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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

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

Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are key links to nutritional condition and growth regulation in teleost. To understand the endocrine mechanism of growth regulation in grouper, we cloned the cDNAs for grouper GH and IGF-I and examined their mRNA expression during different nutritional status. Grouper GH cDNA is 936 base pairs (bp) long excluding the poly-A tail. It contained untranslated regions of 85 and 231bp in the 5'- and 3'-ends, respectively. It has an open reading frame of 612bp coding for a signal peptide of 17 amino acids (aa) and a mature hormone of 187aa residues. Based on the aa sequence of the mature hormone, grouper GH shows higher sequence identity (>76%) to GHs of perciforms than to GHs of cyprinids and salmonids (53-69%). Grouper preproIGF-I cDNA consisted of 558bp, which codes for 186aa. This is composed of 44aa for the signal peptide, 68aa for the mature peptide comprising B, C, A, and D domains, and 74aa for the E domain. Mature grouper IGF-I shows very high sequence identity to IGF-I of teleost fishes (84-97%) compared to advanced groups of vertebrates such as chicken, pig, and human (80%). Using DNA primers specific for grouper GH and IGF-I, the changes in mRNA levels of pituitary GH and hepatic IGF-I in response to starvation and refeeding were examined by a semi-quantitative RT-PCR. Significant elevation of GH mRNA level was observed after 2 weeks of food deprivation, and increased further after 3 and 4 weeks of starvation. GH mRNA level in fed-controls did not change significantly during the same period. Hepatic IGF-I mRNA level decreased significantly starting after 1 week of starvation until the 4th week. There was no significant change in IGF-I mRNA levels in fed-controls. One week of refeeding can restore the GH and IGF-I mRNA back to its normal levels. Deprivation of food for 1-4 weeks also resulted in cessation of growth and decrease in condition factor.
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PMID:Changes in mRNA expression of grouper (Epinephelus coioides) growth hormone and insulin-like growth factor I in response to nutritional status. 1624 24

The metabolism of critical illness is characterised by a combination of starvation and stress. There is increased production of cortisol, catecholamines, glucagon and growth hormone and increased insulin-like growth factor-binding protein-1. Phagocytic, epithelial and endothelial cells elaborate reactive oxygen and nitrogen species, chemokines, pro-inflammatory cytokines and lipid mediators, and antioxidant depletion ensues. There is hyperglycaemia, hyperinsulinaemia, hyperlactataemia, increased gluconeogenesis and decreased glycogen production. Insulin resistance, particularly in relation to the liver, is marked. The purpose of nutritional support is primarily to save life and secondarily to speed recovery by reducing neuropathy and maintaining muscle mass and function. There is debate about the optimal timing of nutritional support for the patient in the intensive care unit. It is generally agreed that the enteral route is preferable if possible, but the dangers of the parenteral route, a route of feeding that remains important in the context of critical illness, may have been over-emphasised. Control of hyperglycaemia is beneficial, and avoidance of overfeeding is emphasised. Growth hormone is harmful. The refeeding syndrome needs to be considered, although it has been little studied in the context of critical illness. Achieving energy balance may not be necessary in the early stages of critical illness, particularly in patients who are overweight or obese. Protein turnover is increased and N balance is often negative in the face of normal nutrient intake; optimal N intakes are the subject of some debate. Supplementation of particular amino acids able to support or regulate the immune response, such as glutamine, may have a role not only for their potential metabolic effect but also for their potential antioxidant role. Doubt remains in relation to arginine supplementation. High-dose mineral and vitamin antioxidant therapy may have a place.
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PMID:Nutritional interventions in critical illness. 1734 68


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