed 35 days later by ventromedial hypothalamic (VMH) knife cut or sham surgery (forming groups Bypass-VMH, Bypass-Sham, Sham-VMH, and Sham-Sham). Bypassed rats receiving VMH cuts (Bypass-VMH group) ate more food and gained more weight than did either Bypass-Sham or Sham-Sham groups. The hyperphagia and obesity of the Bypass-VMH rats was, however, substantially less than that of the sham bypass VMH cut rats (Sham-VMH group). Bypass-VMH rats that had their intestinal tract reconnected increased their food intake and ultimately became as obese as the Sham-VMH rats. Two additional groups received VMH knife cut or sham surgery followed 50 days later by jejunoileal bypass surgery (VMH-Bypass and Sham-Bypass groups). At the time of the bypass the VMH-Bypass group was hyperphagic and obese, but after surgery they underate and lost weight until they eventually stabilized their body weight at a level below that of the Sham-Bypass group. The body weight of the VMH-Bypass group was also 167 g less than that of the Bypass-VMH group. Thus, the order of surgery significantly influences the food intake and body weight level of rats with VMH knife cuts and jejunoileal bypass.

Animals↗
PubMed1975

Influence of hypothalamic hyperphagia on tolerance of lung to explosive decompression.

A study was made of the effect of hypothalamic hyperphagia on the tolerance of lung to explosive decompression in male Long-Evans rats. The control and hypothalamic hyperphagic rats were explosively decompressed together from 1 atm to an ambient pressure of 30 min Hg in 0.04s. The hypothalamic-lesiones rats gained from 252 g average weight to 460 g, a 82% gain. The respective figures for the controls. were from 248 g to 336 g and 36%. It was also observed that a considerable amount of fat was accumulated between pleura and lungs in experimental animals. The average accumulation of fat between pleura and lungs in experimental rats was 3.23 g, while the value of the control group was only 0.42 g. The difference was statistically significant. Such an increase of fat accumulation in the thoracic cage could decrease the tidal volume. The severity of decompression-induced pulmonary hemorrages might thus be decreased. On the other hand, it also seems possible that the soft fat cushion between pleura and lungs might damp the bruising of the pulmonary tissue against the resistant thoracic wall to a certain extent, thus resulting in a decreased susceptibility to decompression-induced lung damage. Besides , the mortality in obese rats undergoing explosive decompression was also significantly lower than that of the controls

Adaptation, Physiological↗
PubMed1978

Potentiation of hyperphagia and relief of hypothermia in the genetically obese mouse (genotype, ob/ob) by alpha-methyl tyrosine.

DL-alpha-methyl-p-tyrosine methyl ester hydrochloride affected the hyperphagia and hypothermia characteristic of the genetically obese mouse (genotype, ob/ob) throughout an experimental period of 5 days. Intraperitoneal injections of 100 mg/kg body weight, daily, resulted in a significant increase in the average daily food consumption by 60 per cent, already elevated 35 per cent above that of lean litter-mates. The drug, administered at the same dose, caused a similar percentage elevation of food intake in the lean litter-mates. Rectal temperatures of obese mice were raised significantly throughout the 5-day period by an average of 0.95 degrees C, following administration of the drug. There was a significant rise of 0.75 degrees C in the rectal temperature of lean mice on 2 of the 5 days in the period. Body weight remained unchanged. Further experiments are necessary to determine the site of action at which DL-alpha-methyl-p-tyrosine brings about these effects at this dose in lean and obese mice.

Animals↗
PubMed1995

Role of hyperphagia in structural changes of small intestine during lactation.

The present study was conducted to investigate the cause of the structural changes of small intestine during lactation in albino rats. Anatomical measurements (total length, total wet weight and total dry weight) and histological studies of small intestine were undertaken in virgin control rats, lactating control rats, lactating rats with restricted food intake and lactating rats with restricted litter size. Restriction of food intake prevented the growth of small intestine during lactation, while restriction of litter size had no effect. Results indicate that the structural changes in small intestine are due to work hypertrophy secondary to hyperphagia and not due to any hormonal factors.

Animals↗
PubMed2002

The use of dextroamphetamine to treat obesity and hyperphagia in children treated for craniopharyngioma.

BACKGROUND: Obesity and attention difficulties are known complications following surgical treatment for craniopharyngioma. Treatments to date have been largely disappointing. OBJECTIVE: To examine the use of the central nervous system stimulant dextroamphetamine sulfate to regulate appetite and subsequent weight gain in children treated for craniopharyngioma. SETTING: A multidisciplinary clinic specializing in pediatric brain tumors. PATIENTS: Five consecutive patients with significant weight gain and poor attention following surgical treatment for craniopharyngioma were selected for the study. INTERVENTION: Children enrolled in the study were treated with dextroamphetamine, and growth, laboratory, and behavioral assessments were conducted for 24 months. RESULTS: Mean +/- SD body mass index (weight in kilograms divided by height in meters squared) increased from 21 +/- 3.5 before the operation to 32 +/- 2.8 by the start of the protocol. Body mass indices remained stable throughout the protocol. No changes were observed in insulin levels or caloric intake, but the children were more active when taking dextroamphetamine. Parents noted a significant improvement in hyperactivity (mean +/- SD, 1.2 +/- 0.4 to 0.6 +/- 0.2; P =.05), scored with the Conners Parent and Teacher Rating Scales. Teachers noted a similar improvement. CONCLUSIONS: During dextroamphetamine treatment, weight gain stabilized in children who had experienced obesity following surgical resection for craniopharyngioma. In addition, parents and teachers noted significant improvements in children's overall activity and attention. Further studies are needed to determine if the improvements are stable and if earlier intervention can prevent the initial obesity.

Analysis of Variance↗