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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High-fat diet-feeding increases body weight and adiposity in Syrian hamsters (Mesocricetus auratus), effects due in part to decreased energy expenditure. The effects of voluntary exercise- or cold exposure-induced increases in energy expenditure were examined in fat- or chow-fed, female Syrian hamsters. In Experiment 1, voluntary exercise (10 weeks) caused a moderate hyperphagia and actually increased body weight in both diet groups through increases in lean body mass. Carcass lipid was not affected by by exercise in chow-fed hamsters and only slightly reduced in fat-fed animals. In Experiment 2, chronic (8 weeks) cold exposure (5 degrees C) increased energy intake to the same extent in both dietary groups relative to the warm-exposed (23 degrees C) controls. High-fat diet-induced obesity was largely prevented by cold exposure. Cold exposure reduced lean body mass in chow-fed hamsters, but this carcass component was spared by fat-feeding. These results indicate that the increased metabolic demands of cold exposure were more effective in preventing this form of diet-induced obesity than those of voluntary exercise (80% and 17% reductions in carcass lipid, respectively). These results are discussed in terms of possible beneficial effects of eating a lipid-rich diet prior to winter.
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PMID:Dietary obesity in exercising or cold-exposed Syrian hamsters. 671 40

Neonatal administration of monosodium glutamate (MSG) produces in rats neurotoxic degeneration of the circumventricular system, including the medial-basal hypothalamus, depleting several neuropeptides and neurotransmitters in this area. In addition, a number of behavioral and neuroendocrine responses are impaired, including a significant decrease in the analgesic response to cold-water swims (CWS). The present study examined whether the alterations in the analgesic responses following CWS and 2-deoxy-D-glucose (2-DG) induced by neonatal MSG treatment were due either to direct alterations in a pain-inhibitory system, or alternatively, to alterations in a system that processes the stressful consequences or properties of a stimulus. To accomplish this, the analgesic, hypothermic, and locomotor responses following CWS and the analgesic, hyperphagic, and locomotor responses following 2-DG were assessed in rats treated neonatally (days 2, 4, 6, 8, and 10) with either MSG or a vehicle solution. MSG-treated rats displayed significant reductions in both their analgesic and hypothermic responses following CWS, suggesting that MSG treatment impairs an animal's ability to process sufficiently the stimulus properties of the swim as stressful. While MSG treatment potentiated 2-DG analgesia, it reduced 2-DG hyperphagia, suggesting that MSG treatment also impairs coping responses to glucoprivation. These data indicate the importance of the circumventricular system in the coding of stimuli as potential stressors and in the subsequent activation of requisite systems necessary to provide a sustained, coordinated, and synchronous coping response.
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PMID:Impairments in analgesic, hypothermic, and glucoprivic stress responses following neonatal monosodium glutamate. 673 8

The past 10-15 years have produced a significant increase in knowledge and theories concerning the regulation of energy balance, but the precision of this regulation is still uncertain. However, the fact that investigators have had to resort to a variety of techniques and ploys (some of them bizarre) to produce marked pertubations in body weight is in itself an indication that the regulatory system can be very robust. Although control of food intake obviously plays a major role in this system, control of energy expenditure (i.e. DIT) also has to be considered as an important factor in the maintenance of energy balance. In this review most of the evidence for DIT and its biochemical origins has been derived from studies on experimental animals. Many of the overfeeding studies carried out on man are consistent with the animal work, but because of differences in interpretation and some equivocal results, the role of DIT in human metabolism is still a contentious issue. This problem may not be fully resolved to everyone's satisfaction until complete, continuous, and very precise energy balance measurements are made on chronically overfed lean subjects. Before this expensive and arduous experiment is undertaken, evidence for thermogenesis in man will continue to depend on acute measurements of the metabolic response to various stimuli. An increasing number of studies (e.g. 35, 80) have demonstrated the existence of NST in man, and the possibility that this could originate from BAT is supported by histological (62, 148) and thermographic data (130). Conversely, reductions in cold tolerance (2, 18) and thermogenic responses to noradrenaline (82) with increasing adiposity are similar to the blunted responses seen in genetically obese animals, which suggests that human obesity may also involve an impairment in thermogenesis. At the present time these ideas concerning the important of DIT in man and its role in obesity remain somewhat speculative, but no doubt this area will now be the subject of further research. Similarly, the impact of early nutritional influences on subsequent energy balance regulation and resistance to obesity will receive more attention following the report (144) that hyperphagia in rats during early life results in a reduced body fat content and leanness in adulthood. The relative contributions and interactions between intake and output in energy balance need clarifying, and in terms of central organization, the mechanisms of appetite control should now be considered for their relevance to the control of thermogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of energy balance. 676 16

During cold-induced nonshivering thermogenesis, interscapular brown adipose tissue (BAT) lipoprotein lipase (LPL) activity and lipogenesis are elevated. Because of the many similarities between cold- and diet-induced thermogenesis, we examined the effect of ad libitum access to a 32% sucrose solution on caloric intake, adiposity, and BAT enzyme activities in male rats. Daily caloric intakes of sucrose-fed animals were elevated by 20%-25%, and 8 wk of sucrose feeding doubled carcass fat content. This sucrose-feeding induced obesity was associated with increases in circulating triglyceride and insulin levels as well as increased retroperitoneal white adipose tissue LPL activity. However, the increased carcass lipid content accounted for less than half of the excess calories ingested by the sucrose-fed rats. Sucrose feeding stimulated in vivo lipogenesis in BAT and elevated BAT fatty acid synthetase and acetyl-CoA carboxylase activities but not LPL activity. These findings suggest that overeating enhances endogenous lipogenesis but not uptake of circulating triglyceride in BAT. Thus, both cold- and diet-induced thermogenesis increase BAT lipogenesis, while only cold-induced thermogenesis is associated with elevated LPL activity in BAT.
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PMID:Effect of sucrose overfeeding on brown adipose tissue lipogenesis and lipoprotein lipase activity in rats. 682 91

Rats fed a varied and palatable "cafeteria" diet exhibited hyperphagia, increases in resting metabolic rate (VO2) and the thermogenic response to noradrenaline as well as hypertrophy of brown adipose tissue (BAT). In streptozotocin-diabetic rats, cafeteria feeding failed to produce increases in VO2 or the response to noradrenaline, although BAT mass was greater than in their respective stockfed controls. Replacement doses of insulin (protamine-zinc-insulin, PZI) at two levels (2 and 4 units/rat every alternate day) failed to restore the thermogenic response of diabetic rats to the cafeteria diet. Acute replacement (8 units PZI) 12hr before the measurements resulted in resting and noradrenaline-stimulated values for VO2 that were similar to those of non-diabetic cafeteria rats. These findings suggest an insulin requirement for diet-induced thermogenesis and the failure of diabetic rats to maintain body temperature when exposed to cold (5 degrees C) suggests a further insulin requirement for cold-induced thermogenesis. In non-diabetic cafeteria rats, plasma insulin levels were significantly lower than those of stock fed controls in spite of a high carbohydrate intake and normal blood glucose.
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PMID:A role for insulin in the diet-induced thermogenesis of cafeteria-fed rats. 701 42

The effect of two experimental manipulations designed to mobilize lipids from adipose tissue have been investigated in rats with parasagittal knife cuts in the ventromedial hypothalamus (VMH). Those animals which displayed hyperphagia during the initial 5 days VMH knife cuts were then restricted in food intake to reduce body weights to levels comparable to that of the sham-operated controls. Two weeks following the knife-cut lesions, or sham operations, animals in the first experiment were exposed to the cold for 60 min, and those in the second experiment were injected with 2-deoxy-D-glucose (2-DG). The injections of 2-DG increased the level of glycerol in the control animals but not in the animals with VMH knife cuts. Both groups showed a rise in glucose. Plasma insulin and triglycerides were the same in both groups. Exposure to the cold increased the level of glycerol in both groups. The insulin levels were lower in the corresponding groups with knife cuts. These studies show that VMH knife cuts do not produce hyperinsulinemia in pair-gained rats.
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PMID:Obesity-inducing hypothalamic knife cuts: effects on lipolysis and blood insulin levels. 705 66

The rise in resting oxygen consumption (VO2) during the 2-3 h following intragastric feeding (50 kJ [12 kcal]) was significantly greater in hyperphagic cafeteria-fed rats and hyperthyroid rats, but was markedly reduced in 3-day fasted and genetically-obese Zucker rats, compared to their respective stock-fed controls. In control and hyperthyroid animals this response was almost completely abolished by administration of propranolol. In another group of rats, resting VO/ was elevated by 8 per cent after 12 h of cafeteria feeding and was maximally increased by 20 per cent after 2.5 days on the diet. In rats previously cold-adapted (15 days at 5 degrees C) the maximal response (20 per cent) to cafeteria feeding was seen after only 12 h on the diet. These results suggest that the acute thermic response to food involves a sympathetic activation of thermogenesis, similar to that induced by chromic hyperphagia and cold-exposure, and can be influenced by genetic background plane of nutrition and thyroidal status.
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PMID:Factors influencing the acute effect of food on oxygen consumption in the rat. 706 15

Mild, non-noxious, oscillating pinches to a rat's tail elicits hyperphagia. The present study examined whether tail-pinch (TP) would exert hyperalgesic and hyperactive effects in rats that also exhibit the overeating response. The first experiment assessed TP effects upon reactivity to electric shock as measured by flinch-jump thresholds. Significant decreases in jump thresholds were observed 0 and 15, but not 30, min following TP. This effect persisted regardless of whether food was present or absent during TP. The second experiment assessed TP effects upon reactivity to heat as measured by hot-plate latencies. In contrast to jump thresholds, the shortened hot-plate latencies observed following TP persisted into the recovery period. In examining TP effects upon activity levels (Experiment 3), it was found that animals display similar patterns of temporally-declining activity regardless of whether TP was administered or not. Finally, TP selectively decreased the analgesic responses to two different doses of morphine and two different cold-water swim temperatures (Experiment 4). The TP-induced reductions occurred when TP was administered either before or after the analgesic manipulation. These data are discussed in terms of the nociceptive selectivity of the TP effect, and its influences upon analgesic processes.
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PMID:Modulation of antinociceptive responses following tail pinch stress. 720 Jan 85

Feeding a "cafeteria" diet for 2 wk to male Holtzman rats resulted in a weight gain that was, on average, only slightly more than that of control rats fed a regular chow diet. Wet weight, DNA, and total protein content of interscapular brown adipose tissue were more than doubled in the cafeteria-fed rats and proliferation of mitochondria paralleled tissue growth. After 2 wk of recovery from cafeteria feeding, the expanded size of the tissue had completely regressed to a normal level. Brown adipose tissue mitochondria of cafeteria-fed rats bound 3 times more purine nucleotides than mitochondria of chow-fed control rats, but no change in the proportion of polypeptides with molecular weight in the region of 32,000 could be detected. The changes in brown adipose tissue and its mitochondria in cafeteria-fed rats correspond to those seen previously in noradrenaline-treated rats, i.e., tissue growth accompanied by mitochondrial proliferation and an unmasking of proton conductance pathways. The increase in 32,000-mol-wt polypeptides seen in brown adipose tissue mitochondria of cold-acclimated rats does not occur in the cafeteria-fed rats. Control mechanisms are presumed to differ, either quantitatively or qualitatively, in the two situations, cold exposure and overeating, which both cause growth of brown adipose tissue.
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PMID:Brown adipose tissue of cafeteria-fed rats. 727 Jun 79

The effects of repeated treatment with the metabolic stressor 2-deoxy-D-glucose (2-DG: 500 mg/kg/day, 7 days) upon some ingestive and psychological behaviours were investigated, and compared with those elicited by repeated immobilization or cold exposure (2 hr/day, 7 days). Because all these stressors affect central serotonergic systems, 5-HT1A and 5-HT2A receptor-mediated behaviours were also analysed. Both 2-DG administration and immobilization decreased daily food intakes and increased the weight of the adrenals, while all stressors reduced body weight gain. In addition, 2-DG triggered hyperphagia (and reduced body weight loss) throughout the 7 light phases, and hypophagia (and reduced body weight gain) throughout the 7 dark phases. However, the other stressors had only temporary effects during the light phases. These results suggested that immobilized and cold exposed rats, but not 2-DG-treated rats had progressively adapted to their stressors. Furthermore, 2-DG-treated rats exhibited decreased ambulation when placed in the open field, but no change in social interaction. Forepaw treading and flat body posture responses to the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) were not altered by the stressors, but both of them slightly amplified 8-OH-DPAT-induced hypothermia. This change was associated with a decreased head shake response to the 5-HT2A agonist 1-(4-iodo-2,5-dimethoxy-phenyl)-2-aminopropane (DOI) in 2-DG-treated rats, compared with that measured in the other groups. This study opens the possibility that alterations in feeding rhythms has functional consequences on 5-HT2A receptors.
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PMID:Effects of repeated 2-deoxy-D-glucose administration on ingestive, psychological, and 5-HT-related behaviours in the rat. 793 5


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