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

Organisms often shown enhanced growth during recovery from starvation, and can even overtake continuously fed conspecifics (overcompensation). In an earlier paper (Ecology 84, 2777-2787), we studied the relative role played by hyperphagia and resource allocation in producing overcompensation in juvenile (non-reproductive) animals. We found that, although hyperphagia always produces growth compensation, overcompensation additionally requires protein allocation control which routes assimilate preferentially to structure during recovery. In this paper we extend our model to cover reproductively active individuals and demonstrate that growth rate overcompensation requires a similar combination of hyperphagia and allocation control which routes the part of enhanced assimilation not used for reproduction preferentially towards structural growth. We compare the properties of our dynamic energy budget model with an earlier proposal, due to Kooijman, which we extend to include hyperphagia. This formulation assumes that the rate of allocation to reserves is controlled by instantaneous feeding rate, and one would thus expect that an extension to include hyperphagia would not predict growth overcompensation. However, we show that a self-consistent representation of the hyperphagic response in Kooijman's model overrides its fundamental dynamics, leading to preferential allocation to structural growth during recovery and hence to growth overcompensation.
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PMID:Resource allocation, hyperphagia and compensatory growth. 1552 53

Eating disorders (ED), such as anorexia nervosa (AN) and bulimia nervosa (BN), are complex psychiatric disorders where different genetic and environmental factors are involved. Several lines of evidence support that brain-derived neurotrophic factor (BDNF) plays an essential role in eating behaviour and that alterations on this neurotrophic system participates in the susceptibility to both AN and BN. Accordingly, intraventricular administration of BDNF in rats determines food starvation and body weight loss, while BDNF or its specific receptor NTRK2 knockout mice develop obesity and hyperphagia. Case-control studies also suggest a BDNF contribution in the aetiology of ED: we have previously reported a strong association between the Met66 variant within the BDNF gene, restricting AN (ANR) and minimum body mass index (minBMI) in a Spanish sample, and a positive association between the Val66Met and -270C/T BDNF SNPs and ED in six different European populations. To replicate these results, avoiding population stratification effects, we recruited 453 ED trios from eight European centres and performed a family-based association study. Both haplotype relative risk (HRR) and haplotype-based haplotype relative risk (HHRR) methods showed a positive association between the Met66 allele and ANR. Consistently, we also observed an effect of the Met66 variant on low minBMI and a preferential transmission of the -270C/Met66 haplotype to the affected ANR offspring. These results support the involvement of BDNF in eating behaviour and further suggest its participation in the genetic susceptibility to ED, mainly ANR and low minBMI.
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PMID:Association of BDNF with restricting anorexia nervosa and minimum body mass index: a family-based association study of eight European populations. 1565 4

The possible role of neuropeptide Y (NPY) was studied in rats with hypermetabolism and hyperphagia induced by thyroxine (50-100-200 microg/day s.c. for 3-4 weeks). Both metabolic rate and body temperature increased quickly with thyroxine treatment, while hyperphagia started to develop only after 2 weeks of treatment. The weight gain rate progressively decreased or stopped. The NPY-induced hyperphagia was not altered significantly during thyroxine treatment (in severe thyrotoxicosis it was rather suppressed); the fasting-induced hyperphagia was smaller than in controls following 1 week of treatment, and it became enhanced only after 3 weeks, when the deficit in body weight indicated a certain level of starvation already prior to the food deprivation. The NPY-antagonist D-Tyr27,36,D-Thr32-NPY27,36 suppressed this fasting-induced hyperphagia, suggesting that endogenous NPY is involved in this late phase. In conclusion, hyperthyroidism per se does not increase the NPY activity, instead the quickly developing hyperthermia may inhibit the NPY actions; NPY may, however, be activated by a concurrent hypermetabolism-induced starvation.
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PMID:Hyperphagia of hyperthyroidism: is neuropeptide Y involved? 1610 82

In this review, the mechanism of our "toxic environment's" effects on insulin and weight gain in the genesis of obesity is elaborated. The composition of our diet is highly insulinogenic. The insulin drives energy into fat, and interferes with leptin signaling in the VMH. This results in weight gain and the sense of starvation, which results in decreased SNS activity, reducing energy expenditure and physical activity; and increased vagal activity, which promotes yet further insulin release and energy storage. Thus, hyperinsulinemia turns the leptin negative feedback system into a "vicious cycle" of obesity (see Figure 3, page 905). Externally, this appears as "gluttony and sloth" but it is biochemically driven. How does this work? A thin, insulin-sensitive, 13-year-old boy might consume a daily allotment of 2,000 kcal, and burn 2,000 kcal daily (or 50 kcal/kg fat-free mass) in order to remain weight-stable, with a stable leptin level. However, if that same 13-year-old became hyperinsulinemic and/or insulin resistant, perhaps as many as 250 kcal of the daily allotment would be shunted to storage in adipose tissue, promoting a persistent obligate weight gain. Due to the obligate energy storage, he now only has 1,750 kcal per day to burn. The hyperinsulinemia also results in a lower level of leptin signal transduction, conveying a CNS signal of energy insufficiency. The remaining calories available are lower than his energy expenditure; the CNS would sense starvation. Through decreased SNS tone, he would reduce his physical activity, resulting in decreased quality of life; and through increased vagal tone, he would increase caloric intake and insulin secretion, but now at a much higher level. Thus, the vicious cycle of gluttony, sloth, and obesity is promulgated. Is this personal responsibility, when a kid's brain thinks it's starving? Is it personal responsibility when the American Academy of Pediatrics still recommends juice for toddlers? Is it personal responsibility when the Women, Infant and Children program subsidizes fruit juice but not fruit? Is it personal responsibility when the first ingredient in the barbecue sauce is high-fructose corn syrup? Is it personal responsibility when high-fiber fresh produce is unavailable in poor neighborhoods? Is it personal responsibility when the local fast food restaurant is the only neighborhood venue that is clean and air-conditioned? Is it personal responsibility when in order to meet the criteria for No Child Left Behind, the school does away with physical education class? Is it personal responsibility when children are not allowed out of the house to play for fear of crime? We must get the insulin down. Fixing the "toxic environment" by altering the food supply and promoting physical activity for all children can't be done by government, and won't be done by Big Food. This will require a grassroots, bottom-up effort on the part of parents and community leaders. We as pediatricians must lead the way.
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PMID:The 'skinny' on childhood obesity: how our western environment starves kids' brains. 1746 96

Dmbx1 is a paired-class homeodomain transcription factor. We show here that mice deficient in Dmbx1 exhibit severe leanness associated with hypophagia and hyperactivity and that isolation of a Dmbx1(-/-) mouse from its cohabitants induces self-starvation, sometimes leading to death, features similar to those of anorexia nervosa in humans. Interestingly, overexpression of agouti in Dmbx1(-/-) mice failed to induce aspects of the A(y)/a phenotype, including hyperphagia, obesity, and diabetes mellitus. In Dmbx1(-/-) mice, administration of agouti-related protein increased cumulative food intake for the initial 6 h but significantly decreased it over 24- and 48-h periods. In addition, Dmbx1 was shown to be expressed at embryonic day 15.5 in the lateral parabrachial nucleus, the rostral nucleus of the tractus solitarius, the dorsal motor nucleus of the vagus, and the reticular nucleus in the brainstem, all of which receive melanocortin signaling, indicating involvement of Dmbx1 in the development of the neural network for the signaling. Thus, Dmbx1 is essential for various actions of agouti-related protein and plays a role in normal regulation of energy homeostasis and behavior.
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PMID:Dmbx1 is essential in agouti-related protein action. 1787 59

Hypothalamic neurons that express agouti-related protein (AgRP) and neuropeptide Y (NPY) are thought to be important for regulation of feeding, especially under conditions of negative energy balance. The expression of NPY and AgRP increases during lactation and may promote the hyperphagia that ensues. We explored the role of AgRP neurons in reproduction and lactation, using a mouse model in which AgRP-expressing neurons were selectively ablated by the action of diphtheria toxin. We show that ablation of AgRP neurons in neonatal mice does not interfere with pregnancy, parturition, or lactation, suggesting that early ablation allows compensatory mechanisms to become established. However, ablation of AgRP neurons after lactation commences results in rapid starvation, indicating that both basal feeding and lactation-induced hyperphagia become dependent on AgRP neurons in adulthood. We also show that constitutive inactivation of Npy and Agrp genes does not prevent pregnancy or lactation, nor does it protect lactating dams from diphtheria toxin-induced starvation.
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PMID:Role of agouti-related protein-expressing neurons in lactation. 1797 21

During starvation, after a short dynamic period of adaptation (phase I), a metabolic steady state is reached in which proteins are spared and lipids provide most of the energy expended [phase II (P2)]. However, protein breakdown increases dramatically once a lower threshold of body lipids is reached [phase III (P3)]. Body composition, energy intake, energy expenditure, and energy efficiency were determined in 8 groups of rats (fed, food-deprived up to P2 or P3 of starvation and refed for 3 d, 7 d, or until body mass restoration) to determine whether the kinetics of lipid and/or protein reserve recovery may be slowed down when refeeding occurs after the lipid threshold has been reached. Despite larger losses, P3 refed rats restored their body reserves as efficiently as those refed in P2. Whatever the nutritional status at the onset of refeeding, rehydration occurred first and hyperphagia played a more important role than hypometabolism in the restoration of the lost reserves. However, the pattern of body component gains was different during early refeeding. In P3 refed rats, body lipids were restored preferentially by significant contribution from endogenous lipid production. Thus, the extent of lipid depletion has important consequences for the restoration pattern of the body reserves. It depends not only on the intensity of the energy restriction (partial or total) as already demonstrated but also on the metabolic status at the onset of refeeding. These results may have significant implications on the way refeeding should be conducted after severe energy depletion.
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PMID:Restoration of body energy reserves during refeeding in rats is dependent on both the intensity of energy restriction and the metabolic status at the onset of refeeding [corrected]. 1842 92

Neonatal feeding problems are observed in several genetic diseases including Prader-Willi syndrome (PWS). Later in life, individuals with PWS develop hyperphagia and obesity due to lack of appetite control. We hypothesized that failure to thrive in infancy and later-onset hyperphagia are related and could be due to a defect in the hypothalamus. In this study, we performed gene expression microarray analysis of the hypothalamic response to maternal deprivation in neonatal wild-type and Snord116del mice, a mouse model for PWS in which a cluster of imprinted C/D box snoRNAs is deleted. The neonatal starvation response in both strains was dramatically different from that reported in adult rodents. Genes that are affected by adult starvation showed no expression change in the hypothalamus of 5 day-old pups after 6 hours of maternal deprivation. Unlike in adult rodents, expression levels of Nanos2 and Pdk4 were increased, and those of Pgpep1, Ndp, Brms1l, Mett10d, and Snx1 were decreased after neonatal deprivation. In addition, we compared hypothalamic gene expression profiles at postnatal days 5 and 13 and observed significant developmental changes. Notably, the gene expression profiles of Snord116del deletion mice and wild-type littermates were very similar at all time points and conditions, arguing against a role of Snord116 in feeding regulation in the neonatal period.
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PMID:Neonatal maternal deprivation response and developmental changes in gene expression revealed by hypothalamic gene expression profiling in mice. 2019 75

Uncontrolled type 1 diabetes leads to hyperphagia and severe ketosis. This study was conducted to test the hypothesis that ketone bodies act on the hindbrain as a starvation signal to induce diabetic hyperphagia. Injection of an inhibitor of monocarboxylate transporter 1, a ketone body transporter, into the fourth ventricle normalized the increase in food intake in streptozotocin (STZ)-induced diabetic rats. Blockade of catecholamine synthesis in the hypothalamic paraventricular nucleus (PVN) also restored food intake to normal levels in diabetic animals. On the other hand, hindbrain injection of the ketone body induced feeding, hyperglycemia, and fatty acid mobilization via increased sympathetic activity and also norepinephrine release in the PVN. This result provides evidence that hyperphagia in STZ-induced type 1 diabetes is signaled by a ketone body sensed in the hindbrain, and mediated by noradrenergic inputs to the PVN.
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PMID:Involvement of brain ketone bodies and the noradrenergic pathway in diabetic hyperphagia in rats. 2123 34

Alterations of both central and peripheral feeding regulatory substances occur in the acute phases of anorexia nervosa (AN) and bulimia nervosa (BN) and, generally, reverse after recovery. Some of these alterations are believed not only to sustain the altered eating behavior but also to contribute to certain psychopathological aspects and/or etiopathogenetic processes of eating disorders (EDs). It has been suggested that EDs are clinical conditions linked to reward-related mechanisms leading to a kind of addiction to self-starvation and/or overeating. Most of the feeding regulatory substances, which are dysregulated in EDs, are also implicated in the modulation of reward, emotional, and cognitive functions, thus representing possible links between altered nutritional regulation, motivated behaviors and reward processes. In this chapter, the ED literature dealing with ghrelin, brain-derived neurotrophic factor, opioid peptides, and endocannabinoids, which have prominent effects on eating behavior, body weight, reward, emotional, and cognitive functions, is reviewed in view of the above suggested links. Moreover, the potential therapeutics of new medications developed on the basis of neuroendocrine aberrations found in EDs is also presented.
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PMID:New frontiers in endocrinology of eating disorders. 2124 77


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