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

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
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PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

The performance of three widely used rat lines (Sprague-Dawley, Wistar, and Long Evans hooded) were evaluated in behavioral test systems that are sensitive to benzodiazepines. The in vivo effects of flunitrazepam and the brain [3H]Ro 15-1788 binding were determined and compared in these rat lines. The behavioral end points evaluated in this study were anxiolysis, measured using the automated elevated plus-maze; sedation by modification of locomotor activity; hyperphagia following food deprivation; protection for pentylenetetrazol-induced convulsions; and hypothermia. There were comparable results in the hypnotic, hypothermic, anticonvulsant, and feeding tests in these lines following flunitrazepam administration. However, the behavior of the Long Evans hooded rat was most amenable to the detection of drug-induced changes in the anxiety test. There was no difference in the maximum number of binding sites (Bmax) or the affinity (Ki) of the Ro 15-1788 or flunitrazepam binding in either the cerebellum or whole brain (minus cerebellum) in the three rat lines as determined by the competitive binding against [3H]Ro 15-1788. Thus, while these rat lines exhibited similar behavioral profiles in most tests the modest differences in the baseline responses and the ability to detect anxiolysis at lower doses of flunitrazepam observed with Long Evans hooded rats makes them particularly suited for these types of studies.
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PMID:Comparison of behavioral and central BDZ binding profile in three rat lines. 136 Jan 63

The sensitivity to insulin hypoglycemic convulsions has been shown to decrease at early times (16 and 24 hr) and increase at later times (1 week) after gold thioglucose (GTG) treatment. Systemically administered GTG is well known to produce hyperphagia, resulting in obesity, and cytological damage focused relatively selectively in the ventromedial hypothalamic area (VMH). Both of these effects on insulin hypoglycemic convulsions occur before the weight gain, but at a time when histological damage visible with cresyl violet stain has already appeared. Both of these changes reflect a difference in the convulsive response to hypoglycemia, rather than a differences in the degree of hypoglycemia in response to insulin. No functional change in the convulsive sensitivity was found at still earlier times during the latency in establishing the histological damage visible with cresyl violet. These results suggest that GTG lesions a relatively discrete brain region involved in adjusting the functional response of the brain to hypoglycemia, including a composite of two opposite regulatory components. The significance of such a control center in relation to energy metabolism in brain is discussed. Moreover, it has been postulated that the glucose moiety of GTG binds to glucoreceptors in the VMH to focus the cytoxicity of the gold thioportion at that site. These results are also discussed in relation to this proposed mechanism for concentration and hence localization of GTG toxicity in the VMH.
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PMID:Change in sensitivity to insulin hypoglycemic convulsions after gold thioglucose treatment: time course of development. 679 12

Systemic gold thioglucose (GTG) is well known to produce hyperphagia, resulting in obesity, and histological damage focused relatively selectively in the ventromedial hypothalamus (VMH). Although structurally very different, bipiperidyl mustard (BPM) produces apparently similar effects. However, a proposed mechanism for concentration and hence localization of GTG toxicity depends on its structural similarity to glucose, binding it to glucoreceptors and focusing the cytotoxicity of the gold thio-portion. We recently showed that GTG treatment also produces an early decrease and a later increase in sensitivity to insulin hypoglycemic convulsions. We report here that BPM also produces a similar biphasic change in sensitivity to insulin hypoglucemic convulsions. For both, the differences are in the brain's convulsive response to hypoglycemia, rather than in the degree of hypoglycemia in response to insulin. Thus, GTG and BPM cytotoxic lesions appear similar in this regard as well. BPM is another way of producing a relatively discrete brain lesion which alters the brain's functional adjustment to hypoglycemia. The significance of this control center and its relationship to the control(s) of feeding and systemic metabolism are discussed.
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PMID:Effects of bipiperidyl mustard (BPM) lesions on insulin hypoglycemic convulsions. 681 53

The first surviving Polish publications on epilepsy were written in the 16th and 17th centuries. Many causes of epileptic seizures are quoted and they are divided into two categories: internal and external. Internal causes (causa interna) include imbalance in the basic bodily humors, that is, yellow bile, black bile, phlegm, and blood. According to medieval writers, the principal cause of epilepsy was vapor, a damp, cold volatile substance originating in the excessive production of one of the basic organismic liquids. Vapor allegedly stuck to the openings leading to the cerebral ventricles or blocked them entirely, resulting in convulsions. External causes (causa externa) include overeating and excessive drinking, teething, spoiled milk, poisons, badly treated spots and fever, cold air, moonlight, and wearing donkey hide. Medical treatments for epilepsy included surgical interventions (bloodletting) and pharmacological interventions. The latter included laxatives, sea onion (scilla maritima, urginea maritima), and ground human skull, all of which were supposed to protect the body from vapors. Medical practitioners of that time also advised that the factors and circumstances conducive to epileptic seizures be observed and identified so that patients could be isolated from these alleged causal factors and their seizures reduced or ended.
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PMID:Treating epilepsy: a review of Polish historical sources. 2177 14

The obesity epidemic has led to the postulation that highly palatable foods may be "addictive" for some individuals. This idea is supported by the fact that there are overlaps in brain circuitry that underlie addictive behavior as well as overeating. In this paper, we discuss the utility of the concept of "food addiction" as it may relate to treating certain disordered eating behaviors. Using criteria set forth in the DSM-IV for substance-use disorders, we review data that have emerged from animal models suggesting that overeating, in the form of binge eating, fits some of the criteria for substance abuse. Further, we discuss preclinical data revealing that the addiction-like behavioral changes observed in response to overeating are concomitant with neurochemical changes that are similar to those observed in response to drugs of abuse. With this background and evidence in mind, we conclude this article with a discussion as to how "food addiction" research may translate into clinical strategies and pharmaceutical treatments useful in curtailing overeating.
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PMID:Overlaps in the nosology of substance abuse and overeating: the translational implications of "food addiction". 2199 87

The concept of addiction is loaded with connotations and is often used for its political as much as its medical utility. The scientific case for 'food addiction' as a clinical phenotype currently rests on its association with generic diagnostic criteria for substance-related disorders being applied to everyday foods and eating-related problems. This has fused the concept of obesity with addiction regardless of whether it fits the definition. The hedonic, or reward, system can account for the ingestion of foods and drugs, confirming that they share neural substrates that differentiate liking and wanting. These are normal processes that are recruited for natural homeostatic behaviours and can explain the phenomenon of hedonic overeating as a consequence of human motivation pushed to extremes by an obesogenic environment. Food addiction constitutes a medicalization of common eating behaviours, taking on the properties of a disease. The use of this medical language has implications for the way in which society views overeating and obesity.
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PMID:Food addiction and obesity: unnecessary medicalization of hedonic overeating. 2854 63