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

With the use of ethanol in hyperalimentation regimens and for the inhibition of premature labor, there is increased opportunity for exposure of the fetus to this potentially toxic substance. We reviewed the literature regarding the effects of ethanol on the fetus and neonate, and illustrate its potential toxicity by the report of a case of neonatal depression secondary to acute maternal ethanol ingestion.
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PMID:Acute transplacental ethanol intoxication. 119 Jan 80

The concentrations and synthesis of monoamines in various hypothalamic nuclei and the influence of monoaminergic drugs on food intake were studied in two rat lines produced by selective outbreeding for voluntary high and low alcohol drinking. The hypothalamic nuclei of the alcohol-preferring AA rats contained slightly more serotonin than those of the alcohol-avoiding ANA rats, but the accumulation of 5-hydroxytryptophan after inhibition of aromatic amino acid decarboxylase was the same in both lines. There was no significant difference in the basal concentrations of catecholamines between the lines, but the accumulation of L-DOPA was significantly greater in the ANA than the AA rats, suggesting differences in catecholamine turnover. This difference was significant in the paraventricular nucleus, which is involved in the regulation of food intake. Clonidine (an alpha 2-agonist) and 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, a 5-HT1A agonist) induced hyperphagia and 1-(3-trifluoromethylphenyl)piperazine (TFMPP, a 5-HT1B agonist) induced hypophagia dose-dependently in both rat lines. Clonidine tended to be more potent in the ANA than the AA rats. Food intake following a 20-h fast was significantly lower in the ANA than AA rats. These results suggest that the alcohol-avoiding ANA and alcohol-preferring AA rats have different hypothalamic monoamine mechanisms controlling food intake, which could also partially account for their differential alcohol acceptance.
Alcohol
PMID:Hypothalamic monoamines and food intake in alcohol-preferring AA and alcohol-avoiding ANA rats. 182 11

Two hundred one non-treatment seeking women with alcoholism, anxiety disorders, alcoholism and anxiety disorders, or neither alcoholism nor anxiety disorders were interviewed to assess core psychopathology associated with eating disorders using the Eating Disorders Examination and DSM-IIIR psychiatric diagnoses using the Schedule of Affective Disorders and Schizophrenia-Lifetime version. Alcoholic women had significantly higher mean scores on each of the Eating Disorders Examination subscales of Restraint, Overeating, Eating Concern, Shape Concern, and Weight Concern compared with nonalcoholic women. Women with anxiety disorders had significantly elevated scores on subscales of Overeating, Eating Concern, and Weight Concern compared with women without anxiety disorders. Women with both alcoholism and anxiety disorders had higher rates of bulimia nervosa and/or eating disorder NOS compared with women with either disorder alone. Implications of these findings are discussed in the context of the co-morbid association between alcoholism, eating disorders, and anxiety disorders.
Alcohol Clin Exp Res 1996 Oct
PMID:Eating pathology among women with alcoholism and/or anxiety disorders. 890 68

The obese Zucker rat is an animal model of genetically inherited obesity demonstrating remarkable hyperphagia. In the present study, to try to clarify the relationship between obesity and gastric function including gastric mucosal integrity, the gastric acid secretion, emptying, and mucosal resistance against ulcerogenic agents were compared in lean and obese Zucker rats. Male lean and obese Zucker rats were housed at 25 degrees C under 12-hr/12-hr lighting cycle (on at 7:00 AM). The gastric acid output of obese Zucker rats was markedly smaller than that of lean Zucker rats, whereas there was no significant difference in gastric emptying in both groups. The degree of mucosal lesion formation induced by ulcerogenic agents was assessed by measuring the total length of all mucosal lesions observed (ulcer index; mm). The intragastric administration of indomethacin (20 mg/kg) produced hemorrhagic mucosal lesions in both lean and obese groups of Zucker rats, but the ulcer index was remarkably smaller in obese Zucker rats than that of their lean littermates (5.2 +/- 1.2 mm vs. 17.5 +/- 3.5 mm, mean +/- SEM, P < 0.01). In addition obese Zucker rats exhibited stronger resistance against the intragastric challenge of absolute ethanol (1 ml/rat), a necrotizing agent, with its ulcer index being 8.5 +/- 2.7 mm, compared with lean Zucker rats whose ulcer index was 26.4 +/- 5.4 mm (P < 0.01). The bilateral subdiaphragmatic vagotomy decreased both gastric acid secretion and the ulcer index of indomethacin-induced gastric injury observed in both obese and lean Zucker rats, whereas there was no significant difference in the ulcer index of ethanol-induced gastric injury. These results suggest that obese Zucker rats exhibit enhanced resistance against ulcerogens and decreased acid output. It is also speculated that the vagal system might be involved in inhibition of acid secretion and formation of indomethacin ulcers in obese Zucker rats.
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PMID:[Pathophysiological study on the mucosal defense system of genetically obese Zucker rats]. 899 42

Administration of the cannabinoid CB1 receptor antagonist SR141716 (3-10 mg/kg i.p.) abolished neuropeptide Y-induced overeating and significantly reduced ethanol and sucrose intake in CB1 wild-type (+/+) mice. In CB1 receptor knockout (-/-) mice, neuropeptide Y totally lost its capacity to increase food consumption. Similarly, sucrose and ethanol intakes were significantly lower in CB1-/- vs. CB1+/+ mice. In CB1 deficient mice, SR141716 had no effect in these models.
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PMID:Overeating, alcohol and sucrose consumption decrease in CB1 receptor deleted mice. 1277 Jul

Ethanol toxicity on liver is a function of duration of alcoholism, amount of daily intake of alcohol and patient's nutrition. The threshold of alcohol toxicity on the liver is about 40 g of ethanol daily in men and 20-30 g in women, however liver cirrhosis develops in no more than 8-20% of patients exceeding this values. Ethanol is oxidized in the liver to acetaldehyde--a compound considerably more toxic than ethanol itself. Despite small amount of alcohol dehydrogenase (ADH) found in gastric mucosa, the metabolism of ethanol in this site may have an important hepatoprotective effect. The oxidation of ethanol is associated with a change of hepatocyte redox homeostasis, which leads to a number of metabolic disorders such as lactic acidosis, hyperlipidaemia and hyperuricaemia. Chronic ethanol consumption does not influence ADH activity, but has a profound stimulatory effect on microsomal enzymes, in particular cytochrome CYP2E1. This fact is responsible for development in alcoholic liver associated with rise of oxygen consumption, excessive production of free radicals and increased metabolism of ethanol, vitamin A and testosterone. Ethanol and acetaldehyde have a deleterious effect, both the direct and indirect, on hepatocytes e.g., generating radical oxygen species and damaging intestinal mucosal barrier. Cellular oxidative stress that is caused by both an excess of free radicals and the antioxidatives' deficiency (glutathion, vitamin E, phosphatidylcholine), may be the principal factor responsible for progression of alcoholic liver disease. Among other factors accelerating alcohol-related liver lesion there are certain drugs, high fat diet, infection with HCV and genetic factors (female sex, enzymatic polymorphic forms of ADH and ALDH, hemochromatosis). Great importance in pathogenesis of necrotic and inflammatory hepatic events is being attributed to portal endotoxaemia and cytokines induced within the liver, in particular TNF-alpha and interleukin 8. These cytokines play a key role in development of alcoholic hepatitis, which clinical severity ranges from subclinical to fatal forms. Apart from abstinence, the treatment of alcohol liver disease is based on hyperalimentation, since alcoholism is generally associated with protein malnutrition. In severe forms of alcohol hepatitis corticosteroids are recommended.
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PMID:[Alcoholic liver disease]. 1290 Dec 71

Alcohol is frequently mentioned as a disinhibitor of restrained eating behavior although only a small number of studies have investigated this disinhibition effect. The present study was conducted to fill this gap. A total of 116 female college students participated in a questionnaire-based assessment and a taste-test experiment. Before the taste test, half of the participants consumed a preset amount of alcohol-laced orange juice, the other half were given plain orange juice. The dependent variable was the amount of savory crackers eaten during the taste test. The Dutch Eating Behavior Questionnaire (DEBQ), the Three-Factor Eating Questionnaire (TFEQ), and the Restraint Scale (RS) were used to measure eating behavior dimensions, which formed the independent variables in various regression analyses. No disinhibition effect was found. On the contrary, participants scoring high on restraint (DEBQ, TFEQ) proved to consume even less food than those having lower scores. Participants that rated high on the scales measuring tendency toward overeating consumed more food than participants with low scores. These results support earlier contentions that the validity of the Restraint Theory's statement that dieting leads to overeating is questionable.
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PMID:Absence of a disinhibition effect of alcohol on food consumption. 1500 Sep 59

Findings of earlier studies support the idea of a possible relation between dietary fat and ethanol intake, but it is unclear whether acute exposure to fat can increase ethanol consumption directly. In the current series of experiments, we examined whether daily overeating of fat, a single high-fat meal, or the injection of fat can increase ethanol intake. In Experiment 1, adult Sprague-Dawley rats were maintained on a high-fat diet (50% fat) for 7 days and switched subsequently to a laboratory chow diet while being trained to drink 9% ethanol. Rats that had eaten the greatest amount of the high-fat diet subsequently drank the most ethanol. In Experiment 2, a 1-h meal of the high-fat diet (50% fat) produced a significant increase in 7% ethanol consumption in comparison with what occurred after consumption of an equicaloric, low-fat (10% fat) meal. In Experiment 3, the orosensory effect of fat was eliminated with an intraperitoneal injection of a fat emulsion, Intralipid (20% fat, 5.0 ml). The injection of Intralipid, in comparison with saline, increased the ingestion of 9% ethanol. This finding is in contrast to what occurred with injection of an equicaloric, 50% glucose solution, which suppressed ethanol intake. These findings provide new evidence to support a positive relation between dietary fat and the consumption of ethanol.
Alcohol
PMID:A high-fat meal or injection of lipids stimulates ethanol intake. 1590 13

The functional role of corticosterone (CORT) in regulating migratory hyperphagia and lipogenesis was investigated in an annual migrant, the dark-eyed junco (Junco hyemalis). Intraperitoneal injections of either dexamethasone (9 microg DXM/500 microL of 5% EtOH in saline, n=10) to inhibit an increase in baseline CORT or saline (5% EtOH, n=9) were given every 48 h for 15 d after transfer from short (10.5L:13.5D) to long (15.5L:8.5D) days. Food intake, body mass, furcular fat deposition scores, and nocturnal migratory activity were recorded for 29 d after photostimulation. Both groups showed the same increase in daily food intake over the study period (DXM=52%, control=41%). Controls began to increase baseline CORT and mass about 2 wk after photostimulation. DXM-treated birds maintained low CORT and did not increase mass or CORT until injections ceased, at which time they gained mass at the same rate shown earlier by controls. DXM-treated birds did not show greater levels of migratory activity despite experiencing an increase in energy intake during the CORT-inhibited period. Collectively, the results support the migration modulation hypothesis, illustrating how an increase in baseline CORT is needed to support the development of migratory condition. We address the apparent conflict with earlier studies on CORT and migratory food intake and propose a model in which migratory hyperphagia is supported by changes in centrally regulated responses to CORT that can occur even if CORT remains low and lipogenesis is regulated predominantly by peripheral mechanisms that require an increase in baseline CORT.
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PMID:The role of corticosterone in supporting migratory lipogenesis in the dark-eyed Junco, Junco hyemalis: a model for central and peripheral regulation. 1716 Aug 85

The studies described in this report provide interesting animal models for exploring some of the metabolic and neural antecedents to the over-consumption of fat and alcohol. The results provide strong support for the existence of positive feedback loops that involve a close relation between circulating lipids and orexigenic peptides in dorsal regions of the hypothalamus. The peptides involved in these circuits include galanin, enkephalin, dynorphin and orexin. These peptides are expressed in the paraventricular nucleus and perifornical lateral hypothalamus, and they have very different functions from peptides expressed in the arcuate nucleus. Through mechanisms involving circulating lipids that rise on energy-dense diets, these peptides in the dorsal hypothalamus are each increased by the consumption of fat and ethanol; these nutrients, in turn, stimulate further production of these same peptides that promote overeating and excess drinking. These mechanisms involving non-homeostatic, positive feedback circuits may be required under conditions when food supplies are scarce and periods of gorging are essential to survival. However, they have pathological and sometimes life-threatening consequences in modern society, where fat-rich foods and alcoholic drinks are abundantly available and are contributing to the marked rise over the past 25 years in obesity and diabetes in both children and adults.
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PMID:Overconsumption of dietary fat and alcohol: mechanisms involving lipids and hypothalamic peptides. 1748 72


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