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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were designed to determine whether variations in diet composition could modify the secretion of human growth hormone. Eight men and seven women ingested experimental diets for 10-12 days. Each experimental diet was preceded by a control diet for five days. Experimental diets studied in men were a) 2300 calorie, 80% carbohydrate (8 men); b) 2300 calorie, 75% high-fat (7 men); c) 2300 calorie, 70% high-protein (5 men); d) 3600 calorie, "control" (40% carbohydrate, 40% fat, 20% protein) (5 men); and e) 3600 calorie, 80% high-carbohydrate (5 men). A control diet and a high-carbohydrate (5 men). A control diet and a high-carbohydrate diet at the 2300 calorie level were studied in women. Each diet study was terminated by a 72 hour fast. Serum samples were collected hourly for 24 hours after each control period, on the eigth, ninth, or tenth day of each study, and during the final day of each fast. High-carbohydrate diets at the 2300 calorie level caused a significant decrease of growth hormone values in serum in each of eight men (sign test of significance, P less than .01). The mean figures were likewise significantly decreased. Isocaloric diets of high fat and high protein did not alter growth hormone concentrations in serum. A high-caloric diet similar to the control diet in composition was without effect on growth hormone secretion in men; however, a high-carbohydrate diet at the higher caloric level again depressed growth hormone values in plasma. On the third day of a 72 hour fast, growth hormone values in serum increased 287% in men, from a mean control serum concentration of 4.4 +/- 0.8 ng/ml to 11.9 +/- 5.0 ng/ml (P less than .01). Women, unlike men, had no significant decrease in growth hormone concentrations in serum over a 24 hour period after the high-carbohydrate diet, and the increase after starvation was significantly less than that in men, achieving significance only when evaluated by paired analysis. Growth hormone values in serum after the infusion of arginine followed a similar pattern, i.e., decreased after high carbohydrate but unaffected by other diets in men; high carbohydrate diets did not alter the growth hormone response of women to arginine.
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PMID:Diet-induced alterations of hGH secretion in man. 77 53

In 24 normal and 24 obese subjects of both sexes circulating substrates (blood sugar, free fatty acids, ketone bodies) and hormones (insulin, growth hormone, pancreatic glucagon) were determined during 6 days of total fast. In normals the blood sugar fell to lower levels than in the obese. Plasma free fatty acids and ketone concentrations rose faster in normal than in obese subjects, and faster in females than in males. Plasma insulin concentrations declined to a greater extent in obese than in normal subjects. In all groups studied a significant increase of the pancreatic glucagon level within 1-3 days of fasting was observed, however, its rise occurred faster in normal females than in males. Growth hormone (GH) rose significantly in normal males but not in obese males. Following high overnight fasting values in some normal females showed no significant increase in GH levels but significantly higher GH values than obese females after 1-6 days of fasting. After summarizing starvation-induced metabolic changes common to all study groups the respective differences found between males and females and between normal and obese subjects are discussed.
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PMID:[Metabolic differences between males and females and between normal and obese subjects during total fast]. 93 57

Growth hormone (GH) cells of rats were studied on days, 2, 4 and 7 of starvation. Immunoperoxidase staining for light microscopy confirmed the presence of GH in the pituitaries of all groups of animals. Electron microscopy revealed crinophagy in the cytoplasm of GH cells on days 4 and 7. By ultrastructural morphometry, volume density and the diameter of secretory granules in the cytoplasm of GH cells remained unchanged. Blood GH determinations showed a significant decrease on day 4 of the starvation period. On day 7 most of the values were in the range of the controls. Blood prolactin levels fell significantly on day 7. It appears that the pituitary is capable of secreting GH even in rats completely deprived of exogenous nutrients.
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PMID:Effect of starvation on pituitary growth hormone cells and blood growth hormone and prolactin levels in the rat. 95 50

Growth hormone concentration has been assayed in 105 children (45 girls and 60 boys) during starvation and following its stimulation with clonidine and insulin and during the sleep. A significant difference between growth hormone concentration during fasting and after stimulation has been noted. No statistically significant difference between growth hormone concentrations during the sleep and following insulin has been found. The most intensive growth hormone release has been observed during the sleep. Test with clonidine is technically simple and may be performed also in the out-patient clinics.
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PMID:[Growth hormone concentration following various factors stimulating its release]. 130 18

Catch-up (compensatory) growth following transient growth retardation due to illness or starvation has long been recognized in biology and in clinical medicine. This report summarizes work utilizing experimental models in rats in efforts to elucidate the control of catch-up growth. The results support the hypothesis that the catch-up growth mechanism includes a set-point or reference for body size appropriate for age and that the control resides in the central nervous system. Growth hormone (GH) secretion is increased during catch-up growth, although the results also show that increased GH secretion is not required for catch-up growth acceleration. Environmental light modulates the effect of catch-up growth on GH secretion. The mechanisms for sensing a deficit in body size and for stimulating catch-up growth acceleration remain unknown.
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PMID:The control of catch-up growth. 287 34

The effect of growth hormone-releasing factor (GRF) on feeding behavior in rats was examined. Starvation-induced feeding was suppressed by intraventricular administration of 1 nmol and 4 nmol of synthetic human GRF (hGRF). Food intake was not affected when the peptide was administered by intraperitoneal injection. Furthermore, centrally administered hGRF also suppressed feeding in hypophysectomized rats. These results suggest that GRF suppression of food intake is mediated through the central nervous system independent of its effect on pituitary growth hormone secretion.
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PMID:The satiety effect of growth hormone-releasing factor in rats. 392 93

The present experiments were undertaken to study the effect of complete food removal on body weight, pituitary growth hormone (GH), plasma GH and glucose concentration in male and female Wistar rats. Plasma and pituitary GH levels were measured by means of a specific radioimmunoassay. Plasma glucose concentration decrease during the initial 60 h fasting in males and 72 h in females, and remained fairly constant thereafter in both groups. Pituitary GH content was unchanged in males and females by 36 h and 60 h, respectively, after the onset of starvation. Thereafter, pituitary GH decreased progressively with increase of the starvation period. In spite of the changes in pituitary GH, plasma GH concentration in fasted male and female rats was similar to or higher than in controls. In fact, during an initial period, up to 72 h in males and 96 h in females, plasma GH levels in fasting rats were similar to control values. With longer starvation periods, plasma GH concentration rose above control values. After 24 h of refeeding 102 h fasted rats, plasma GH concentrations were comparable to control levels. In addition, after an initial loss of 10 g after 24 h fasting, body weight of both male and female animals decreased, and by the end of the starvation period it was about 50% of control weight. From these results it seems that complete food removal has a direct effect on pituitary GH. Furthermore, the fact that changes in plasma GH concentrations were evidentiated just before the period when plasma glucose was maintained at constant levels in fasted rats of both sexes supports the hypothesis that growth hormone plays a physiological role in the regulation of glucose homeostasis during starvation.
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PMID:Effects of starvation on pituitary and plasma growth hormone in rats. 724 Jun 70

Substrate fluxes in response to growth hormone administration depend on both the calorie as well as acid-base balance. Growth hormone's acidogenic action as a consequence of promoting fatty acid utilization yields protons required for driving hepatic glutamate efflux; effective uncoupling of nitrogenous precursors from ureagenesis and recycling as glutamate bound for the periphery appears dependent upon this mechanism. Subsequent peripheral retrieval of the salvaged glutamate requires insulin-like growth factor-1 (IGF-1) activated uptake and acid-base homoeostasis. In addition to this nitrogen sparing acidogenic effect, growth hormone is also basogenic in combination with IGF-1 and acting on the kidney as a target organ. Therefore acid-base and nitrogen homoeostasis are normally attuned to one another through the co-ordinated action of growth hormone/IGF-1 on substrate fluxes. However during starvation ketoacid production as the consequence of incomplete fatty acid oxidation and ketone excretion swamps the basogenic limb and full-blown metabolic acidosis prevails; under this condition growth hormone's effectiveness in sparing nitrogen for anabolic processes is curtailed as glutamate (emanating from the liver) and glutamine (derived from muscle proteolysis) are directed to the kidneys, supporting ammoniogenesis: nitrogen balance is now sacrificed for acid-base homoeostasis. Underlying this state is an intracellular acidosis that may contribute to insulin resistance and developing hyperglycaemia in response to growth hormone. In acute injury, an additional acid load contributed from muscle proteolysis and cytokines reinforces an intracellular acidosis that further blunts growth hormone responsiveness and suppresses coupled IGF-1 production. From this perspective growth hormone's acidogenic and basogenic actions should balance for an effective anabolic response during hypermetabolic catabolic illnesses.
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PMID:The role of growth hormone in substrate utilization. 958 78

Anorexia nervosa is a syndrome of unknown etiology. It is associated with multiple endocrine abnormalities. Hypothalamic monoamines (especially serotonin), neuropeptides (especially neuropeptide Y and cholecystokinin) and leptin are involved in the regulation of human appetite, and in several ways they are changed in anorexia nervosa. However, it remains to be clarified whether the altered appetite regulation is secondary or etiologic. Increased secretion of corticotropin-releasing hormone and proopiomelanocortin seems to be secondary to starvation, however, there is evidence that it may maintain and intensify anorexia, excessive physical activity and amenorrhea. Hypothalamic amenorrhea, which is a diagnostic criterion in anorexia nervosa, is not solely related to the low body weight and exercise. Growth hormone resistance with low production of insulin-like growth factor I and high growth hormone secretion reflect the nutritional deprivation. The nutritional therapy of patients with anorexia nervosa might be improved by administering an anabolic agent such as growth hormone or insulin-like growth factor I. So far none of the endocrine abnormalities have proved to be primary, however, there is increasing evidence that some of these might participate in a vicious circle.
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PMID:A review of endocrine changes in anorexia nervosa. 1022 46

Numerous endocrine abnormalities are associated with anorexia nervosa and bulimia nervosa. The principal complication is amenorrhoea. Hypothyroidism and hypercortisolism have been described as a protective mechanism to conserve energy. Growth hormone concentrations are often increased as a result of starvation. Insulin and blood sugar concentrations are decreased, but prolactin concentrations are remain normal. Considerable evidence exists of hypothalamic dysfunction in patients with eating disorders. This dysfunction is reflected in disturbances of endocrine function. Endocrine disturbances may be not solely related to the low body weight. Hypothalamic monoamines, neuropeptides and leptin are involved in the regulation of human appetite, and in several ways they are changed in eating disorders. However, it remains to be clarified whether the altered appetite regulation is secondary or etiologic.
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PMID:[Endocrine and reproductive disturbances in anorexia nervosa and bulimia nervosa]. 1126 7


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