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

Basal plasma gastrin levels were significantly higher in obese rats induced by ventromedial hypothalamic lesions (VMH rats) than in sham-operated controls. Gastrin secretion in response to insulin hypoglycemia and a liquid diet load was higher in VMH rats than in controls. The antral gastrin concentration was also elevated in VMH rats. Pair-fed rats with VMH lesions showed increased gastrin secretion as did the non-pair-fed group. These results show that gastrointestinal hormone secretions as well as pancreatic endocrine function are abnormal in obese rats with VMH lesions. Increased gastrin secretion is probably induced by factors other then hyperphagia, such as disturbance of the autonomic nervous system due to the VMH lesions.
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PMID:Alterations of gastrin secretion in obese rats with ventromedial hypothalamic lesions. 636 Sep 24

Two experiments were performed to investigate in some detail the behavioural and metabolic effects of the administration of regular insulin to golden hamsters. In Experiment 1 dose-response curves describing the effects of insulin upon both food intake and plasma glucose (PG) were generated. Dosages of less than 20 units/kg did not cause increases in food intake, while dosages of 10 units/kg or greater produced significant hypoglycemia at +6 hr post-injection. There was also a significant inverse linear relationship (r = -.528) between individual hamsters' food intakes and PG levels over the range of insulin dosages. In Experiment 2, insulin (30 units/kg) caused increases in meal frequency but not in meal size, and hyperphagia developed within +3 hr of insulin administration. When food was not available, insulin caused PG levels to fall below control levels at +1 hr and to remain depressed until at least +6 hr post-injection. However when hamsters were allowed to eat, PG did not fall significantly below control levels until +3 hr and began to recover at +5 hr post-injection. Results are discussed in relation to several apparent peculiarities in the hamster's behavioural response to regular insulin, specifically the small magnitude and the slow development of insulin-induced hyperphagia, and the hamster's relative insensitivity to the hyperphagic effect of insulin.
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PMID:Characteristics of insulin-induced hyperphagia in the golden hamster. 637 4

Two experiments were performed to investigate whether insulin-induced hyperphagia (IIH) serves an adaptive function in counteracting hypoglycemia in hamsters. In Experiment 1, insulin-injected hamsters having free access to food during a six-hour feeding test had neither higher plasma glucose (PG) concentrations nor lower frequencies of neurological impairment at the end of the test than did hamsters whose food intake was restricted to control levels. In Experiment 2, it was observed that PG fluctuations did not act as a trigger for meal-onset in insulin-injected hamsters, nor was PG affected by consumption of a meal during IIH. The withholding of food for periods longer than the typical intermeal interval (IMI) of insulin-injected hamsters (= 50 min) resulted in a marked increase in the frequency of neurological deficits among hamsters having PG levels lower than about 40 mg/dl. However animals with similarly low PG concentrations, but deprived of food for less than 50 min showed no signs of impairment, suggesting that some alternate metabolic fuel is available during the IMI and prevents the occurrence of behavioural deficits. The results of these experiments suggest that a simple glucostatic interpretation of IIH in hamsters is inadequate, and although hyploglycemia may play a role in hamster IIH, other factors must also be considered. In Experiment 3, the effect of a hyperphagia-inducing dose of insulin upon stomach emptying was investigated. It was found that both insulin-injected and control hamsters have similar amounts of food in their respective pregastric and gastric pouches at both the onset and offset of meals, but that both pouches empty far more rapidly under the influence of insulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Food consumption, plasma glucose and stomach-emptying in insulin-injected hamsters. 639 Apr 72

The effects of adrenalectomy on food intake, weight gain, plasma glucose, and corticosterone levels were investigated in normal untreated controls and gold thioglucose-(GTG) treated hyperphagic obese mice. Adrenalectomy of normal untreated mice was followed by a transient reduction in food intake and body weight with a return, after approximately 7 days, to levels which paralleled those of untreated sham-operated mice. Plasma corticosterone levels were significantly depressed in all untreated adrenalectomized mice. Plasma glucose levels were not affected by adrenalectomy. In sharp contrast to the response of untreated adrenalectomized mice, adrenalectomy of GTG-treated hyperphagic obese mice was followed by a sudden and persistent drop in food intake (anorexia) and body weight. These mice were unable to maintain their body weight. Despite this condition, the mice did not appear to be physically debilitated until a short time (6-12 h) before their death which was preceded by a period of severe hypoglycemia. These findings indicate that the hyperphagia and weight gain of GTG-treated obese mice is dependent on adrenal hormones. The anorexia after adrenalectomy of GTG-treated hyperphagic obese mice may be the result of a direct dependence of central or peripheral structures involved in the regulation of food intake on adrenal hormones. Alternatively, these structures may be affected by the action of metabolites or hormones which arise as a consequence of adrenal insufficiency.
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PMID:Anorexia after adrenalectomy in gold thioglucose-treated obese mice. 640 38

An 81-yr-old male with pulmonary emphysema was hospitalized because of malnutrition and hypoglycemia. This patient developed ventilatory failure requiring mechanical assistance 12 h after initiation of iv hyperalimentation. Severe hypophosphatemia (0.1 mg/dl), mild hypocalcemia, hypomagnesemia, and hypokalemia were subsequently and concomitantly documented. Repeated attempts to wean him from the respirator failed until hypophosphatemia was corrected. When difficulties are encountered in weaning patients from mechanical ventilation, attention should be directed toward detection of hypophosphatemia. This may be crucial in the presence of chronic lung disease.
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PMID:Hypophosphatemia as a reversible cause of refractory ventilatory failure. 662 64

The sensitivity to insulin hypoglycemic convulsions has been shown to decrease at early times (16 and 24 hr) and increase at later times (1 week) after gold thioglucose (GTG) treatment. Systemically administered GTG is well known to produce hyperphagia, resulting in obesity, and cytological damage focused relatively selectively in the ventromedial hypothalamic area (VMH). Both of these effects on insulin hypoglycemic convulsions occur before the weight gain, but at a time when histological damage visible with cresyl violet stain has already appeared. Both of these changes reflect a difference in the convulsive response to hypoglycemia, rather than a differences in the degree of hypoglycemia in response to insulin. No functional change in the convulsive sensitivity was found at still earlier times during the latency in establishing the histological damage visible with cresyl violet. These results suggest that GTG lesions a relatively discrete brain region involved in adjusting the functional response of the brain to hypoglycemia, including a composite of two opposite regulatory components. The significance of such a control center in relation to energy metabolism in brain is discussed. Moreover, it has been postulated that the glucose moiety of GTG binds to glucoreceptors in the VMH to focus the cytoxicity of the gold thioportion at that site. These results are also discussed in relation to this proposed mechanism for concentration and hence localization of GTG toxicity in the VMH.
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PMID:Change in sensitivity to insulin hypoglycemic convulsions after gold thioglucose treatment: time course of development. 679 12

Systemic gold thioglucose (GTG) is well known to produce hyperphagia, resulting in obesity, and histological damage focused relatively selectively in the ventromedial hypothalamus (VMH). Although structurally very different, bipiperidyl mustard (BPM) produces apparently similar effects. However, a proposed mechanism for concentration and hence localization of GTG toxicity depends on its structural similarity to glucose, binding it to glucoreceptors and focusing the cytotoxicity of the gold thio-portion. We recently showed that GTG treatment also produces an early decrease and a later increase in sensitivity to insulin hypoglycemic convulsions. We report here that BPM also produces a similar biphasic change in sensitivity to insulin hypoglucemic convulsions. For both, the differences are in the brain's convulsive response to hypoglycemia, rather than in the degree of hypoglycemia in response to insulin. Thus, GTG and BPM cytotoxic lesions appear similar in this regard as well. BPM is another way of producing a relatively discrete brain lesion which alters the brain's functional adjustment to hypoglycemia. The significance of this control center and its relationship to the control(s) of feeding and systemic metabolism are discussed.
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PMID:Effects of bipiperidyl mustard (BPM) lesions on insulin hypoglycemic convulsions. 681 53

We studied a patient with lung cancer, who exhibited severe systemic derangements of metabolism causing cachexia preceding the appearance of a large bulky tumor. The data described herein left no doubt that lung cancer growing in the patient acted as a powerful hypoglycemic factor, setting in motion widespread metabolic disorders. Inappropriate secretion of insulin may be involved in the manifestation of hypoglycemia. However, no ectopic secretion of insulin, glucagon, ACTH and aldosterone appeared to be associated with the carcinoma in the patient. From the present and previous observations, it is stressed that progressive energy loss from the patient occurs by virtue of a combination of severe anorexia and the establishment of a systemic energy-losing cycle dependent on an interplay of glycolysis in the cancer cells and stimulated gluconeogenesis in the host tissues, which in turn results in derangements of protein, lipid and electrolyte metabolism. Attempts to ameliorate the patient's distress and counterbalance the effect of the tumor by parenteral hyperalimentation were not satisfactory and resulted in only a temporary improvement. This study also demonstrated that marked granulocytosis was the result of production of an excess granulopoietic colony stimulating activity by the cancer cells.
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PMID:Hypoglycemia, hypopotassemia and hyperleukocytosis associated with squamous cell carcinoma of the lung. 697 22

A spontaneous recessive mutation appearing in strain 129/J mice at the diabetes (db) locus on Chromosome 4 has been characterized. The new allele, designated db3J, produced hyperphagia and severe obesity. Mutants weighed in excess of 70 g by 6 months of age, compared to 22-28 g for lean littermates. Although the disease was similar to the mild hyperglycaemia-severe obesity syndrome exhibited by db gene presentation on the C57BL/6J inbred background, the syndrome in 129/J mice reduced lifespan, with mutants exhibiting sudden weight loss, hypoglycaemia, and a 67% mortality between 6 and 14 months of age. Mutant males, but not females, were transiently hyperglycaemic between 2 to 4 months of age, attaining a maximum mean blood sugar of 196 +/- 27 (SEM) mg/dl. Thereafter glucose levels declined to normoglycaemic values (80-100 mg/dl), and with increasing age, mutants of both sexes became hypoglycaemic (60 mg/dl at 9 months). Mutants of both sexes were extremely hyperinsulinaemic at the earlier ages, with mean plasma insulin at months 5 reflecting 30-fold elevations above normal for males and 18-fold for females. These levels diminished with age, the decline being more marked in males. Plasma glucagon levels were 3-fold elevated in the younger mutants of both sexes (86 pg/ml versus 28 pg/ml in normal mice), mean levels increasing to almost 5-fold above mean control vaues in the older age group (198 pg/ml versus 41 pg/ml in normal mice). Histopathological findings were limited to pancreas. Increasing necrosis of the exocrine, but not endocrine, pancreas was noted in aging mutants. Aldehyde fushsin staining of the mutant pancreas revealed hyperplastic islets filled with heavily granulated B-cells. B-cell hyperplasia was accompanied by a 30-fold increase over controls in pancreatic insulin content in the 8 month old mutants, whereas pancreatic glucagon content was only doubled. Morphometric analysis showed less than a 2-fold increase in the mean number of A-cells per islet. Thus, an interesting feature of expression of the diabetes gene in the 129/J strain is the persisting hyperglucagonaemia in the face of moderating hyperinsulinaemia.
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PMID:A new mutation (db3J) at the diabetes locus in strain 129/J mice. I. Physiological and histological characterization. 699 69

Concurrent diabetes mellitus and hyperadrenocorticism were diagnosed in 30 dogs over a 2-year period. Clinical signs included polyuria, hepatomegaly, polyphagia, abdominal distension, truncal alopecia, anorexia, and vomiting. Because of the similar clinical and laboratory findings for hyperadrenocorticism and diabetes mellitus, hyperadrenocorticism was initially overlooked in some dogs. Insulin resistance, characterized by high daily insulin requirements, developed in the diabetic dogs with untreated hyperadrenocorticism. Therapy with o,p'-DDD resulted in precipitous declines in insulin requirements. By lowering the dosage of o,p'-DDD and supplementing with glucocorticoids during the o,p'-DDD loading period, serious hypoglycemia was avoided. Control of coexisting hyperadrenocorticism lessened the severity of the diabetes mellitus, but insulin therapy remained a necessity in all dogs.
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PMID:Diagnosis and management of concurrent diabetes mellitus and hyperadrenocorticism in thirty dogs. 700 30


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