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PubMed1997

Increased hypothalamic neuropeptide Y concentration or hyperphagia in streptozotocin-diabetic rats are not mediated by glucocorticoids.

Hypothalamic neuropeptide Y containing neurones are overactive and may mediate hyperphagia in insulin-deficient diabetic rats, but the factors stimulating them remain uncertain. To determine the possible role of glucocorticoids, we investigated the effects of the glucocorticoid receptor blocker mifepristone (RU486) on food intake and regional hypothalamic neuropeptide Y concentrations in streptozotocin-diabetic rats. RU486 (30 mg/kg) or corn oil vehicle control was given orally for 3 weeks to diabetic rats. Food intake and neuropeptide Y levels in the hypothalamic arcuate and paraventricular nuclei were increased in untreated diabetic rat groups (P < 0.01), and though RU486 did increase plasma corticosterone levels (P < 0.01) it did not have any effect on either feeding or neuropeptide Y levels (P = NS). These negative findings suggest that glucocorticoids may not be responsible for increasing hypothalamic neuropeptide Y or for hyperphagia in insulin-deficient diabetes.

Animals↗
PubMed1999

Role of the ventromedial hypothalamus in prolactin-induced hyperphagia in ring doves.

Prolactin (PRL) strongly stimulates feeding activity and body weight gain in ring doves, and of the brain loci tested to date, the ventromedial hypothalamus (VMH) is the most effective site of PRL action in promoting these changes. To determine if the VMH is essential for this response, we examined the effects of VMN destruction on spontaneous feeding and on changes in food intake induced by intracerebroventricular (i.c.v.) injections of PRL. Male birds were selectively destroyed by radiofrequency lesions (n = 6). A group of sham-lesioned males (n = 6) served as controls. Lesioned birds exhibited a transient increase in food intake that peaked around the seventh postoperative day and declined to baseline levels by day 12. In contrast to this pattern, body weights of lesioned birds increased in parallel with food intake, but remained elevated throughout the 3-week postoperative period. During the peak period of hyperphagia in the lesioned group, food intake and body weight increases were two to three times greater in lesioned birds than in controls. After postoperative feed intake had stabilized, each bird received 5 daily i.c.v. injections of ovine PRL. Food intake and body weight increased dramatically in both groups in response to PRL treatment, and no group differences were observed in response to magnitude. We conclude that VMH destruction strongly perturbs feeding and body weight regulation in doves. However, VMH integrity is not essential for the expression of PRL-induced hyperphagia.

Animals↗
PubMedDate not supplied

Reversal of delta 9-THC hyperphagia by SR141716 and naloxone but not dexfenfluramine.

Presatiated adult male Lister hooded rats received oral administration of the exogenous cannabinoid Delta-9-tetrahydrocannabinol (Delta(9)-THC; 1.0 mg/kg) in combination with subcutaneous injection of either the cannabinoid CB1 antagonist N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide (SR141716; 0, 0.05, 0.1, 0.5 or 1.0 mg/kg), the CB2 antagonist N-[(1S)-endo-1,3,3-trimethyl bicyclo[2.2.1]heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528; 0, 0.05, 0.1, 0.5 or 1.0 mg/kg), the general opioid antagonist naloxone (0.1, 0.5, 1.0 or 5.0 mg/kg) or the 5-HT agonist dexfenfluramine (0.05, 0.1, 0.5, 1.0 or 5.0 mg/kg). Food (chow) intake was measured over 2 h from the onset of the dark period. Delta(9)-THC induced significant hyperphagia, which was attenuated by subanorectic doses of SR141716 and naloxone. Neither SR144528 nor dexfenfluramine affected Delta(9)-THC-induced feeding. These data confirm mediation of Delta(9)-THC hyperphagia by central-type CB1 receptors, and support a functional relationship between cannabinoid and opioid systems in relation to appetite regulation. Stimulation of CB1 receptors may promote feeding by actions on food reward rather than by inhibition of serotonergic satiety mechanisms.

Animals↗
PubMed2003

Evidence for involvement of neuropeptide Y and melanocortin systems in the hyperphagia of lactation in rats.

Hypothalamic neuropeptide Y (NPY) systems are upregulated during lactation in rats. Because NPY is central to the hypothalamic control of energy balance, the present studies tested the hypothesis that NPY contributes to the marked hyperphagia during lactation. A 4-day infusion of [D-tyr (27,36), D-thr (32)] NPY (27-36) (D-NPY(27-36)), a peptide analogue of NPY that antagonizes NPY-induced feeding, into the third ventricle at 1 microg/h transiently inhibited nocturnal feeding in nonlactating female rats. However, this antagonist had no effect on nocturnal feeding, but did transiently reduce food intake during the light hours, when infused into the third ventricle at the same dose in lactating females. An essentially similar pattern of results was obtained with chronic infusion into the third ventricle of the anorexigenic peptide alpha-melanocyte-stimulating hormone (alpha-MSH, 1 microg/h), in nonlactating and lactating rats. Both D-NPY(27-36) and alpha-MSH transiently reduced nocturnal food intake in lactating rats by approximately 10% when infused at the higher dose of 5 microg/h, and a marked inhibition of approximately 40% of both nocturnal and diurnal feeding was produced by a combined infusion of both at 5 microg/h. These results provide the first pharmacological evidence implicating specific neuromessengers in mediating the hyperphagia of lactation, and suggest that, while an action of NPY may contribute to the increased food intake seen in lactating animals, other systems are also involved. In particular, a reduction in melanocortin signaling during lactation may allow for an increased orexigenic influence of the agouti-related protein (AgRP), which is co-expressed with NPY.

Animals↗
PubMed1990

Does dietary hyperphagia contradict the lipostatic theory?

It has frequently been suggested that body weight or fat somehow exerts an inhibitory influence on food intake in a way that acts to maintain a stable body weight or fat. The principal evidence supporting this idea is that animals that have been induced to overeat and become overweight by various means, eat less than control rats when they are permitted to eat freely. If the degree of suppression of appetite by overweight is as large as several experiments suggest, then dietary hyperphagia should be self-limiting. Any overeating induced by dietary treatments should disappear after animals become moderately overweight. Animals fed some kinds of hyperhagia-promoting diets do show this pattern. However, animals fed other kinds of diets do not show this pattern, and with most diets, dietary hyperphagia continues for extended periods. This implies that either 1) overweight does not suppress appetite as much as suggested by various authorities, 2) dietary manipulations can override normal regulatory mechanisms, or 3) certain diets induce irreversible changes in body fat that are not evident from changes in body weight.

Adipose Tissue↗
PubMed1987

Carbohydrate-induced hyperphagia and obesity in the rat: effects of saccharide type, form, and taste.

Adult female rats were fed, in addition to chow and water, a carbohydrate source that differed in type (glucose, sucrose, or polysaccharide), form (32% solution, powder, or gel), or taste (very sweet, minimally sweet, or bitter). A control group was fed only chow and water during the 40-day experiment. The groups fed the glucose solution, sucrose solution, or one of three polysaccharide solutions (Polycose, maltose-dextrin 10, maltose-dextrin 42) all overrate and gained more body weight and fat than did the control group. The carbohydrate solution groups did not differ in their total caloric intake, weight gain, percent body fat, or basal insulin level. The polysaccharide groups, however, consumed more carbohydrate than did the sugar groups. The groups fed glucose, sucrose, or Polycose in powder form consumed less carbohydrate and total calories, gained less weight and fat, and had lower insulin levels than did the groups fed the saccharides in solution form. The powder groups did not reliably differ from the control group on these measures. Rats fed Polycose in solution form or in a solid gel form (32% Polycose + 1% agar) were similar in their carbohydrate intake, total caloric intake, weight gain, and percent body fat. Rats fed Polycose solutions that were minimally sweet (32% Polycose), sweet (0.2% saccharin + 32% Polycose), or bitter [0.05% sucrose octa acetate (SOA) + 32% Polycose] did not differ in their Polycose intake, total caloric intake, weight gain, or percent body fat. The results demonstrate that saccharide form is more important than saccharide type or taste in promoting hyperphagia and obesity in rats. The Polycose gel findings further indicate that it is the water of hydration, not liquidity that is responsible for the hyperphagia-inducing effect of carbohydrate solutions.

Animals↗
PubMed2000

Hypothalamic galanin is up-regulated during hyperphagia and increased body weight gain induced by disruption of signaling in the ventromedial nucleus.

Disruption of signaling in the ventromedial nucleus (VMN) by colchicine (COL) produces transient (4 days) hyperphagia and weight gain. Microinjection of galanin into various hypothalamic sites stimulates feeding, so we tested the hypothesis that galanin is up-regulated in COL-treated rats by analyzing galanin concentrations in micropunched hypothalamic sites. Galanin was increased in the paraventricular nucleus on Days 1 through 4 after COL-injection. Galanin was also elevated in three other hypothalamic sites, the dorsomedial nucleus, lateral hypothalamic area, and perifornical hypothalamus, on Days 2-4 and in the lateral preoptic area, on Day 1 only. In the median eminence-arcuate nucleus and amygdala an initial decrease on Day 1 was followed by a then progressive increase through Day 4. These increases occurred despite marked elevations in blood insulin and leptin, hormones known to suppress hypothalamic galanin. When COL- or saline-treated rats were injected intracerebroventricularly with galanin, it stimulated feeding further in the hyperphagic COL-treated rats, but the relative response over basal consumption was similar in both COL-treated and control rats. These results in VMN disrupted rats suggest that neurochemical rearrangements, including increased availability of galanin, may contribute to the hyperphagia and increased weight gain; additionally, it seems that neurons in the VMN normally exert a restraint on galanin signaling.

Animals↗
PubMed2001

Chronic administration of neuropeptide Y into the lateral ventricle of C57BL/6J male mice produces an obesity syndrome including hyperphagia, hyperleptinemia, insulin resistance, and hypogonadism.

Neuropeptide Y (NPY) is involved in the central regulation of appetite, sexual behavior, and reproductive function. We have previously shown that chronic infusion of NPY into the lateral ventricle of normal rats produced an obesity syndrome characterized by hyperphagia, hyperinsulinism and collapse of reproductive function. We further demonstrated that acute inhibition of LH secretion in castrated rats was preferentially mediated by the NPY receptor subtype 5 (Y(5)). In the present study, the effects of chronic, central infusion of NPY, or the mixed Y2-Y5 agonist PYY(3-36), were evaluated both in normal male C57BL/6J mice and Sprague-Dawley rats. After a 7-day infusion to male mice, both NPY and PYY(3-36) at 5 nmol per day, induced marked hyperphagia leading to significant increases in body and fat pad weights. Furthermore, both compounds markedly reduced several markers of the reproductive axis. In the rat study, PYY(3-36) was more active than NPY to inhibit the pituitary-testicular axis, confirming the importance of the Y5 subtype for such effects. In the mouse, chronic NPY infusion induced a sustained increase in corticosterone and insulin secretion. Plasma leptin levels were also markedly increased possibly explaining the observed reduction in gene expression for hypothalamic NPY. Gene expression for hypothalamic POMC was reduced in the NPY- or PYY(3-36)-infused mice, suggesting that NPY exacerbated food intake by both acting through its own receptor(s), and reducing the satiety signal driven by the POMC-derived alpha-MSH. The present study in the mouse suggests in analogy with available rat data, that constant exposure to elevated NPY in the hypothalamic area unabatedly enhances food intake leading to an obesity syndrome including increased adiposity, insulin resistance, hypercorticism, and hypogonadism, reminiscent of the phenotype of the ob/ob mouse, that displays elevated hypothalamic NPY secondary to lack of leptin negative feedback action.

Animals↗
PubMed2003

Peptides associated with hyperphagia in adults with Prader-Willi syndrome before and during GH treatment.

UNLABELLED: Prader-Willi syndrome (PWS) is a complex genetic disorder characterised by mild mental retardation and distinct physical, behavioural, and psychiatric features. One of the cardinal symptoms is excessive eating, which--if left untreated--leads to extreme obesity. In the present study we have examined circulating levels of peptides with documented association to hyperphagia in young adults with PWS. Since growth hormone (GH) is often used nowadays to correct GH insufficiency during childhood PWS, we also studied the impact of GH administration on the peptides. Seventeen adults, 9 men and 8 women, 17-32 years of age with a mean BMI of 35+/-3.2 kg/m(2) participated. All had clinical PWS (Holm's criteria). Genetic testing was performed in all patients and in 11 the diagnosis was confirmed. They were randomized to treatment with either placebo or GH (Genotropin, Pharmacia Corporation) for 6 months. Subsequently all received open label treatment to provide all subjects with 12 months active GH treatment. Doses were individually titrated. Weight, BMI, oxytocin (baseline only), leptin, Neuropeptide Y (NPY), and ghrelin were evaluated at baseline and after 6 and 12 months. At baseline plasma mean oxytocin was within and serum ghrelin just above the normal range (14.7+/-1.2 pmol/L and 0.87+/-0.12 microg/L, respectively). Serum leptin levels were high above and plasma NPY levels within the lower normal range (47.8+/-29.1 microg/L and 13+/-1 pmol/L, respectively). Results were independent of genotype. No changes in mean BMI, ghrelin, leptin or NPY were seen following GH treatment. CONCLUSION: Leptin levels were in general high reflecting obesity and as a consequence NPY levels were low. In simple obesity oxytocin levels are high, while ghrelin levels are suppressed. In view of the adiposity oxytocin circulated in abnormally low and ghrelin in abnormally high concentrations in our patients. GH treatment of PWS patients did not change ghrelin, leptin or NPY. We suggest that both oxytocin and ghrelin are involved in the pathogenesis of hyperphagia seen in PWS.

Adolescent↗
PubMed2000

Upregulation of uncoupling protein 2 mRNA in genetic obesity: lack of an essential role for leptin, hyperphagia, increased tissue lipid content, and TNF-alpha.

Uncoupling protein 2 (UCP2) has been proposed to play a prominent role in the regulation of energy balance. UCP2 mRNA expression is upregulated in white adipose tissue (WAT) and liver, but is not altered in skeletal muscle in genetically obese ob/ob mice. The mechanisms involved in the upregulation of UCP2 in obesity have not been investigated. We have now examined the potential role of leptin, hyperphagia, increased tissue lipid content, and overexpression of tumor necrosis factor (TNF)-alpha in the upregulation of UCP2 mRNA expression in the liver and WAT in ob/ob mice. Treatment of ob/ob mice with leptin for 3 days significantly reduced their food intake but had no effect on the upregulation of UCP2 mRNA levels in the liver or WAT. To investigate the effect of feeding and higher tissue lipid content on the upregulation of UCP2 in liver and WAT, we compared UCP2 mRNA levels in ad-libitum fed and 72-h fasted control and ob/ob mice. In controls, fasting had no effect on UCP2 mRNA levels in liver, but increased UCP2 mRNA in WAT suggesting that the effects of fasting on UCP2 mRNA levels are tissue-specific. In ob/ob mice, fasting did not lower UCP2 mRNA levels in liver or WAT suggesting that the upregulation of UCP2 in ob/ob mice is not merely a direct consequence of increased food intake. 72-h fasting lowered hepatic total lipid content by 34% and 36% in control and ob/ob mice, respectively, without any corresponding decrease in hepatic UCP2 mRNA levels, suggesting that the enhanced UCP2 expression in the liver of ob/ob mice is not secondary to lipid accumulation in their livers. Although TNF-alpha has been shown to acutely increase UCP2 mRNA levels in liver and WAT, and is overexpressed in adipose tissue in obesity, deletion of the genes for both TNF receptors in ob/ob mice produces a further increase in UCP2 mRNA expression in liver and adipose tissue indicating a paradoxical inhibitory role. Taken together, these results suggest that the upregulation of UCP2 mRNA levels in the liver and WAT of ob/ob mice is not due to the lack of leptin, hyperphagia, increased tissue lipid content, or over-expression of TNF-alpha.

Adipose Tissue↗
PubMed2005

Hyperphagia induced by GABAA receptor-mediated inhibition of the nucleus accumbens shell: dependence on intact neural output from the central amygdaloid region.

To investigate the role of corticolimbic input in modulating feeding-related nucleus accumbens (Acb) circuitry, researchers temporarily deactivated sites within the basolateral amygdaloid complex (BLA) or central amygdaloid region (CeA) via GABA(A) agonist (muscimol) infusions and measured feeding responses following muscimol infusions into the Acb shell. Hyperphagia elicited by intra-Acb shell muscimol was not altered by coinfusions of intra-BLA muscimol. In contrast, muscimol infusions into the CeA dose-dependently reduced feeding elicited either by intra-Acb shell GABA(A) receptor stimulation or by food deprivation and produced a syndrome of forepaw treading. Intra-CeA tetrodotoxin infusions also blocked intra-Acb shell muscimol-induced hyperphagia. Hence, feeding elicited by intra-Acb shell GABA(A) receptor stimulation requires intact neural output from the CeA but not the BLA.

Amygdala↗
PubMed2006

Neural mechanisms underlying hyperphagia in Prader-Willi syndrome.

OBJECTIVE: Prader-Willi syndrome (PWS) is a genetic disorder associated with developmental delay, obesity, and obsessive behavior related to food consumption. The most striking symptom of PWS is hyperphagia; as such, PWS may provide important insights into factors leading to overeating and obesity in the general population. We used functional magnetic resonance imaging to study the neural mechanisms underlying responses to visual food stimuli, before and after eating, in individuals with PWS and a healthy weight control (HWC) group. RESEARCH METHODS AND PROCEDURES: Participants were scanned once before (pre-meal) and once after (post-meal) eating a standardized meal. Pictures of food, animals, and blurred control images were presented in a block design format during acquisition of functional magnetic resonance imaging data. RESULTS: Statistical contrasts in the HWC group showed greater activation to food pictures in the pre-meal condition compared with the post-meal condition in the amygdala, orbitofrontal cortex, medial prefrontal cortex (medial PFC), and frontal operculum. In comparison, the PWS group exhibited greater activation to food pictures in the post-meal condition compared with the pre-meal condition in the orbitofrontal cortex, medial PFC, insula, hippocampus, and parahippocampal gyrus. Between-group contrasts in the pre- and post-meal conditions confirmed group differences, with the PWS group showing greater activation than the HWC group after the meal in food motivation networks. DISCUSSION: Results point to distinct neural mechanisms associated with hyperphagia in PWS. After eating a meal, the PWS group showed hyperfunction in limbic and paralimbic regions that drive eating behavior (e.g., the amygdala) and in regions that suppress food intake (e.g., the medial PFC).

Adolescent↗
PubMed1980

Effect of induced hypothalamic hyperphagia and forced-feeding on organ weight and tissular development in Landes geese.

The effects of induced hypothalamic hyperphagia and forced-feeding were studied in 30 geese of the Landes breed. They were housed in individual cages under a dark-light cycle of 12 hrs light-12 hrs darkness. Eleven geese with ventromedian hypothalamic (VMH) lesions and 8 controls were fed ad libitum. A third lot of 11 force-fed animals was pair-fed with the operated geese. The study lasted 4 weeks after an adaptation period to the new environmental conditions. The daily food intake of the geese and their weekly liveweight gain were monitored. After VMH lesions, the mean food intake of the geese increased by 169 p. 100 so that after each treatment their liveweight increased and they became obese (P less than 0.001). The tissue distribution of the group with lesions showed a higher amount of subcutaneous fat (P less than 0.05), while the mesenteric fat (P less than 0.05) was more abundant after forced-feeding. The liver weight was much higher in all cases; its increment reached 311 p. 100 in geese with VMH lesions and 193 p. 100 in the force-fed. However, those values were too low when compared to the means obtained by traditional forced-feeding. Hyperphagia in the geese was very marked as compared to that in rats, but it was insufficient to produce a considerable hepatic steatosis.

Animals↗
PubMed1983

Pancreatic hydrolases in cold-induced hyperphagia of rats fed a low or high-fat diet.

Rats fed either a low (2p. 100) or high (40 p. 100)-fat diet were exposed to 22 or 5 degrees C. The resulting hyperphagia adequately compensated energy losses as judged from body weight. The cold-induced hyperphagia was accompanied by a non-parallel increase in pancreatic hydrolases. Amylase and lipase were not increased above the adaptive levels they had respectively reached in the heat with a high-starch or high-lipid diet. Chymotrypsinogen, on the contrary, responded to increased intake of both diets. It also responded to the higher protein concentration in the high-fat diet caused by isocaloric replacement of starch by fat. Colipase varied independently of lipase and was increased additively by fat and protein intakes. Consequently, although limiting for lipase in the warm, colipase rose to a 1:1 ratio in the cold. Increased intake had a consistent pleiotropic effect evidenced by an increase of amylase with the high-fat diet and of lipase with the low-fat diet. The net effect was a significant increase in the lipid-digesting potential of the organism of lipid-fed animals upon exposure to cold, while the starch-digesting potential remained unaffected in starch-fed animals.

Animals↗
PubMed1983

The significance of hyperphagia and diet composition on the metabolism in ventromedial hypothalamic lesioned male rats.

The metabolic consequences of ventromedial hypothalamic lesion were studied in a group of aged male rats which were obese and had decreased response to insulin. The effects of hyperphagia and ventromedial hypothalamic lesion per se were separated by comparing experimental animals fed isocalorically with controls and animals fed ad libitum. Ventromedial hypothalamic lesion as such led to increases in the glucose conversion to fatty acid and in lipoprotein lipase activity in adipose tissue. Protein catabolism as reflected by plasma urea levels, was enhanced. The lipoprotein lipase activity in heart tended to be lower after VMH lesion. These metabolic changes were amplified in the VMH lesioned rats fed ad libitum. The liver glycogen content was lowered by VMH lesion, but this effect was abolished by hyperphagia. In parallel experiments the influence of diet composition was studied by feeding similar groups with diet of high fat content. The glucose incorporation in fatty acids was in all groups markedly and similarly inhibited by the high fat diet. The increase in lipoprotein lipase activity in heart and adipose tissue of control rats with high fat intake could not be demonstrated in any of the groups with ventromedial hypothalamic lesion. The plasma urea level in the control group was not affected by the diet, but tended to increase in the ventromedial hypothalamic lesioned groups on high fat intake. These findings demonstrate that the well known metabolic effects of ventromedial hypothalamic lesions are also manifest in obese insulin resistant male rats. Furthermore, the responses to changes in diet composition are different from those of the control rats.

Adipose Tissue↗
PubMed1965

THE EFFECT OF HYPERGLYCEMIA ON HYPOTHALAMIC GOLD UPTAKE AND HYPERPHAGIA IN GOLDTHIOGLUCOSE-TREATED MICE.

The accumulation of gold in the hypothalamus and the development of hyperphagia and obesity were studied in mice given a single intravenous injection of goldthioglucose at various levels of blood glucose concentration. It was found that the glucose concentration prevailing at the time of goldthioglucose injection was correlated directly with the level of free and bound goldthioglucose in the blood 3 minutes later, with the hypothalamic uptake of gold, with the extent of the hypothalamic lesion, and with the severity of the subsequent hyperphagia and obesity. Hyperglycemia was associated with an increased gold deposition throughout the brain. A gold content of 88 +/- 12 microg/mg wet tissue in the hypothalamus of fasted animals was associated with clearcut lesions in all animals studied, whereas a similar gold content in the control brain lobes of hyperglycemic animals was not associated with lesions in any animal. This finding indicates that some regions in the brain (e.g. the ventral hypothalamus) are more susceptible than others to damage by goldthioglucose.

Animals↗
PubMed2006

Ruminal fermentation and fill change with season in an arctic grazer: responses to hyperphagia and hypophagia in muskoxen (Ovibos moschatus).

We studied castrated adult muskoxen fed a standard diet of grass hay and supplement throughout the year to determine seasonal changes in digesta passage, fill, and fermentation without the confounding effects of reproductive demands or changes in food quality. Although food intake increased by 74% between spring and autumn, mean retention times of fluid and particulate digesta markers were maintained between seasons in both the rumen (9-13 h) and the intestines (27-37 h). The rumen contained 84.5% of digesta and accounted for 79% of dry matter digestion in the whole digestive tract. Ruminal fluid space and whole-gut digesta fill increased by 31%-34%, while ruminal rates of in situ degradation increased by more than 100% between spring and autumn for cellulose and hemicellulose. Hyperphagia in autumn was accompanied by increased bacterial counts in ruminal fluid (30%), declines in ruminal pH, and increases in the concentration of fermentation acids (16%) when compared with spring hypophagia. Consumption of fresh hay and supplement increased the concentrations of acids most markedly during winter and spring when bacterial counts were low. Low food intakes in winter and spring may limit the microbial population, whereas hyperphagia in autumn may foster a much more active microflora that requires consistent supplies of substrate. Plasticity of fill and fermentation in muskoxen minimizes winter costs and maximizes nutrients and energy gained from coarse forages in small home ranges throughout the year.

Animals↗
PubMed1990

Growth, thermogenesis, and hyperphagia.

Resting metabolic rate is demonstrated to be a function of fat-free mass and a growth variable related to food-energy-input imbalance rate. By use of obligatory energy expenditure terms, the two-reservoir energy model applied to hyperphagia shows that growth of the fat-free mass is rapid whereas that of the fat store is slow and that the growth of both is bounded. Most of the excess energy at the onset of hyperphagia initially goes into the fat store, but this decreases with time until the greater fraction is diverted to the fat-free mass. The two-reservoir model predicts that weight gain per unit of excess energy is not constant but decreases monotonically until ultimately reaching an asymptotic value. Departure of theory and experiment in the long term suggests that facultative considerations become increasingly important.

Adipose Tissue↗