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

The study was designed to evaluate hepatic mitochondrial function during ketotic states. The ketogenic models studied were streptozotocin-induced diabetic ketoacidosis, 48 h of starvation, and after growth hormone administration. In the last-mentioned model we observed increased free fatty acids but not ketonemia. Oxidative phosphorylation was measured using the citric acid cycle substrates pyruvate and succinate, the amino acid glutamate, a ketone body beta-hydroxybutyrate, and a long-chain fatty acid palmitoyl-l-carnitine. State 3 (ADP stimulated) and state 4 (ADP limited) respiration, respiratory control ratio (state 3/state 4), and the ADP/O ratios were normal in the controls and the experimental groups. Uncoupled respiration produced by dinitrophenol with a variety of substrates was unchanged in the experimental groups compared to the controls. Fatty acid oxidation was studied in detail. The rate of utilization of palmitoyl-l-carnitine by controls or experimental groups did not depend on the product formed (citrate, acetoacetate). No significant changes were observed in the oxidation of palmitoyl-CoA (+ carnitine) or with an intermediate-chain fatty acid hexanoate. The specific activity of hepatic mitochondria carnitine palmitoyltransferase did not change in any of the three experimental groups. It is concluded that during diabetic ketoacidosis, starvation, and growth hormone administration, there is (a) no alteration in hepatic mitochondrial function; (b) no change in the intrinsic capacity of hepatic mitochondria to oxidize fatty acids; and (c) no change in the specific activity of mitochondrial carnitine palmitoyltransferase. The mechanism by which the body restrains flux through the mitochondrial oxidative machinery remains to be fully determined.
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PMID:Hepatic mitochondrial function in ketogenic states. Diabetes, starvation, and after growth hormone administration. 12 19

Large subcutaneous doses (2 mg/21 days) of estradiol valerate (EV) given over several months will induce a prolactin and growth hormone-secreting pituitary tumor in female rats. The medial basal hypothalami (MBHs) of such EV-treated animals were examined at different time intervals with light and electron microscopes to determine whether EV affects the MBH and to relate any observed effects to the process of tumorigenesis. The MBHs of extensively treated rats exhibited profound glial and neuronal changes. The filament content of astrocytes was greatly increased and large dense pleomorphic inclusions filled both astrocytic perikarya and processes. Degenerating neuronal elements have been observed in the neuropil of extensively treated animals. Dark cells identified as M cells were seen to engage in phagocytosis and were loaded with dense inclusions. Some neurons in MBH contained large quantities of lipofuscin that was different in appearance from that of normal females of the same age. The glial reaction developed gradually. At earlier stages of EV treatment there were fewer reactive glia and these contained fewer inclusions. Myelin figures often occurred in these early inclusions. Reactive glia in EV-treated rats did not appear in the preoptic area, dorsomedial nucleus or lateral hypothalamus but were found in ventromedial nucleus. Retired breeders and starvation-stressed rats resembled normal controls. These pathological changes in MBH may result from a direct effect of EV on the hypothalamus. It is possible that, in addition to its effects on the hypophysis, EV suppresses or injures hypophysiotropic cells in MBH, thus releasing pituitary chromophobes from inhibitory hypothalamic influences. This could result in hypersecretion and neoplasia.
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PMID:Cytopathological effects of estradiol on the arcuate nucleus of the female rat. A possible mechanism for pituitary tumorigenesis. 17 Aug 18

Various hormonal and non-hormonal agents were tested for their ability to induce ornithine decarboxylase (EC 4.1.1.17) in primary cultures of fetal rat liver cells that retain many of the differentiated functions of hepatocytes. The only agents to induce ornithine decarboxylase in this cell type were fetal calf serum, prostaglandin E1 and cyclic AMP derivatives. Also, the amino acid arginine would induce ornithine decarboxylase in this cell type following arginine starvation for 24 h. These observations are in contrast to the wide range of hormones, e.g. insulin, hydrocortisone, glucagon and growth hormone, than can induce ornithine decarboxylase in vivo in the adult rat liver but which are all without effect on fetal rat liver cells.
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PMID:Factors regulating the induction of ornithine decarboxylase in fetal rat liver cells in culture. 21 27

In the first part of the study oral glucose tolerance tests (GTT) or insulin tolerance tests (ITT) were performed in 22 lean and 22 obese nondiabetics before and after fasts of at least 6 days' duration. Deterioration of glucose tolerance was greater in lean than in obese individuals. Plasma levels of factors known to influence glucose tolerance (glucagon, growth hormone, free fatty acids, ketones) were significantly higher in fasting lean than in fasting obese subjects. Furthermore, delayed insulin rise (GTT) and decreased insulin sensitivity (ITT) were observed after starvation in lean subjects but not in the obese, which could explain the greater deterioration of glucose tolerance in the lean population. In the second part of the study glucose and fructose tolerance were compared during 4-hour infusions of these substrates (0.5 g/kg/h) in 8 normal subjects before and after two 4-day fasts. After starvation, glucose as well as fructose infusion resulted in plasma levels of the infused hexose significantly higher than in control, and the rise in plasma lactate and pyruvate was delayed. These results contradict the view widely held in the literature, that fructose metabolism remains unimpaired in the fasting state.
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PMID:[Carbohydrate intolerance during complete fasting]. 33 74

To investigate further the alterations in pituitary-thyroid function seen during starvation, we have measured basal and TRH-stimulated serum levels of thyrotropin (TSH), prolactin (PRL), growth hormone, thyroxine (T4), triiodothyronine (T3), free T4, free T3, and reverse T3 during prolonged fasting in seven obese men. Fasting was associated with a significant decrease in serum (4, (3, and free T3, while there was an increase in serum reverse T3; these values tended to return toward pre-fast levels as the fast continued beyond 3 weeks. No significant changes were seen in basal serum TSH, PRL, growth hormone, or free T4. Although the TSH response to TRH was diminished during fasting, PRL, T4, and T3 responses were unchanged. In addition to transient alterations in the peripheral metabolism of T4, these findings suggest that alterations in the thyroid hormone binding capacity of serum carrier proteins may occur during fasting. The blunted TSH response to TRH despite reduction of serum T3 concentration suggests that subtle alterations in hypothalamic-pituitary function may also occur.
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PMID:Alterations in basal and TRH-stimulated serum levels of thyrotropin, prolactin, and thyroid hormones in starved obese men. 41 Aug 22

In order to determine the endocrine and metabolic state of thyrotoxicosis we measured blood glucose and plasma insulin response to ingestion of a mixed meal in 19 euthyroid and 9 hyperthyroid subjects. Moreover concentrations of glucose, free fatty acids (FFA), glycerol, acetoacetate (AcAc) beta-hydroxybutyrate (beta-OHB), insulin and human growth hormone (hGH) were determined in the blood of both healthy and hyperthyroid patients after an overnight and a 39-h fast. In another group of thyrotoxics the overnight fasting respiratory quotient (RQ) was measured. After a mixed meal blood glucose and plasma insulin changes of FFA, AcAc and beta-OHB was significantly higher in thyrotoxics, whereas hGH increase did not appear significantly greater in these subjects. There was no statistical difference between the respiratory quotient mean values found in hyperthyroid and in control subjects. In conclusion, these data indicate that in thyrotoxicosis absolute insulin response to a mixed meal is normal and that food deprivation considerably increase lipid mobilization from adipose tissue and causes an exaggerated starvation ketosis. The RQ mean valoue suggests that in the hyperthyroid state lipid-derived fuel as well as carbohydrate-derived fuel contributes to the increased oxygen consumption.
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PMID:Studies on metabolic alterations after a mixed meal and during a 39-hour fast in thyrotoxicosis. 48 28

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

Ten days of total energy deprivation evoked the following endocrine changes in 12 healthy, normal-weight males: early and marked reductions and increments in the blood levels of T3 and reverse T3, respectively, with rapid returns to pre-starvation levels after refeeding; a slight and late decrease in the blood levels of T4; a minute reduction of the blood levels of TSH; a pronounced increase in the blood levels of growth hormone, but a return towards pre-exposure levels even before discontinuation of starving; a minor and gradual enhancement of the blood levels of cortisol, and an increase in nocturnal urinary adrenaline excretion. It is assumed that these changes reflect a complex regulatory mechanism, the purpose of which is to secure adequate energy supply to vital organs.
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PMID:Effects of total energy withdrawal (fasting) on thelevels of growth hormone, thyrotropin, cortisol, adrenaline, noradrenaline, T4, T3, and rT3 in healthy males. 83 66

Oral glucose tolerance tests were performed on 14 lean and 14 obese nondiabetic subjects before and after a 6-day fast. In addition, insulin tolerance tests were performed on 8 lean and 8 obese subjects before and after starvation. Both in lean and obese subjects glucose tolerance deteriorated during starvation, but much more so in the lean population. During fasting, insulin elevation after a glucose load was significantly delayed in lean subjects but not in the obese. Circulating levels of factors known to affect glucose tolerance, such as glucagon, growth hormone, free fatty acids, and ketone bodies were higher in fasting lean than in fasting obese individuals. In normals fasting resulted in a significant decrease of the blood glucose response to insulin injection, whereas in fasting obese subjects glucose response was unchanged. The results obtained suggest that the effect of fasting on insulin release and insulin sensitivity was more pronounced in lean than in obese subjects, which resulted in greater deterioration of glucose tolerance in the lean population.
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PMID:Mechanism of glucose intolerance during fasting: differences between lean and obese subjects. 89 29

Multiple endocrine determinations were carried out on 101 patients with anorexia nervosa. Ninety-five percent of the patients studied were female, and in 94% of patients the anorexia nervosa began before 30 years of age. Evidence of gonadal dysfunction was the predominant manifestation, both clinically and by laboratory studies. Amenorrhea occurred before or concurrent with onset of weight loss in 65% of the women. The average weight loss was 28% of the weight before illness began. In an additional 11%, the disease began before menarche. The mean age of menarche in patients with secondary amenorrhea was 13 years. Urinary excretion of pituitary gonadotropin was undetectable in 44 of 65 patients and was below 19 rat units per 24 hours in the remaining patients. Serum luteinizing hormone level was below 8 microgram/dl in 15 of 27 patients studied and serum follicle-stimulating hormone was below 10 microgram/dl in 7 of 27 patients studied. Mean serum or urinary estrogens, or both, were low in more than 50% of the patients. Elevation of serum corticosteroids or loss or reversal of diurnal variation, or both, was noted in 50% of patients. Fasting serum growth hormone levels were elevated in 45% of the patients. Mean total and free serum thyroxine, thyroid-stimulating hormone, and triiodothyronine levels were low. These hormonal alterations in the hypothalamic-pituitary axis in patients with anorexia nervosa probably represent adaptive and protective mechanisms for chronic starvation and weight loss.
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PMID:Hypothalamic-endocrine dysfunction in anorexia nervosa. 92 47


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