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)

This study was performed to examine the effect of overeating on in vivo and in vitro insulin secretion in normal mice. Six week old male CRJ-ICR mice were maintained on a cookie and chocolate mashed diet (C.C. diet) until 30 weeks of age; control mice received an ordinary mouse chow. The mice on the C.C. diet (C.C. mice) consumed 125-130% of the daily caloric intake of control mice throughout the study. C.C. mice developed mild hyperglycemia with relative obesity from 16 weeks of age. Fed blood glucose levels at 30 weeks of age for C.C. mice were 158.3 +/- 6.7 mg/dl as opposed to 127.2 +/- 3.1 mg/dl for controls (p less than 0.01). In experimental mice at 18 weeks of age, plasma insulin response after intraperitoneal glucose load (2 mg/g BW) and insulin secretion at 30 mM glucose from the perfused pancreas were similar to those in control mice. However, at 30 weeks of age, insulin secretion at 30 mM glucose from perfused pancreas in C.C. mice was significantly suppressed compared with that of control mice (p less than 0.02). Conversely, in vivo insulin secretory response to intraperitoneal glucose load was significantly increased in C.C. mice (p less than 0.05). There were no differences in insulin secretion at 15 mM glucose from perfused pancreas. These results indicate that impairment of beta-cell secretory capacity develops in impaired glucose tolerant mice with obesity, while in vivo studies show a high insulin response to glucose. This alteration of beta-cell function may be the initial change during the development of the hyperglycemia-induced defect in insulin secretion.
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PMID:The effects of overeating on insulin secretion in normal mice. 184 Oct 30

Vanadate and vanadyl, two forms of vanadium, have been reported to exert insulin-like effects in vivo and in vitro. In the present study we compared the effectiveness of oral sodium metavanadate (NaVO3), sodium orthovanadate (Na3VO4) and vanadyl sulphate pentahydrate (VOSO4.5H2O) treatment in alleviating some signs of diabetes in streptozotocin-induced diabetic rats. Vanadium compounds were administered in aqueous solutions of NaCl (80 mM) at concentrations of 0.20 mg/ml (NaVO3), 0.50 mg/ml (Na3VO4), and 1.1 mg/ml (VOSO4.5H2O) for two weeks. Control rats, either diabetic or non-diabetic, drank solutions of NaCl (80 mM). Although some signs of diabetes (hyperglycaemia, hyperphagia, polydipsia) were significantly ameliorated by the vanadium treatment, negative side effects were also observed in all of the vanadium-treated diabetic rats. Those effects included some deaths, decreased weight gain, and tissue vanadium accumulation, which are consistent with the reported toxicity of vanadium in non-diabetic rats. Vanadyl sulphate was the most effective compound of those tested in normalizing blood glucose levels. However, the results here reported suggest that chronic administration of vanadyl or vanadate in the drinking water is not a viable alternative treatment to insulin in human diabetes.
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PMID:Improvement of glucose homeostasis by oral vanadyl or vanadate treatment in diabetic rats is accompanied by negative side effects. 186 88

Little is known about effective treatment for severe diarrhea in the insulin-dependent diabetic patient. A 41-year-old woman was admitted to our hospital because of hyperglycemia and dysuria. She had stopped insulin self-injection therapy for 2 years and diarrhea had become worse, resulting in malnutrition. Following enteral alimentation by elemental diet (ED) with continuous subcutaneous insulin infusion (CSII), frequency of diarrhea remarkably decreased and general nutritional condition was improved. At the first step, the patient was given 600 kcal/d ED through the tube sustained in the jejunum. Total calorie intake for 24 hours was gradually increased to the level of 2400 kcal/d and this therapy continued for 5 months. During this period, blood glucose level was kept in almost normal range (between 100 and 200 mg/dL) through the continuous insulin infusion of regular insulin (1.0-1.5 U/h). Thereafter, general conditions were improved and frequency of diarrhea gradually decreased. When this treatment was stopped, watery diarrhea, steatorrhea, and hypoalbuminemia completely disappeared and she gained 12 kg of body weight. Furthermore, spontaneous urination appeared following this treatment. This case suggests that the enteral hyperalimentation combined with strict control of blood glucose, using the CSII, may be an effective therapy for such severe diarrhea with malnutrition in diabetes.
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PMID:Enteral hyperalimentation with continuous subcutaneous insulin infusion improved severe diarrhea in poorly controlled diabetic patient. 190 53

This study was performed to investigate the consequences of developing obesity on glucose homeostasis in animals showing hyperphagia plus vagal hyperinsulinemia and rats that were normophagic and hyperinsulinemic. Male rats were lesioned in the ventromedial hypothalamus (VMH) and kept either under ad libitum or absolute (oral or intragastrical) pair-feeding conditions for 4 weeks. Hyperphagic rats, as well as normophagic VMH rats, became obese, but only ad lib-fed obese rats displayed glucose intolerance to intravenous (IV) glucose infusions. Orally pair-fed VMH rats also showed normal oral and intragastric glucose tolerance, but in intragastrically fed VMH animals and controls, oral and intragastric glucose tolerance was decreased. These results indicate that (1) obesity as a consequence of VMH lesions is not dependent on hyperphagia, confirming earlier reports, and also independent of the ingestion of bulk meals. (2) beta-cell release of insulin to IV glucose infusion is not sufficient when hyperphagia and vagally mediated hyperinsulinemia coincide, and is therefore dependent on several factors; and (3) oral glucose intolerance develops when preabsorptive reflexes are blunted, irrespective of whether the animals were hyperinsulinemic or not.
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PMID:Hyperinsulinemia and glucose tolerance in obese rats with lesions of the ventromedial hypothalamus: dependence on food intake and route of administration. 194 35

This study investigated the effect of fasting, self-selected meals and isocaloric oral glucose and fat meals and intravenous (i.v.) feeding on plasma zinc concentrations in men. Plasma zinc remained stable when volunteers fasted all day, but self-selected meals and 600 kCal of dextrose or fat emulsion caused significantly reduced plasma zinc concentrations [mean (SD) 12.1 (1.4), 12.3 (0.6) and 12.2 (0.7) mumol/L at 1400 h, respectively, compared with a fasting level of 13.9 (1.6) mumol/L at 0800 h, P less than 0.05]. In patients undergoing intravenous hyperalimentation, plasma zinc decreased from 12.0 (1.4) mumol/L at 0800 h to 10.0 (1.1) mumol/L at 1400 h [mean (SD), P less than 0.01]. These data show that both enteral and i.v. feeding cause a decline in plasma zinc and that glucose alone is not responsible for this post-prandial fall since ingestion of isocaloric amounts of glucose or fat have a similar effect.
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PMID:Effect of fasting, self-selected and isocaloric glucose and fat meals and intravenous feeding on plasma zinc concentrations. 195 45

Diabetes is characterized by hyperphagia, polydipsia, polyuria, and elevations in blood and urinary glucose. It has also been documented that beta-adrenergic responsiveness is reduced in diabetes. The intestinal glucosidase inhibitor, acarbose (BAY G 5421), decreases postprandial glycemia by delaying carbohydrate absorption. The purpose of this study was to evaluate the effects of chronic acarbose treatment (20 and 40 mg/100 g of diet) on the metabolic and adrenergic parameters altered in streptozotocin (STZ) (50 mg/kg, intravenously [IV] )-induced diabetes. Metabolic parameters were measured daily for 8 weeks. Diabetic rats were hyperphagic, polydipsic, and polyuric within 1 week of STZ treatment. Acarbose treatment did not consistently effect the food intake but did reduce water intake, urinary output, blood glucose, and the urinary loss of glucose associated with STZ-induced diabetes. Adrenergic responses were assessed by monitoring the increase in tail skin temperature (TST) associated with administration of isoproterenol. Diabetic rats were less responsive than controls and acarbose treatment restored responses toward that of the controls. Additionally, 3H-NE release from the tail artery was elevated in the diabetic rat and restored to normal in the acarbose-treated animals. Collectively these data suggest that acarbose treatment is effective in reducing the severity of metabolic and autonomic complications associated with STZ-induced diabetes.
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PMID:Beneficial effects of dietary acarbose in the streptozotocin-induced diabetic rat. 196 Nov 20

The increased food intake in the rat during the first two hours of the dark cycle was significantly inhibited by central pretreatment with either the selective kappa opioid antagonist, nor-binaltorphamine (NorBNI, 20 micrograms, i.c.v., 53-54%) or naltrexone (NTX, 20 micrograms, i.c.v., 47-60%). Short-term (2 h) intake of a high-fat diet was significantly inhibited by central NorBNI (1-20 micrograms, 33-79%) and NTX (20 micrograms, 47-51%). Hyperphagia induced by the anti-metabolic glucose analogue, 2-deoxy-D-glucose was significantly inhibited by central NorBNI (20 micrograms, 40-68%) and NTX (20 micrograms, 28-69%). These data suggest that the kappa receptor subtype, in addition to other opioid receptor subtypes, influence these forms of feeding behavior.
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PMID:Suppression of nocturnal, palatable and glucoprivic intake in rats by the kappa opioid antagonist, nor-binaltorphamine. 196 62

Diabetes (db) is an autosomal recessive mutation located in the midportion of mouse chromosome 4 that results in profound obesity with hyperphagia, increased metabolic efficiency, and insulin resistance. To clone this gene and generate a molecular map of the region around this mutation, two genetic crosses were established: an intraspecific backcross between C57BL/6J db/db females and C57BL/6J db/db x DBA/2J +/+ F1 (B6D2 db/+ F1) male mice and an interspecific intercross between B6D2 db/+ F1 males and C57BL/6J db/db x Mus spretus F1 (B6spretus db/+ F1) females. The progeny of both crosses were characterized for genotype at the db locus to map a series of restriction fragment length polymorphisms relative to the db locus. Measurements of body weight, body length, and plasma concentrations of glucose and insulin in the animals allowed the assignment of genotype (db/db vs. db/+ or +/+). A total of 132 progeny of the intraspecific cross and 48 db/db progeny of the interspecific cross were typed for individual restriction fragment length polymorphisms to generate a gene order of: centromere-brown (Mt4)-P lambda Mm3(2)-Ifa (Inta)-Cjun-db-D4Rp1-Glut1-Mtv-13-Lck. Several of the genes that are linked to db [Cjun, glucose transporter (Glut1) and Lck] map to human chromosome 1p, suggesting that db may be part of a syntenic group between human 1p and the distal portion of mouse chromosome 4. In addition, phenotyping of the progeny of these crosses revealed a wide range in plasma concentrations of glucose and insulin among the obese progeny, with some animals developing overt diabetes and other remaining euglycemic. Distributions of age-controlled plasma [glucose] and [insulin] among the intraspecific-cross obese progeny were not bimodal, suggesting a role for polygenic differences between the progenitor strains (C57BL/6J and DBA/2J) in the development of overt diabetes.
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PMID:Molecular mapping of the mouse db mutation. 197 28

Insulin levels in a 7-year-old boy with hyperphagia and obesity following an episode of meningoencephalitis were studied sequentially during the course of progressive weight gain. High fasting insulin levels (1183 pmol/L) and strikingly high insulin release in response to glucose (7892 pmol/L) were found within weeks of the onset of the illness. The abnormality in insulin secretion occurred prior to the marked weight gain. Hyperinsulinemia was not accompanied by hypoglycemia. Early hyperinsulinemia may be a primary event in the development of hyperphagia and obesity following hypothalamic injury.
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PMID:Hypothalamic or central obesity is associated with an early rise in plasma insulin concentration. 201 20

Changes in preference for sweet tasting solutions have previously been reported in diabetic rats. The present study was designed to use detailed analyses of drinking patterns to investigate changes in sweet taste perception in rats made diabetic with a streptozotocin (SZ) injection and tested with saccharin and a broad range of sucrose concentrations. Although meal patterns in diabetic rats have been studied extensively, drinking patterns and their relation to meal patterns have not been described. A second goal of this research was to use the detailed patterns of eating and drinking of the diabetic rat in an effort to understand the resulting hyperphagia. Rats were given IP injection of SZ or saline. Following the SZ injection, the rats showed marked increase in blood glucose levels, an increase in food and fluid intake and they failed to gain weight. The SZ-injected rats showed a loss of preference for saccharin and for high concentrations of sucrose. Patterns of sucrose ingestion that are correlated with taste perception were distorted in the diabetic rats. The detailed pattern analysis of eating showed that the diabetic-induced hyperphagia resulted from a marked increase in length of eating bouts. The increase in fluid intake in the diabetic rats resulted from both an increase in frequency and length of drinking bouts. Circadian patterns of both food and fluid ingestion were maintained in the diabetic rats.
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PMID:Ingestion patterns of food, water, saccharin and sucrose in streptozotocin-induced diabetic rats. 201 74


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