It's normal for bears to exhibit hyperphagia, or excessive hunger, during the summer months.
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But they also inevitably encounter some of the park's 2,200 brown bears, who, around July enter into a state of hyperphagia — aka, eating nonstop.
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He was born with a genetic abnormality that leads to cognitive delays, hyperphagia (insatiable hunger), slurred speech, and moods that veer unexpectedly from loving to violent.
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An abnormal surge in appetite, known as hyperphagia, dominates the lives of those suffering from PWS, which typically kills three out of every 100 patients each year.
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To prepare their bodies, they must enter a state known as hyperphagia, in which they eat nearly nonstop until they become practically unrecognizable to the rangers who know them.
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Certainly there is an odd magic at work at Belarussian Xata, where, as the meal progresses, the food grows increasingly rich — a kind of homage to hyperphagia, the fattening period before hibernation — yet the spirit stays light.
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High cortisol levels, in combination with high insulin levels, may be responsible for stress-induced eating, as research shows high cortisol reactivity is associated with hyperphagia, an abnormally increased appetite for food, during stress. Furthermore, since glucocorticoids trigger hunger and specifically increase one's appetite for high-fat and high-sugar foods, those whose adrenal glands naturally secrete larger quantities of glucocorticoids in response to a stressor are more inclined toward hyperphagia. Additionally, those whose bodies require more time to clear the bloodstream of excess glucocorticoids are similarly predisposed. These biological factors can interact with environmental elements to further trigger hyperphagia.
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Haploinsufficiency of SIM1 has been shown to cause severe early-onset obesity in a human girl with a de novo balanced translocation between chromosomes 1p22.1 and 6q16.2 and has been suggested to cause a Prader-Willi-like phenotype in other cases. Additionally, studies in mice have shown that haploinsufficieny of Sim1 causes obesity that is due to hyperphagia and do not respond properly to increased dietary fat. Overexpression of SIM1 protects against diet induced obesity and rescues the hyperphagia of agouti yellow mice, who have disrupted melanocortin signaling. The obesity and hyperphagia may be mediated by impaired melanocortin activation of PVN neurons and oxytocin deficiency in these mice.
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It has been demonstrated that modulating Sim1 levels postnatally also leads to hyperphagia and obesity, suggesting a physiological role for Sim1 separate from its role in development.
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In Klüver–Bucy syndrome, an individual will display placidity, hyperorality, hypersexuality, and hyperphagia. This condition results from bilateral destruction of the amygdaloid bodies of the limbic system.
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The ventromedial nucleus (VMN) is most commonly associated with satiety. Early studies showed that VMN lesions caused over-eating and obesity in rats. However, the interpretation of these experiments was summarily discredited when Gold's research demonstrated that precision lesioning of the VMN did not result in hyperphagia. Nevertheless, numerous studies have shown that the immediacy of hyperphagia and obesity syndrome are a consequence of VMN lesions or procaine injections, and point to the VMN's role in satiety.
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Although hunger may arise from energy or nutrient deficits, as would be expected in the set-point theories of hunger and eating, hunger may arise more commonly from anticipated pleasure of eating, consistent with the positive-incentive perspective. Gramlich distinguished the overeating responses to these stimuli as homeostatic hyperphagia and hedonic hyperphagia respectively. Accordingly, hunger and eating are subject to feedback control from homeostatic, hedonic, and cognitive processes. Although these mechanisms interplay and overlap to some extent, they can nonetheless be individually separated.
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Reversed vegetative symptoms include only oversleeping (hypersomnia) and overeating (hyperphagia), as compared to insomnia and loss of appetite. These features are characteristic of atypical depression (AD). However, there have been studies claiming that these symptoms alone are sufficient to diagnose the condition of AD.
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The rapid onset obesity aspect of ROHHAD is usually the first diagnostic indicator of the disease. Patients often present with hyperphagia and rapid weight gain. This rapid weight gain is defined as 20-30 pounds over a 6-12 month period, and typically occurs between the ages of 1.5 and 11.
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Their cries are weak, and they have difficulty waking up. Another sign of this condition is a thin upper lip. More aspects seen in a clinical overview include hypotonia and abnormal neurologic function, hypogonadism, developmental and cognitive delays, hyperphagia and obesity, short stature, and behavioral and psychiatric disturbances. Holm et al.
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In psychology, disinhibition is a lack of restraint manifested in disregard of social conventions, impulsivity, and poor risk assessment. Disinhibition affects motor, instinctual, emotional, cognitive, and perceptual aspects with signs and symptoms similar to the diagnostic criteria for mania. Hypersexuality, hyperphagia, and aggressive outbursts are indicative of disinhibited instinctual drives.
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Patients with Kleine–Levin syndrome (KLS) experience recurring episodes of prolonged sleep (hypersomnia). In most cases, patients sleep 15 to 21 hours a day during episodes. Excessive appetite (hyperphagia) and unusual cravings are present in half to two thirds of cases. About half of patients, mainly male patients, experience dramatically increased sexual urges (hypersexuality).
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Likewise, hyperphagia (excessive eating) may be a result of hormonal imbalances, mental disorders (e.g., depression) and others. Dyspepsia, also known as indigestion, can also affect appetite as one of its symptoms is feeling "overly full" soon after beginning a meal. Taste and smell ("dysgeusia", bad taste) or the lack thereof may also effect appetite.
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Kleine–Levin syndrome (KLS) is a rare disorder characterized by persistent episodic hypersomnia and cognitive or mood changes. Many patients also experience hyperphagia, hypersexuality and other symptoms. Patients generally experience recurrent episodes of the condition for more than a decade and may return at a later age. Individual episodes generally last more than a week, sometimes lasting for months.
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Hedonic hunger or hedonic hyperphagia is "the drive to eat to obtain pleasure in the absence of an energy deficit." Particular foods may have a high "hedonic rating" or individuals may have increased susceptibility to environmental food cues. Weight loss programs may aim to control or to compensate for hedonic hunger. Therapeutic interventions may influence hedonic eating behavior.
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Diagnostic criteria for KLS was established by Schmidt in 1990, and the International Classification of Sleep Disorders further refined them. KLS is classified as a sleep disorder, specifically one of recurrent hypersomnia. Before 2005, hyperphagia and hypersexuality were thought to occur in all cases. That was changed with the guidelines published that year, which noted that they did not always occur.
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Appetite has a relationship with every individual's behavior. Appetitive behaviour also known as approach behaviour, and consummatory behaviour, are the only processes that involve energy intake, whereas all other behaviours affect the release of energy. When stressed, appetite levels may increase and result in an increase of food intake. Decreased desire to eat is termed anorexia, while polyphagia (or "hyperphagia") is increased eating.
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The ACADS gene has also been implicated in delaying the onset of Prader-Willi Syndrome, which is characterized by hypotonia, growth failure, and neurodevelopmental delays in the first years of life, and hyperphagia and obesity much later. In Genome Wide Association Studies (GWAS), SCAD has been associated with a reduced amount of insulin release shown by an oral glucose tolerance test, or OGTT.
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Feeding behaviors in children with ONH often include hyperphagia (overeating), resulting in obesity; or hypophagia (reduced food intake) with or without weight loss. Children also frequently experience aversion to specific textures of food. Disturbance of circadian sleep rhythm, resulting in abnormal sleep- wake cycles, is noted in one-third of children with ONH. This disturbance could result in behavioral problems and disruption of family life.
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Zugunruhe has been artificially induced in experiments by simulating long days. Some studies on White-crowned Sparrows have suggested that prolactin is involved in the pre-migratory hyperphagia (feeding), fattening and Zugunruhe. However, others have found that prolactin may merely be associated with lipogenesis (fat accumulation). Researchers have been able to study the endocrine controls and navigational mechanisms associated with migration by studying Zugunruhe.
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Many of the parabiotic pairs died throughout the experiment before its conclusion. In each pair, one rat became obese and exhibited hyperphagia. The weight of the rat with the surgical lesion rose rapidly for a few months, then reached a plateau as a direct result of the surgical procedure. After the procedure, the rat with the impaired hypothalamus ate voraciously while the paired rat's appetite decreased.
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The paired rat became obviously thin throughout the experiment, even rejecting food when it was offered. Some of the paired rats starved to death. Lesions subsequently made in the hypothalamus of two paired rats resulted in hyperphagia and obesity. That result verifies that the paired rat decreased its eating in a direct response to the signals in the blood from the rat with the lesion.
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In a crisis, corticotropin-releasing hormone (CRH) is secreted by the hypothalamus, suppressing appetite and triggering the release of glucocorticoids from the adrenal gland. These steroid hormones increase appetite and, unlike CRH, remain in the bloodstream for a prolonged period of time, often resulting in hyperphagia. Those who experience this biologically instigated increase in appetite during times of stress are therefore primed to rely on emotional eating as a coping mechanism.
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AgRP induces obesity by chronic antagonism of the MC4-R. Overexpression of AgRP in transgenic mice (or intracerebroventricular injection) causes hyperphagia and obesity, whilst AgRP plasma levels have been found to be elevated in obese human males. Understanding the role AgRP plays in weight gain may assist in developing pharmaceutical models for treating obesity. AgRP mRNA levels have been found to be down regulated following an acute stressful event.
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Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author. Research diagnostic criteria have been proposed and include evening hyperphagia (consumption of 25% or more of the total daily calories after the evening meal) and/or nocturnal awakening and ingestion of food two or more times per week. The person must have awareness of the night eating to differentiate it from the parasomnia sleep-related eating disorder (SRED).
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By inhibiting the rewarding effects of cocaine, CART has a potential use in treating cocaine addiction. CART peptides are inhibitors of food intake (anorectic) and closely associated with leptin and neuropeptide Y, two important food intake regulators. CART hypoactivity in the hypothalamus of depressed animals is associated with hyperphagia and weight gain. CART is thought to play a key role in the opioid mesolimbic dopamine circuit that modulates natural reward processes.
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Individuals may have increased hedonic hunger susceptibility to environmental food cues. Genetic variability may influence hedonic hyperphagia. Variation in hedonic hunger levels from person to person may be key in determining success in weight loss tactics and a person's ability to cope with tempting foods that are readily available. To assess this, a Power of Food Scale (PFS) has been developed that quantifies a person's appetitive anticipation (not consumption).
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The male grizzly bear's hibernation ends in early to mid-March, while females emerge in April or early May. In preparation for winter, bears can gain approximately , during a period of hyperphagia, before going into hibernation. The bear often waits for a substantial snowstorm before it enters its den: such behavior lessens the chances predators will find the den. The dens are typically at elevations above on north-facing slopes.
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When leptin binds with the leptin receptor, it activates a number of pathways. Leptin resistance may be caused by defects in one or more part of this process, particularly the JAK/STAT pathway. Mice with a mutation in the leptin receptor gene that prevents the activation of STAT3 are obese and exhibit hyperphagia. The PI3K pathway may also be involved in leptin resistance, as has been demonstrated in mice by artificial blocking of PI3K signalling.
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After 20 minutes, the mean firing rate returned rapidly toward the PRE level. The elevated firing of hippocampal place cells during SWS after spatial exploration could explain why there were elevated levels of slow-wave sleep in Datta's study, as it also dealt with a form of spatial exploration. In rats, sleep deprivation causes weight loss and reduced body temperature. Rats kept awake indefinitely develop skin lesions, hyperphagia, loss of body mass, hypothermia, and, eventually, fatal sepsis.
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It is traditionally characterized by hypotonia, short stature, hyperphagia, obesity, behavioral issues (specifically obsessive–compulsive disorder-like behaviors), small hands and feet, hypogonadism, and mild intellectual disability. However, with early diagnosis and early treatment (such as with growth hormone therapy), the prognosis for persons with PWS is beginning to change. Like autism, PWS is a spectrum disorder and symptoms can range from mild to severe and may change throughout the person's lifetime. Various organ systems are affected.
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A limitation of food sources in early spring and wild berry and nut crop failures in summer may contribute to American black bears regularly feeding from human-based food sources. These bears often eat crops, especially during autumn hyperphagia when natural foods are scarce. Favored crops include apples, oats and corns. American black bears can do extensive damage in areas of the northwestern United States by stripping the bark from trees and feeding on the cambium.
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Two major factors found to contribute to binge eating in bulimia nervosa (BN) patients are: stress and negative emotions. One model of BN produces stress-induced hyperphagia, where rats go through periods of restricted food and then are allowed free access to food; this mimics the intermittent self-imposed fasting and yielding to food of BN patients. Sham-feeding rat models have been used to present the defect in the satiety mechanisms in BN due to vomiting or purging after food intake.Davis, J.D., Campbell, C.S. (1973).
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These two types of cells are neuropeptide Y (NPY)-expressing cells, which cause hyperphagia and energy conservation, and cells that pro-opiomelanocortin (POMC), which are related to hypophagia and increased energy expenditure. NPY and norepinephrine are both localized in select neurons in the brain and periphery. A norepinephrine reuptake inhibitor, such as nisoxetine, could potentially cause anorexia by decreasing activity of cells that express NPY and norepinephrine. In lean and obese mice, selective and combined norepinephrine and dopamine reuptake inhibition reduces food intake and body weight.
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In the late 1960s, non-selective serotonin receptor antagonists demonstrated a relationship between serotonin receptors and food intake. Later, animal studies showed that serotonin receptor agonists might act as a mediator of satiety. Serotonin has been implicated as a critical factor in the short-term regulation of food intake and in promoting loss of weight associated with hyperphagia. Studies using pharmacological and genetic tools demonstrated that the 5-HT2C receptor subtype was one of the principal mediators through which serotonin exerts its anorectic effects in rodents.
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Male groundhogs average slightly larger than females and, like all marmots, they are considerably heavier during autumn (when engaged in autumn hyperphagia) than when emerging from hibernation in spring. Adult males average year-around weight , with spring to fall average weights of while females average , with spring to fall averages of .North Carolina Wild, Wildlife Profiles, Woodchuck, Marmota monax Seasonal weight changes indicate circannual deposition and use of fat. Groundhogs attain progressively higher weights each year for the first two or three years, after which weight plateaus.
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Prader-WIlli (PWS) and Angelman syndrome (AS) are distinct neurogenetic disorders caused by chromosomal deletions, uniparental disomy or loss of the imprinted gene expression in the 15q11-q13 region. Whether an individual exhibits PWS or AS depends on if there is a lack of the paternally expressed gene to contribute to the region. PWS is frequently found to be the reason for secondary obesity due to early onset hyperphagia - the abnormal increase in appetite for consumption of food. There are known three molecular causes of Prader–Willi syndrome development.
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Given that the hypothalamic arcuate nucleus regulates many basic processes, including appetite, a link may well exist. In the hypothalamus of people with PWS, nerve cells that produce oxytocin, a hormone thought to contribute to satiety, have been found to be abnormal. People with PWS have high ghrelin levels, which are thought to directly contribute to the increased appetite, hyperphagia, and obesity seen in this syndrome. Cassidy states the need for a clear delineation of behavioral expectations, the reinforcement of behavioural limits, and the establishment of regular routines.
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The obese gene (then termed ob/ob, now known to be a mutations in the gene responsible for the production of leptin) was determined from one mutant mouse, discovered in 1950. Coleman and researchers further identified a gene on chromosome 4 that led to hyperphagia and obesity in mice. The gene, then termed "db/db" (now known to be a mutation in the leptin receptor) also correlated to the severe onset of diabetes. The experimenters used parabiosis to conjoin a db/db mouse to a normal mouse, and the normal mouse would starve to death after one week.
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Moon face is often associated with Cushing's syndrome or steroid treatment (especially corticosteroids), which has led to it being known as Cushingoid facies. Moon face is a type of corticosteroid- induced lipodystrophy along with "buffalo hump", which in one study occurred in 47% of the 820 patients. Moon face is among the most frequently reported adverse events of systemic glucocorticoids, along with insomnia (58%), mood disturbances (50%), and hyperphagia (49%). Another long-term study of 88 patients on prednisone showed that lipodystrophy, such as moon face, was the most frequent adverse event, suffered by 63% of patients.
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1-(1-Naphthyl)piperazine (1-NP) is a drug which is a phenylpiperazine derivative. It acts as a non-selective, mixed serotonergic agent, exerting partial agonism at the 5-HT1A, 5-HT1B, 5-HT1D, 5-HT1E, and 5-HT1F receptors, while antagonizing the 5-HT2A, 5-HT2B, and 5-HT2C receptors. It has also been shown to possess high affinity for the 5-HT3, 5-HT5A, 5-HT6, and 5-HT7 receptors, and may bind to 5-HT4 and the SERT as well. In animals it produces effects including hyperphagia, hyperactivity, and anxiolysis, of which are all likely mediated predominantly or fully by blockade of the 5-HT2C receptor.
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Most of the members of the box C/D family function in directing site-specific 2'-O-methylation of substrate RNAs. In the human genome, there are 29 tandemnly repeated copies of SNORD116, followed by 48 copies of another C/D box snoRNA, SNORD115, in the Prader–Willi syndrome (PWS) region of chromosome 15. Unlike most other snoRNAs, SNORD116 is expressed prevalently in the brain (but is absent in PWS patients) and lacks any significant complementarity with ribosomal RNA. Mouse models of PWS show similar symptoms to humans (hyperphagia and growth deficiency), providing further evidence that PWS is directly linked to the deletion of SNORD116.
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A human mutant leptin was first described in 1997, and subsequently six additional mutations were described. All of those affected were from Eastern countries; and all had variants of leptin not detected by the standard immunoreactive technique, so leptin levels were low or undetectable. The most recently described eighth mutation reported in January 2015, in a child with Turkish parents, is unique in that it is detected by the standard immunoreactive technique, where leptin levels are elevated; but the leptin does not turn on the leptin receptor, hence the patient has functional leptin deficiency. These eight mutations all cause extreme obesity in infancy, with hyperphagia.
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This is in part due to sexual dimorphism, as male brown bears average at least 30% larger in most subtypes. Individual bears also vary in size seasonally, weighing the least in spring due to lack of foraging during hibernation, and the most in late fall, after a period of hyperphagia to put on additional weight to prepare for hibernation. Therefore, a bear may need to be weighed in both spring and fall to get an idea of its mean annual weight. Skeleton The normal range of physical dimensions for a brown bear is a head-and-body length of and a shoulder height of .
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Nagata-Kuroiwa R., Furutani N., Hara J., Hondo M., Ishii M., Abe T., et al. (2011). Critical role of neuropeptides B/W receptor 1 signaling in social behavior and fear memory. PLoS ONE 6:e16972. doi:10.1371/journal.pone.0016972 Early studies indicated that NPB and NPW had a complex effect on appetite, but generally led to anorexia.Tanaka H., Yoshida T., Miyamoto N., Motoike T., Kurosu H., Shibata K., et al. (2003). Characterization of a family of endogenous neuropeptide ligands for the G protein-coupled receptors GPR7 and GPR8. Proc. Natl. Acad. Sci. U.S.A. 100, 6251–6256. doi:10.1073/pnas.2233339100 Similarly, male rats lacking NPBWR1 exhibited hyperphagia and adult-onset obesity, though why female rats are unaffected is unknown.
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A condition rarely diagnosed, Witzelsucht has been well documented in the recent era in at least two cases: Case #1: A 30-year-old, right-handed man was admitted to the department of neurology for irritability, inappropriate behavior, and morbid hyperphagia with obesity. His inappropriate laughter and persistent pun and joke telling was a sharp contrast to his personality as an intellectual theological scholar, known for his exceptional memory as opposed to his sense of humor. This behavior was generally prompted by environmental stimuli such as physician’s rounds or blood sampling. To the patient, his behavior seemed normal, which explains why he remained nondiscriminating toward his jokes, their context, and their impression on those around him.
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WAGR syndrome (also known as WAGR complex, Wilms tumour-aniridia syndrome, aniridia-Wilms tumour syndrome) is a rare genetic syndrome in which affected children are predisposed to develop Wilms tumour (a tumour of the kidneys), Aniridia (absence of the coloured part of the eye, the iris), Genitourinary anomalies, and mental Retardation. The G is sometimes instead given as "gonadoblastoma," since the genitourinary anomalies can include tumours of the gonads (testes or ovaries). Some WAGR syndrome patients show severe childhood obesity and hyperphagia; the acronym WAGRO (O for obesity) has been used to describe this category and may be associated with the coinciding loss of BDNF a gene that is also on chromosome 11. The condition, first described by Miller et al.
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An orexigenic, or appetite stimulant, is a drug, hormone, or compound that increases appetite and may induce hyperphagia. This can be a medication or a naturally occurring neuropeptide hormone, such as ghrelin, orexin or neuropeptide Y, which increases hunger and therefore enhances food consumption. Usually appetite enhancement is considered an undesirable side effect of certain drugs as it leads to unwanted weight gain, but sometimes it can be beneficial and a drug may be prescribed solely for this purpose, especially when the patient is suffering from severe appetite loss or muscle wasting due to cystic fibrosis, anorexia, old age, cancer or AIDS. There are several widely used drugs which can cause a boost in appetite, including tricyclic antidepressants (TCAs), tetracyclic antidepressants, natural or synthetic cannabinoids, first-generation antihistamines, most antipsychotics and many steroid hormones.
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