Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult male spiny mice (Acomys cahirinus) were challenged with 2-deoxy-D-glucose (2-DG) or regular insulin, and food intake or plasma glucose concentration was measured. Mice did not increase their food intake over baseline levels following treatment with 2-DG (62.5-1000 mg/kg). In contrast, regular insulin injections (1-50 U/kg) stimulated a modest, but significant increase in feeding, which was apparent within 2 hr at a low dose of 1 U/kg. However, a marked hyper- and hypoglycemia (compared to saline controls), respectively, were induced within 30 min by 2-DG (250 and 500 mg/kg) and regular insulin (1 and 3 U/kg). Reduced glucose levels may not account for the insulin-induced hyperphagia.
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PMID:Effect of insulin and 2-deoxy-D-glucose on feeding and plasma glucose levels in the spiny mouse. 307 May 82

Cimetidine is often prescribed for hospitalized patients requiring intravenous nutritional support (ie, total parenteral nutrition). When administered parenterally, the drug may prevent excessive fluid and electrolyte loss in patients with short-bowel syndrome, particularly after resection. It may also help prevent anastomotic ulcers in patients following partial gastrectomy. In patients with hypersecretory disease or high-volume ostomy drainage, cimetidine is clinically useful in moderating secretions, thus reducing fluid and electrolyte loss. Cimetidine can prevent, and perhaps treat, metabolic alkalosis associated with significant losses of nasogastric aspirate. Intravenous administration of the drug to patients requiring nasogastric suction often eliminates the need for addition of hydrochloric acid to their parenteral nutrition admixtures. Cimetidine has been found to be physically compatible and chemically stable in crystalline amino acid/dextrose solutions and in crystalline amino acid/dextrose/lipid admixtures. As cimetidine is widely used in patients receiving total parenteral nutrition, it has become acceptable practice to deliver the drug via parenteral nutrition admixtures. Admixing the drug may be of particular advantage for patients with limited vascular access or for those who are fluid restricted. Cimetidine when given by continuous infusion may be more effective and require less drug per day than if administered via intermittent injection. Moreover, administration of cimetidine by continuous infusion to hyperalimentation patients has been documented to save the institution more than $22,000 a year in materials and labor costs.
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PMID:Cimetidine and parenteral nutrition in the ICU patient. 309 28

We performed a controlled trial of peripheral hyperalimentation in moderate and severe alcoholic hepatitis to determine whether improvement in survival and liver function could be obtained. Twelve patients with moderate and 22 with severe alcoholic hepatitis were randomized to 28 days of peripheral parenteral nutrition (PPN) or standard therapy (ST). In the moderate group, six were treated with each therapy. In the severe group, 10 were treated with PPN and 12 with ST. Routine liver tests, hepatocyte function (galactose elimination capacity), estimated hepatic blood flow (galactose clearance) and assessment of ascites and encephalopathy were performed at randomization and at 28 days. Groups were equally matched at randomization. In the moderate group PPN produced no improvement in morbidity (liver tests) and mortality (no deaths). In the severe group there were seven deaths (4 PPN, 3 ST). PPN produced greater improvement than ST in serum bilirubin and transferrin concentrations and a trend toward greater improvement in prothrombin time, serum albumin and galactose elimination capacity. PPN had no deleterious effect on encephalopathy or ascites as only ST patients developed ascites or encephalopathy after randomization. We conclude that PPN compared to ST (1) provides no benefit in moderate alcoholic hepatitis, but (2) did more rapidly improve morbidity (liver tests) and probably liver function in severe alcoholic hepatitis; (3) PPN did not improve early mortality, and (4) it had no deleterious effect on encephalopathy or ascites.
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PMID:A randomized controlled study of peripheral parenteral nutrition in moderate and severe alcoholic hepatitis. 314 49

The autoperfused heart-lung preparation was developed as a method for extending the acceptable donor-to-recipient interval in clinical heart-lung transplantation. Metabolic substrate enhancement has been shown to be necessary for the survival and homeostasis of the functioning preparation. To define basic metabolic requirements and to determine the resting energy expenditure of the working canine heart-lung preparation, two groups were studied. Ten canine heart-lung blocks were placed in a normothermic autoperfusion circuit. In Group 1 (n = 5), a hyperalimentation solution of balanced substrate was infused (15% dextrose, 4.25% amino acids, 8 meq magnesium sulfate, 30 IU/dl insulin, and 10% lipids). In Group 2 (n = 5), no substrate was given. The preparations were ventilated with a mixture of room air and 5% CO2 at a rate of 4 breaths/min to maintain physiological pH. Myocardial function was assessed by cardiac output determinations and mixed venous gases. Pulmonary function was assessed with arterial blood gases. The oxygen consumption (VO2) and carbon dioxide production (VCO2) were measured with a Metabolic Cart, and the resting energy expenditure was calculated. The mean survival time for Group 1 was 360 minutes, and all preparations were terminated electively. The mean survival time for Group 2 was 219 +/- 43 minutes (p less than 0.01) with congestive heart failure as the common terminal event. All parameters of cardiac function and blood gases remained within physiological limits without significant differences between groups. The resting energy expenditure, a measure of metabolic rate, was 2.5 +/- 0.3 kcal/hr in Group 1 and 1.0 +/- 0.2 in Group 2 at termination (mean +/- SD) (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Energy expenditure of autoperfusing heart-lung preparation. 318 Mar 88

Electrolytic lesions of the ventromedial hypothalamus (VMH) produce an obesity syndrome characterized, in part, by excessive food intake and adiposity. Several hypotheses suggest that VMH lesion-induced hyperphagia results from elevated parasympathetic tone on the viscera expressed via the vagus nerves. To evaluate this possibility, vagally-mediated gastric acid secretion was measured in control and VMH-lesion rats. Initially, Pavlovian conditioning was used to elicit acid secretion to anticipated eating. VMH lesions eliminated the ability to mobilize acid secretion to the expectation of eating even though other behavioural indices of conditioning indicated that VMH rats still expected the food. The generality of the acid secretory deficit in VMH rats was evaluated by activating vagally-mediated acid secretion pharmacologically with insulin or 2-deoxy-D-glucose (2DG). VMH rats significantly increased acid secretion to insulin, although the response was attenuated compared to controls. Acid secretion stimulated by 2DG was normal. Thus the effects of VMH lesions on vagally-mediated acid secretion depend on the way in which the response is activated. The implications of this finding are discussed.
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PMID:Ventromedial hypothalamic lesions eliminate gastric acid secretion elicited by anticipated eating. 321 46

2-Deoxy-D-glucose (2DG) analgesia, mediated in part by endogenous opiate and hypothalamo-hypophysial systems is presumably activated by its stress-related properties. Recently 2DG hyperphagia, but not 2DG hyperglycemia was reduced by central pretreatment with the pancreatic beta-cell toxin, alloxan; this deficit was eliminated by co-administration of 3M D-glucose. The present experiment examined whether intracerebroventricular pretreatment with alloxan (40 or 200 micrograms) altered 2DG analgesia (400 or 700 mg/kg, IP) on the tail-flick and jump tests, and whether 3M D-glucose co-administration ameliorated any deficits. Both alloxan doses significantly reduced 2DG analgesia (400 mg/kg) on both tests. 2DG analgesia (700 mg/kg) was significantly reduced by both alloxan doses on the jump test, but only by the higher alloxan pretreatment on the tail-flick test. 3M D-glucose co-administration ameliorated alloxan-induced analgesic deficits more effectively at the lower 2DG dose. Neither alloxan nor alloxan/3M D-glucose treatments altered basal thresholds. These data pertain both to alloxan's effects upon coding of 2DG effects as stressful, and to the role of diabetes and/or central glucoreceptors in analgesic processes.
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PMID:Intracerebroventricular alloxan reduces 2-deoxy-D-glucose analgesia. 339 8

A comparison of the effects of the short-acting opioid antagonist naloxone, with the irreversible and highly-specific mu-1 antagonist naloxonazine, has categorized the mediation of opioids in some forms of feeding into mu-1 and non-mu-1 components. The mu-1 sites have been implicated in free-feeding, deprivation-induced feeding and morphine-induced hyperphagia, based upon their sensitivity to both naloxone and naloxonazine. However, the ability of naloxone, but not naloxonazine to inhibit feeding, induced by either 2-deoxy-D-glucose glucoprivation, ethylketocyclazocine, dynorphin or (D-ala2., D-leu5.)-enkephalin implies the existence of non-mu-1 opioid receptor mechanisms in these responses. The present study compared the effects of the daily administration of naloxone and naloxonazine (10 mg/kg, i.v.) in rats in three different types of maturational or dietary situations. In adult rats, naloxonazine and naloxone significantly reduced body weight (7% and 4%, respectively) and food intake (21% and 13%, respectively) over 14 days. These effects were more pronounced in adolescent rats where naloxonazine and naloxone significantly reduced the gain in body-weight (53% and 33%, respectively) and food intake (24% and 15%, respectively) over 14 days. In the adolescent rats, the effects of naloxonazine were significantly greater than those of naloxone. In contrast, chronic treatment with neither naloxone nor naloxonazine altered body weight or food intake of rats made obese by dietary manipulations and left on that diet during treatment with antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of effects of chronic administration of naloxone and naloxonazine upon food intake and maintainance of body weight in rats. 341 36

The response of brown adipose tissue (BAT) thermogenesis, as measured by mitochondrial GDP binding, of lean and obese Zucker fa/fa rats to 2-deoxy-D-glucose (2-DOG) has been investigated. 2-DOG reduced BAT mitochondrial GDP binding of lean rats but had no effect in obese rats. Adrenalectomy increased BAT GDP binding in obese rats and restored the 2-DOG inhibitory effect. Corticosterone inhibited GDP binding in lean rats and abolished the 2-DOG inhibitory effect. 2-DOG induced hyperphagia and hyperglycaemia in lean rats, but these effects were either absent or attenuated in the obese. The possibility that a glucocorticoid inhibition of glucose metabolism impairs sympathetic activity in the obese rats is discussed.
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PMID:The effects of 2-deoxy-D-glucose on brown adipose tissue of lean and obese Zucker rats. 372

Several pieces of evidence indicate that brain serotoninergic systems play an inhibitory role in feeding, being specifically involved in regulating satiety and food selection. The anorectic drug fenfluramine has been shown to exert its effects by activating serotoninergic mechanisms. Since fenfluramine influences both central and peripheral serotonin stores, it is difficult to establish the relative contributions of the central and peripheral serotoninergic mechanisms in the regulation of feeding behaviour. In the present paper evidence is presented that changes in feeding come about In the present paper evidence is presented that changes in feeding come about after interventions in either the brain or the periphery. This evidence includes the observation that serotonin itself given subcutaneously causes a dose-related anorexia in rats trained to eat four hours a day, an effect antagonized not only by metergoline but also by xilamidine, a serotonin antagonist that does not cross the blood-brain barrier. Since serotonin given systemically cannot reach the brain, its effect is ascribed to the activation of peripheral mechanisms. Furthermore, as is the case with fenfluramine, subcutaneous administration of serotonin is able to completely counteract the overeating induced by the glucoprivic agents insulin and 2-deoxy-D-glucose (2-DG). It is concluded that activation of peripheral serotoninergic mechanisms is sufficient not only to reduce eating in rats trained to eat four hours a day, but also to control the hyperphagias brought about by insulin or 2-DG.
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PMID:Peripheral and central mechanisms of action of serotoninergic anorectic drugs. 374 Aug 35

The antiobesity effects of (S)-(+)-1-(4-chlorophenylthiomethyl)-N-methylethylamine fumarate (AO-124) were examined in rats and dogs. AO-124 suppressed food intake dose dependently in normal, Zucker fatty and VMH-obese rats, and beagle dogs. Its anorectic activity was not altered by pretreatment with methysergide, a serotonin receptor blocker. AO-124 also reduced the hyperphagia induced by 2-deoxy-D-glucose but not that induced by insulin, noradrenaline or muscimol, suggesting that the anoretic mechanism of AO-124 may be implicated in a glucostatic regulatory system of feeding. In addition, AO-124 decreased insulin secretion in response to an oral, but not an intravenous, glucose load. Such a suppression in insulin secretion may be explained by slow absorption of glucose from the intestine: AO-124 delayed the gastric emptying time of glucose and inhibited the active transport of glucose as observed in the everted small intestine. Two week administration of AO-124 to Zucker fatty rats resulted in a significant reduction of plasma insulin levels, body weight gain, and body lipid without exerting any changes in body protein. These findings indicate that AO-124 may be useful as an antibesity agent on the basis of its unique mechanisms of action.
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PMID:The antiobesity action of (S)-(+)-1-(4-chlorophenylthiomethyl)-N-methylethylamine fumarate (AO-124). 374 36


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