Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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.
 ...
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.
 ...
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.
 ...
PMID:Enteral hyperalimentation with continuous subcutaneous insulin infusion improved severe diarrhea in poorly controlled diabetic patient. 190 53

Lipogenesis was measured in 2 and 5 week gold-thioglucose (GTG) obese mice after a single meal of 0.5 g of standard chow. Compared to control mice the rate of lipogenesis in GTG obese mice, was 4-fold higher in liver and 10-fold higher in white adipose tissue (WAT). In brown adipose tissue (BAT) of GTG-injected mice the lipogenic rate was only 50% of that of controls. These results indicate that the increased lipid synthesis observed in GTG-injected mice is not due solely to hyperphagia and that some other stimuli, such as increased basal insulin levels and/or decreased thermogenesis and insulin resistance in BAT, contribute to the high rates of fat synthesis in this animal model of obesity.
 ...
PMID:Differences in lipogenesis in tissues of control and gold-thioglucose obese mice after an isocaloric meal. 191 74

28 obese women were investigated in the course of the 21st (A) and 30th (B) week of pregnancy. Increased serum levels of GH, T4 and T3 were found in both samples of blood (A and B), while serum insulin, cholesterol and triacylglycerols were increased only at time B. It was suggested that the similar increase of GH, T4 and T3 at time A and B was due to pregnancy because the level of these hormones is usually not increased in non-pregnant obese women, while hyperinsulinemia and often increased values of cholesterol and triacylglycerols are a common finding in non-pregnant obesity. This presumption was confirmed only partially--body weight and the skin folds correlated only with insulin and T3, while GH, cortisol, T4, cholesterol and triacylglycerols correlated only exceptionally. High levels of insulin and T3 may be due to overeating.
 ...
PMID:[Pregnancy and obesity. II. Hormonal and metabolic changes]. 191 57

Hypothalamic concentrations of neuropeptide Y (NPY), a potent central appetite stimulant, increase dramatically in food-restricted and insulin-deficient diabetic rats. This suggest that NPY may drive hyperphagia in these conditions, which are characterized by weight loss and insulin deficiency. To test the hypothesis that insulin deficiency and weight loss are specific stimuli to hypothalamic NPY, we measured NPY concentrations in individual hypothalamic regions in rats with hyperphagia caused by insulin-induced hypoglycemia. Groups of 8 male Wistar rats were injected with ultralente insulin (20-60 U/kg) to induce either acute hypoglycemia (7 h after a single injection) or chronic hypoglycemia (8 days with daily injections). In hypoglycemic rats, plasma insulin concentrations were increased 6- to 7-fold compared with saline-injected controls; food intake was significantly increased with acute and chronic hypoglycemia and weight gain was significantly increased in the chronically hypoglycemic group. NPY concentrations were measured by radioimmunoassay in 8 hypothalamic regions microdissected from fresh brain slices. NPY concentrations were not increased in any region in either acute or chronic hypoglycemia. NPY therefore seems unlikely to mediate hyperphagia in hyperinsulinemia-induced hypoglycemia, supporting the hypothesis that weight loss is a specific stimulus to hypothalamic NPY and that insulin deficiency may be the metabolic signal responsible.
 ...
PMID:Unchanged hypothalamic neuropeptide Y concentrations in hyperphagic, hypoglycemic rats: evidence for specific metabolic regulation of hypothalamic NPY. 192 23

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.
 ...
PMID:Hyperinsulinemia and glucose tolerance in obese rats with lesions of the ventromedial hypothalamus: dependence on food intake and route of administration. 194 35

The basic assumption of brain research utilizing lesions is that any observed changes in behavior or physiological responses must be the result of tissue destruction. Reynolds suggested 25 years ago that in the case of electrolytic ventromedial hypothalamic lesions, the observed hyperphagia and obesity were due instead to metallic ion deposits from the electrode tip irritating adjacent tissue. His "irritative hypothesis" was largely ignored after others reported obesity in rats given nonirritative (i.e., no deposits) VMH lesions. However, recent studies have shown that the experimental observations by both Reynolds and his critics were correct and that the early discrepancies were largely due to the sex of the animals used in the experiments. Obesity can be produced with nonirritative VMH lesions, but the weight gain is only about 60% of that observed with irritative VMH lesions and the animals do not display the characteristic lesion-induced elevations in basal insulin levels. A new combination ablation-irritative hypothesis is proposed in which electrolytic VMH lesion obesity is attributed in part to tissue ablation and in part to metallic ion deposits stimulating (rather than disinhibiting) vagally mediated insulin responses.
 ...
PMID:Ventromedial hypothalamic obesity: a reexamination of the irritative hypothesis. 195 3

Neuropeptide Y (NPY), acting through various medial hypothalamic nuclei, is found to have potent effects on a variety of endocrine, physiological and behavioral systems that modulate energy balance. This peptide affects the release of various hormones, such as corticosterone, insulin, aldosterone and vasopressin, which modulate energy metabolism, as well as food intake. It also has direct impact on energy metabolism through an effect on substrate utilization and lipogenesis. Finally, NPY has a remarkably potent stimulatory effect on feeding behavior, which is characterized by a selective increase in carbohydrate ingestion that is strongest at the beginning of the active feeding cycle and is dependent upon circulating levels of corticosterone. This evidence has led to the proposal that NPY exerts anabolic effects to restore energy balance at specific times of energy depletion. Increased NPY activity may occur at the beginning of the active cycle or after a period of food deprivation. Further evidence, that chronic NPY stimulation produces profound hyperphagia and obesity and that endogenous NPY concentration is increased in genetically obese animals, strongly suggests that hypothalamic NPY may contribute to the development of eating disorders and obesity.
 ...
PMID:Brain neuropeptide Y: an integrator of endocrine, metabolic and behavioral processes. 195 27

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.
 ...
PMID:Molecular mapping of the mouse db mutation. 197 28


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>