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)

Plasma glucose concentration was measured at 3-h intervals in streptozotocin-induced diabetic rats placed on various insulin replacement regimens using three different kinds of insulin. High insulin dosages produced at least periodic hypoglycemia, even though there were no overt signs of insulin overdose. Low- and single-dose regimens produced periods of hyperglycemia. Both high and low doses of protamine zinc insulin normalized diabetes-induced reductions in 5-hydroxyindole-3-acetic acid [5-HIAA; the principal metabolite of 5-hydroxytryptamine (5-HT)] and 5-HT turnover (5-HIAA/5-HT), despite the failure of the low-dose regimen to normalize plasma glucose. Diabetic rats evidenced continued hyperphagia and hyperdipsia during insulin treatment, and insulin treatment also induced hyperphagia and excessive weight gain in nondiabetic rats. Insulin treatment only partially normalized diabetes-induced adrenal hypertrophy. Adrenal hypertrophy is an indication of a continued stresslike physiological state in diabetes even during insulin therapy. This state may be involved in the enhanced risk in diabetic humans for development of anxiety disorders and clinical depression.
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PMID:Metabolic and neurochemical profiles in insulin-treated diabetic rats. 750 9

The diabetogenic effects of streptozotocin (STZ) were studied on blood glucose, plasma insulin, feeding and drinking, body weight, islet morphology, and hypothalamic serotonin (5-HT) release in vehicle-pretreated rats and in rats pretreated with either intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT; a 5-HT nerve fiber depletor), intraperitoneal injection of p-chlorophenylalanine (PCPA; a tryptophan hydroxylase inhibitor), or intraperitoneal injection of p-chloroamphetamine (PCA; a neurotoxin for 5-HT nerve fiber). At four days after STZ administration, vehicle-treated rats displayed hyperglycemia, polydipsia, polyphagia, decreased plasma insulin level, derangement of islet morphology (few insulin cells, accumulation of glucagon cells), and elevated 5-HT release in the hypothalamus. The above diabetogenic effects of STZ were attenuated by brain serotonin depletion induced by 5,7-DHT, PCPA, or PCA. Furthermore, the STZ-induced hyperglycemia or derangement of islet morphology was attenuated by peripheral sympathectomy or adrenalectomy. It is concluded that brain serotonin depletion attenuates diabetogenic effects of STZ by reducing sympathetic efferent activity in rats.
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PMID:Brain serotonin depletion attenuates diabetogenic effects of streptozotocin. 776 35

Effects of salt loading by drinking 0.9% NaCl solution on the myocardial performance in nondiabetic and diabetic Wistar rats were studied using the isolated working heart apparatus. Body weight and fluid and food intakes of these animals were monitored. Blood pressure and plasma levels of glucose, insulin, cholesterol, and triglycerides were also measured. Diabetes was induced by intravenous injection of streptozotocin (60 mg/kg). Diabetic rats were found to develop myocardial dysfunction at 8 weeks after STZ injection, accompanied by significant increases in food and fluid intakes, slowed body weight gain, hyperglycemia, hypoinsulinemia, and hyperlipidemia but without significant changes in blood pressure. Salt loading did not cause significant changes in any of the parameters studied in nondiabetic rats. However, in streptozotocin-diabetic rats given saline to drink, the impaired myocardial function was significantly improved and was associated with a significant reduction in hyperphagia and hyperlipidemia. Plasma glucose levels significantly decreased at weeks 1-3 but increased to the levels of untreated diabetic animals at weeks 4-7. There was an increase in fluid intake, but neither blood pressure nor plasma insulin levels were significantly affected. It is suggested that the improvements in cardiac function and hyperlipidemia in diabetic rats by salt loading may be related to each other; however, the mechanisms for these effects are not clear but are unlikely to be due to changes in glycemic control.
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PMID:Improvement in cardiac function in streptozotocin-diabetic rats by salt loading. 776 68

The present study investigated the effects of ascorbic acid (AA) supplementation on the cardiac performance and the plasma levels of glucose, insulin, triglycerides, cholesterol and free fatty acid in diabetic and non-diabetic rats. Diabetes was induced by intravenous injection of streptozotocin (STZ) 55 mg/kg. AA was given in drinking water in concentrations of 1 g/l or 2 g/l for 8 weeks after STZ injection. Myocardial performance was determined using the isolated perfused working heart preparations. Following AA supplementation, there were no significant changes in any of the parameters measured in non-diabetic rats; however, the occurrence of polydipsia, hyperphagia, hyperlipidemia and myocardial dysfunction in STZ-diabetic rats was significantly alleviated in a dose-dependent manner. Nevertheless, the decreased body weight gain, hypoinsulinemia and hyperglycemia in diabetic animals were not affected. The data show that AA supplementation in STZ-diabetic rats improves both hyperlipidemia and cardiac function. However, the mechanisms of these effects and the correlation between these improvements are not clear.
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PMID:Ascorbic acid supplementation prevents hyperlipidemia and improves myocardial performance in streptozotocin-diabetic rats. 778 89

Several chelates are available for leukocyte labeling. Studies indicate that cells labeled with any of the chelates have a sensitivity for infection of 90% to 95% when imaged at 24 hours postinjection. The sensitivity of 111In-labeled leukocytes at earlier imaging times is more controversial. There has been concern about the utility of labeled leukocytes in musculoskeletal infection. Recent leukocyte studies show a high sensitivity for infected prostheses, even though these infections are often walled off and do not cause systemic symptoms. However, leukocytes frequently miss osteomyelitis of the spine for reasons that are not known. Although some investigators do not recommend the use of 111In-labeled leukocytes in chronic infections, we have found a high sensitivity for infections that are 2 or more weeks old. Autopsy studies from the preantibiotic era indicate that bacterial infections with common organisms have high levels of neutrophil infiltration for months. Labeled lymphocytes from mixed-cell preparations also may play a role in detecting these inflammatory sites. Questions have been raised about the effect of antibiotic therapy on leukocyte sensitivity. Antibiotics do not appear to have a significant effect on scan sensitivity. By reducing the number of bacteria at an inflammatory site, antibiotics reduce the amount of chemotactic inhibitors. In addition, some antibiotics have been shown to directly stimulate leukocyte chemotaxis. Other factors that can theoretically reduce leukocyte function, including hemodialysis, hyperalimentation, hyperglycemia, and steroids, do not appear to reduce labeled leukocyte sensitivity for infection. The specificity of leukocyte uptake is reduced in the gastrointestinal tract and lungs. In these sites, uptake correlates with infection or the true cause of the patients' fever in only 10% to 50% of cases.
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PMID:Indium-111-labeled leukocytes for the detection of infection: current status. 802 76

The insulin receptor was evaluated at different disease stages in the sand rat (Psammomys obesus), a model for nutrition-induced diabetes. Nondiabetic sand rats showed markedly low receptor number in liver compared with albino rats. Their receptor had an intact tyrosine kinase activity but a higher Km for ATP in the phosphorylation reaction of exogenous substrates. The initial effects of overeating (i.e., development of hyperinsulinemia without hyperglycemia) were associated in the sand rat with a dramatic decrease in in vitro and in vivo insulin-induced receptor tyrosine kinase activity in both liver and muscle. In muscle, this coincided with a decrease in receptor number and an increase in basal tyrosine kinase activity. Similar changes were observed upon development of hyperinsulinemia with hyperglycemia. Upon recovery from the diabetic state by diet restriction, the impaired receptor kinase activation was corrected. Complete restoration occurred only in animals that fully recovered from the diabetic state and became normoinsulinemic. These observations indicate that loss and gain of receptor tyrosine kinase activity were dependent on insulin levels. Thus, overeating may lead to the development of hyperinsulinemia through ineffective extraction of excess insulin by the scarce liver receptors. Hyperinsulinemia, in turn, causes a reversible reduction in receptor kinase activity, leading to insulin resistance. This sequence of events may be relevant to diet-related changes in human non-insulin-dependent diabetes mellitus.
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PMID:Hyperinsulinemia induces a reversible impairment in insulin receptor function leading to diabetes in the sand rat model of non-insulin-dependent diabetes mellitus. 812 94

Several metabolic parameters were used to determine the evolution of the diabetic state of streptozotocin diabetic rats treated with aqueous leaf extracts from Myricia uniflora, a plant widely used in northern Brazil for treatment of diabetes. The effect of the extracts on the intestinal absorption of glucose and on the evolution of diabetes of diabetic rats adapted to a high protein, carbohydrate-free diet were also investigated. Treated rats received twice a day, by gavage, during three weeks, 7.5 mg of lyophilized powder, corresponding to about 60 mg of dried leaves, prepared from percolations with boiled water, Treatment of diabetic rats fed a stock, balanced diet did not affect body weight gain but reduced the hyperglycemia, polyphagia, polydipsia, urine volume and the urinary excretion of glucose and urea. Myrcia administration for 3 weeks had no effect on the weight of epididymal and retroperitoneal adipose tissue, or on the concentrations of pancreatic and serum insulin. The intestinal absorption of glucose, measured with a perfusion technique in situ, was markedly inhibited by Myrcia (7.5 mg of lyophilized powder per ml of perfusion solution). The effects of Myrcia treatment on diabetic rats adapted to a carbohydrate-free diet were similar to those obtained in rats fed the stock diet. The data show that aqueous extracts of Myrcia has a beneficial effect on the diabetic state, mainly by improving metabolic parameters of glucose homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of the antidiabetic activity of Myrcia uniflora extracts in streptozotocin diabetic rats. 820 37

Sixty outbred Wistar rats were randomly assigned to five experimental groups: GI-10 non-diabetic control rats; GII-10 untreated diabetic control rats; GIII-10 diabetic rats treated with retard porcine insulin; GIV-20 diabetic rats that received pancreaticoduodenal transplantation (PDT) from normal donor rats; GV-10 diabetic rats submitted to islet of Langerhans transplantation (ILT) into the portal vein. The animals were housed in metabolic cages for six periods of 24 hours during 30 days and body weight, water and food intake, urine output, blood and urinary glucose were recorded. Diabetes was induced by I.V. administration of Alloxan (42 mg/kg of body weight); PDT was performed by microsurgical techniques and islets were prepared without enzymes. To prevent rejection. Cyclosporin A (10 mg/kg of body weight) was utilized in transplanted rats. PDT consistently and significantly (p < 0.05) improved the metabolic abnormalities of the diabetic rats, by restoring the body weight gain, and immediate relief of polydipsia, polyphagia, polyuria, hyperglycemia and glucosuria observed in pre-treatment period. PDT was more effective than ILT and this over insulin therapy on control of the diabetic state. However, the observed complications in GIV and GV, due to surgery and immunosuppression, should be analysed for the real benefits of the alternative therapy can be superior to eventual fails to the conventional therapy with insulin.
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PMID:[A comparative study of pancreatic-duodenal transplantation, islets of Langerhans transplantation, and insulin treatment, in the control of experimental diabetes in the rat]. 824 60

It has been shown that improvement of glucose homeostasis by oral vanadate or vanadyl treatment in streptozotocin-induced diabetic rats is accompanied by severe negative side effects (some deaths, decreased weight gain, alteration in renal function as well as tissue vanadium accumulation) which argue against the use of vanadium compounds in diabetes treatment. The present study was undertaken to assess the effectiveness in alleviating some signs of diabetes in streptozotocin-treated rats with oral therapy with sodium metavanadate (NaVO3) and sodium 4,5 dihydroxybenzene-1,3-disulfonate (Tiron), a chelating agent effective in mobilizing vanadium. In a preliminary experiment, diabetic rats were given aqueous solutions of 0.20 mg NaVO3/ml for 4 days. Vanadium-treated rats which showed blood glucose levels significantly lower (p < 0.001) than vanadate-untreated diabetic rats were selected for subsequent experiments. These animals were given 0.20 mg NaVO3/ml in drinking water and 0, 125.6, 314 or 628 mg Tiron/kg/d by gavage for 2 w. Although most of the animals did not become normoglycemic, several characteristic signs of diabetes (hyperglycemia, hyperphagia and polydipsia) were alleviated by the NaVO3 treatment. The administration of 314 mg Tiron/kg/d (approximately 1 NaVO3: 5 Tiron, mole ratio) did not diminish the ameliorative effects of NaVO3 with respect to diabetes, but significantly decreased the level of vanadium accumulation in target organs. These results show that some of the beneficial effects of NaVO3 are maintained in diabetic animals given Tiron, while the administration of the chelator results in a significant decrease in tissue vanadium accumulation. Accordingly, this would diminish the possibility of toxic side effects derived from prolonged oral vanadium administration.
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PMID:Oral vanadate and Tiron in treatment of diabetes mellitus in rats: improvement of glucose homeostasis and negative side-effects. 830 15

Statistical studies repeatedly have shown an association between systemic insulin resistance and a preponderance of highly glycolytic, relatively insulin-insensitive muscle fibers as well as a low density of muscle capillaries. The nature of the relationship between these observations is, however, not clear. Female rats were made hyperinsulinemic for 7 days by implantation of osmotic minipumps. Elevated adrenergic activity and secretion of glucocorticoids were controlled by another minipump with propranolol and adrenalectomy was controlled with glucocorticoid substitution. This resulted in hyperinsulinemia and moderate hypoglycemia, the latter probably counteracted by overeating and increased glucagon secretion, as indicated by increased body weight and lower liver glycogen contents, respectively. Systemic insulin sensitivity was increased and measured with a hyperinsulinemic-euglycemic clamp technique. This was paralleled by an elevated glucose utilization estimated as uptake of 2-deoxyglucose in parametrial, retroperitoneal, and inguinal adipose tissues and the soleus and extensor digitorum longus muscles. Glycogen synthesis was also elevated in the soleus muscle. Muscle fiber composition changed with hyperinsulinemia and elevated 2-deoxyglucose uptake toward more fast-twitch, type II, particularly type IIb fibers, whereas the proportion of slow-twitch, type I fibers, diminished. Capillary density was elevated per unit muscle surface area as well as per muscle fiber. This was paralleled by increased insulin sensitivity systemically and in muscles. These results suggest that muscle fiber composition alterations may be a consequence rather than a cause of hyperinsulinemia and that capillarization rather than fiber composition is of importance for insulin sensitivity in muscle.
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PMID:Effects of hyperinsulinemia on muscle fiber composition and capitalization in rats. 851 74


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