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

Intravenous hyperalimentation allows complete nutrition and anabolism in patients who cannot be fed by the oral route. However, several complications have been reported, e.g. septicaemia and hyperglycaemina. In 51 intensive-care patients receiving hyperalimentation, 18% were found to be hyperglycaemic in spite of insulin administration. Hyperglycaemia was frequently associated with stress. In 8 patients undergoing major surgery, which was chosen as a stress model, decreased insulin and increased glucagon, growth hormone and cortisone levels were observed. These findings could explain stress-induced glucose intolerance. In a further experiment, 8 intensive-care patients were given alternative intravenous feedings with either 600g of a mixture of glucose, fructose and xylitol in a ration of 1:2:1 or 600g glucose per day. During both regimens insulin administration was required in 4 patients, but the insulin dosage was lower with the mixture. Plasma glucose during glucose infusion was 205+/-25mg/100ml(M+/-SEM) and the sum of plasma glucose, fructose and xylitol during infusion of the mixture was 176+/-33mg/100ml, the difference being of borderline significance (p less than 0.05). The advantages and disadvantages of infusable substrates are summarized on the basis of the available literature and it is concluded that, in general, glucose is preferable. However, if hyperglycaemia is difficult to control, partial replacement of glucose by glucose substitutes or fat emulsions may be advantageous. A routine infusion programme for central venous feeding is suggested. Causes and prevention of side-effects are reviewed. In many patients receiving central venous nutrition less hazardous and less expensive methods could be used such as nasogastric tube feeding, elemental diet or peripheral venous nutrition.
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PMID:[Parenteral hyperalimentation (author's transl)]. 40 48

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

Overt diabetes (NIDDM) was induced by overeating in neonatally streptozocin (60 mg/kg.BW) treated impaired glucose tolerant mice. We imposed a food restriction and a high fiber diet to evaluate the effects of dietary treatment in this NIDDM model mouse. Furthermore, insulin secretion after the dietary treatment was studied using the perfused pancreas technique. One group of IGT mice (SZ) was maintained on ordinary mouse chow during 6 to 14 weeks of age. The others received a cookie and chocolate mashed diet (C.C. diet) to induce overt diabetes during 6 to 10 weeks of age. Thereafter, the mice with induced overt diabetes were divided according to their diet treatment. The C.C. diet was continued in one group (SZC) for 4 weeks, and the others were divided into a food restriction group (SZR: 4 g/mouse/day of ordinary mouse chow, for 4 weeks) and a high fiber diet group (SZF: 20% W/W of cellulose in ordinary mouse chow, for 8 weeks). The mean caloric intake/mouse/day in SZC, SZR and SZF were 140, 80 and 98% of that in SZ, respectively. Amelioration of hyperglycemia and impaired glucose tolerance was noted in SZR and SZF. A better glycemic control was obtained in SZF with keeping a normal growth rate. On the pancreas perfusion, the insulin secretion to 30 mM glucose was improved in SZR and SZF. Furthermore, the incremental first phase peak insulin release to 30 mM glucose in SZF was significantly greater than that in SZC (SZF, 10.5 +/- 1.0 vs. SZC, 4.5 +/- 1.9 microU/min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary treatment ameliorates overt diabetes and decreased insulin secretion to glucose, induced by overeating in impaired glucose tolerant mice. 217 33

Glucose tolerance factor (GTF), the biologically active form of Cr3+, has been ascribed a role in the potentiation of insulin action and glucose homeostasis. The present study investigated the effects of dietary supplementation with GTF-rich brewer's yeast (Saccharomyces cerevisiae) or GTF-deprived Torula yeast (Torulaspora delbrueckii) in genetically diabetic C57BL/KsJ db/db mice. At 15 weeks of age, db/db mice exhibited increased body weight, hyperphagia, hyperglycaemia, hyperinsulinaemia and increased glycosylated haemoglobins compared with control (+/+) mice. During 56 days consumption of diets supplemented with 50g brewer's yeast or Torula yeast per kg, body weights of both groups of db/db mice decreased by 35%, in association with 1.2-1.7 fold increases of food intake, plasma glucose, glycosylated haemoglobins and an 83% decrease of plasma insulin. With the exception of slightly decreased weight loss, addition of brewer's yeast as opposed to Torula yeast did not affect tissue or plasma chromium nor ameliorate any of the parameters monitored including glucose tolerance and insulin sensitivity at 52-54 days. These findings do not support the contention that the glucose intolerance of genetically diabetic C57BL/KsJ db/db mice partly reflects GTF deficiency.
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PMID:Failure of glucose tolerance factor-containing Brewer's yeast to ameliorate spontaneous diabetes in C57BL/KsJ DB/DB mice. 268 Feb 28

A spontaneous maturity onset diabetes obesity syndrome occurs in a small proportion (10-20%) of male CBA/Ca mice. Inbreeding can increase the incidence to 80%. It occurs at 12-16 weeks of age, and is characterized by hyperphagia, obesity, hyperglycaemia, hypertriglyceridaemia, hyperinsulinaemia, and an impaired glucose tolerance. The mice are also resistant to exogenous insulin. Female mice remain normal except for a slight increase in serum insulin. The male obese diabetic mice have a normal life expectancy. It is proposed that CBA/Ca mice can provide examples of a useful model for investigating the aetiology of type 2 diabetes and obesity, and the effectiveness of antidiabetic and antiobesity drugs.
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PMID:Characterization of the spontaneous diabetes obesity syndrome in mature male CBA/Ca mice. 269 42

The aim of this study was to investigate the metabolic effects of short-term fasting in obese diabetic patients and to correlate the observed changes with the activity of hepatic key enzymes in an animal model of obesity-associated diabetes (ob/ob mice, C57BL/6J strain). In obese diabetic patients (ODP), a 72-h fast (causing slight change in body weight) decreased fasting glycemia by 3.82 +/- 0.79 mmoles/l and significantly improved glucose tolerance (OGTT) while reducing basal and stimulated insulinemia, whereas in obese non-diabetic patients (ONDP) only a small decrease in fasting glycemia (1.24 +/- 0.51 mmoles/l) occurred. This suggests that in ODP hyperphagia is a factor contributing to maintain hyperglycaemia and glucose intolerance (in the face of hyperinsulinaemia, indicating insulin resistance). In fed obese hyperglycaemic mice (OHM), which are a good model of the human obesity-associated diabetes, hepatic fructose-1,6-diphosphatase (F16Pase) and glucose-6-phosphatase (G6Pase), involved in glucose production, showed increased activity (+52 and +200 per cent, respectively) compared to control mice (CM), and the ratios of F16Pase and G6Pase to the opposing enzymes phosphofructokinase (PFK1) and glucokinase (GK), i.e. the F16Pase/PFK1 and G6Pase/GK ratios, were increased by 38 and 101 per cent, respectively, suggesting increase in gluconeogenesis and perhaps in glycogenolysis. In the 48-h fasted OHM, F16Pase activity was decreased (-30 per cent) compared to the fed animals, while the activity of G6Pase showed a smaller and statistically not significant change (-22 per cent). In contrast, in the CM a 48-h fasting was associated with a trend toward increased F16Pase (+22 per cent) and G6Pase (+173 per cent). However, since PFK1 and GK decreased to a similar extent in OHM and CM, the F16Pase/PFK1 and G6Pase/GK ratios, basally elevated in the OHM, did not change with fasting, whereas in the CM they showed a striking elevation (+71 and +274 per cent, respectively). The basally elevated F16Pase/PFK1 and G6Pase/GK ratios (functionally linked to glucose production) in the OHM may contribute to maintain hyperglycaemia; in these mice, the lack of further increase in the glucose production-related F16Pase/PFK1 and G6Pase/GK ratios (which occurs in CM) with fasting might allow that the interruption of the afflux of dietary carbohydrates ameliorates the glycaemic level. Similar mechanisms might occur also in the ODP.
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PMID:Metabolic effects of short-term fasting in obese hyperglycaemic humans and mice. 283 Nov 63

The growth and metabolic effects of a radiation-induced rat insulinoma were examined after subcutaneous subscapular transplantation into normal and streptozotocin diabetic NEDH rats. Streptozotocin diabetic rats exhibited hyperglycaemia, hypoinsulinaemia, impaired glucose tolerance without an insulin response, polyuria, polydipsia, hyperphagia and weight loss. Transplantation of tumour fragments gradually improved the physical and metabolic state over the following 3 weeks. Coincident with a progressive rise in plasma insulin between 10 and 17 days, the diabetic rats gained weight and reduced their food intake. The rats remained hyperglycaemic during this time, but developed hypoglycaemia with marked hyperinsulinaemia by 24 days. Furthermore, plasma glucose and insulin concentrations were not increased by an intraperitoneal glucose challenge, indicating greatly accelerated glucose clearance. Both the streptozotocin-treated and normal insulinoma-bearing rats incurred a fatal hypoglycaemic coma by 28-33 days after transplantation. Final body weights, tumour weights and concentrations of glucose and insulin were similar in the two groups. This study demonstrates reversal of streptozotocin diabetes by insulinoma transplantation. The hyperglycaemia and the accompanying diabetic environment did not modify tumour growth and development.
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PMID:Reversal of diabetes by syngeneic transplantation of a radiation-induced rat insulinoma. 303 49

Recordings of rat's diurnal ad libitum feeding patterns and responses to short term food deprivation suggested that analysis of diurnal feeding rhythms could provide a clue for understanding mechanisms involved in control and regulation of food intake. A simultaneous recording of free feeding patterns and of respiratory exchanges showed that a nocturnal positive energy balance and hyperphagia were mainly due to a diversion of ingested nutrients to fat deposition while negative energy balance and hypophagia during daytime were an effect of fat mobilization and oxidation. Further it was demonstrated that a neuroendocrine diurnal cycle underlined the lipogenesis-lipolysis cycle with hyper-insulinism and glucose tolerance at night, hypoinsulinism and glucose intolerance during the day. Similar phenomena were found along with the human scheduled feeding. Negative correlations between nocturnal lipogenesis and subsequent daytime lipolysis and the diurnal cycle of free fed rats compared to experimentally induced and reversible obesity and to seasonal cycles of hibernators give evidence on the nature of the lipostatic mechanism and its monitoring by hypothalamic ventromedial nuclei.
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PMID:[Lipogenesis, lipolysis and feeding rhythms]. 304 94

A genetically mild obesity syndrome of pubertal onset in a highly inbred line of rats differentiated as beta (beta) has been described. It was discovered in both sexes fed a stock diet for rodents. Hyperphagia was not noticeable. Total fat content reached 31 percent of total body weight in mature males. Obesity was associated with normal plasma cholesterol values and hypertriglyceridemia. Fasting blood sugar levels at maturity were within the normal range for rats, but significantly higher than in lean alpha (alpha) controls. This syndrome developed into a mild glucose intolerance and glucosuria in older obese rats.
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PMID:Spontaneous hypertriglyceridemic obesity and hyperglycemia in an inbred line of rats. 344 Jun 79

This study evaluates the role of adrenal hormones in the development of hyperinsulinaemia and impaired glucose homeostasis in genetically obese hyperglycaemic C57BL/6J ob/ob mice. Lean (+/?) and obese mice were bilaterally adrenalectomised or sham operated at 5 weeks of age, and glucose tolerance was examined after 7 and 14 days. Adrenalectomy temporarily reduced food intake and body weight gain in lean mice, and improved glucose tolerance without a significant change in plasma insulin concentrations at both intervals studied. In obese mice adrenalectomy permanently reduced body weight gain and food intake to values comparable with lean mice. Glucose tolerance was improved in adrenalectomised obese mice at both intervals studied, resulting in plasma glucose concentrations similar to adrenalectomised lean mice. Plasma insulin concentrations during the tolerance tests were reduced in adrenalectomised obese mice, but remained higher than in lean mice. Adrenalectomy did not improve the poor insulin response to parenteral glucose in obese mice. The results indicate that adrenal hormones play an important role in the development of glucose intolerance and contribute to the hyperinsulinaemia in obese (ob/ob) mice, in part by promoting hyperphagia.
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PMID:Role of adrenal glands in the development of abnormal glucose and insulin homeostasis in genetically obese (ob/ob) mice. 352 60


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