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

Norepinephrine (NE) and 3-methoxy-4-hydroxyphenylglycol (MOPEG) were determined in medio-basal hypothalamus of adult male rats using high-performance liquid chromatography to study nutritional modulation of noradrenergic turnover. Acute starvation, as well as 3 weeks of semistarvation with a low-protein high-carbohydrate or high-protein low-carbohydrate diet decreased NE turnover significantly, as estimated by MOPEG concentration. Low-protein semistarvation resulted in subnormal concentrations of large neutral amino acids (LNAA), high-protein semistarvation in elevated concentrations. Tyrosine/LNAA ratio and calculated tyrosine flow into brain and brain tyrosine levels were reduced in both types of semistarvation. Corticosterone was low in low-protein and high in high-protein diet. These results suggest that tyrosine availability in brain potentially contributes to reduced NE turnover in starvation.
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PMID:Brain tyrosine availability and the depression of central nervous norepinephrine turnover in acute and chronic starvation in adult male rats. 400 50

Twenty-two patients with anorexia nervosa were studied at 2-week intervals during treatment on psychiatric wards. In order to characterize the metabolic situation in starvation, levels of free fatty acids, beta-hydroxybutyric acid, and acetoacetate were measured. The endocrine adaptation to starvation was studied by measuring triiodothyronine, noradrenaline, and cortisol. Anorectic symptoms were assessed by the Anorexia Nervosa Inventory Scale (ANIS) and mood changes on the basis of a "Befindlichkeits" Scale (BF). Only half of the patients showed metabolic and endocrine signs of starvation on admission to the hospital, despite low body weight. This group had significantly more severe anorectic symptoms (ANIS) and gained weight at a lesser rate. Metabolic signs of starvation disappeared during the first 4 weeks of therapy in most of the patients. The endocrine indicators for starvation normalized much more slowly, with noradrenaline having the slowest pace. "Bulimics" and "restricters" could not be distinguished from one another by metabolic or endocrine observations. The "bulimics," however, showed more severe anorectic symptoms (ANIS) and a more depressed mood.
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PMID:Anorectic behavior, mood, and metabolic and endocrine adaptation to starvation in anorexia nervosa during inpatient treatment. 402 3

Catecholamines induced an increase in the activity of rat adipose tissue and liver phosphopyruvate carboxylases that was maintained for 48h. The response of adipose tissue phosphopyruvate carboxylase was blocked by actinomycin D, corticosteroids and propranolol, whereas corticosteroids and propranolol did not affect the liver enzyme. Cortisol phosphate, like actinomycin D, interfered only with the initiation of the increase in enzyme activity caused by noradrenaline, but not with the process of enzyme accumulation. In contrast, cycloheximide was effective in blocking enzyme induction throughout the course of the catecholamine effect. Adrenocorticotrophic hormone caused a short-term induction of adipose tissue phosphopyruvate carboxylase, which could be blocked by propranolol. Hepatic phosphopyruvate carboxylase, but not the adipose tissue enzyme, was induced by dibutyryladenosine 3':5'-cyclic monophosphate and by glucagon. Both nicotinic acid and nicotinamide decreased the normal induction of adipose tissue phosphopyruvate carboxylase caused by starvation, but only nicotinamide increased the activity of the liver enzyme.
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PMID:The interaction of catecholamines and adrenal corticosteroids in the induction of phosphopyruvate carboxylase in rat liver and adipose tissue. 434 97

1. In rabbits kept unfed for 4 or 24 or 48 hr after delivery by Caesarean section at term, noradrenaline infusion (I.V. for 30 min) caused a similar increase in oxygen consumption but the increase in serum free fatty acid concentration was greatest in rabbits kept unfed for 48 hr.2. The brown adipose tissue of anaesthetized rabbits under 3 hr old took glucose from the circulation but did not release fatty acids. In similar rabbits noradrenaline infusion stimulated the tissue to generate heat, but there was no release of fatty acids even though the rate of triglyceride hydrolysis was high (as judged by the rate of glycerol release).3. In rabbits kept unfed for 48 hr from birth in a warm environment, brown adipose tissue released small amounts of fatty acids but continued to take glucose from the circulation. Heat production in response to noradrenaline infusion was accompanied by an increased release of fatty acids. The fat content of the brown adipose tissue did not fall with starvation.4. The mean serum insulin concentration of rabbits at birth was 54 muu./ml. compared to 23 muu./ml. in the mother. In new-born rabbits kept unfed for 48 hr the insulin concentration had fallen to 14 muu./ml.5. It is concluded (i) that at birth brown adipose tissue has the capacity to generate heat but the tissue is slow to release its stores of fat in response to starvation, (ii) that brown adipose tissue has a high rate of glucose uptake even during starvation and (iii) that the high circulating concentration of insulin may be responsible for the tissue's slow adaptation to the demands of starvation.
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PMID:Brown adipose tissue metabolism in vivo and serum insulin concentrations in rabbits soon after birth. 557 36

Control of glucose and ketone body metabolism is integrated by a variety of hormones. Insulin is the major anabolic hormone, and its actions are antagonized by rapidly acting catabolic hormones, such as glucagon and the catecholamines, and by others such as cortisol, growth hormone and the thyroid hormones, which generally have more delayed effects. In the normal human subject, the effects of catabolic hormones to raise blood glucose are limited by a compensatory increase in insulin secretion, and these effects are enhanced in insulin deficiency. Hyperketonaemic actions of the catabolic hormones may result from increased supply of non-esterified fatty acids from lipolysis, although glucagon has a major direct action to increase ketogenesis at the liver. As expected, these actions are also restricted in normal humans by the compensatory rise in insulin secretion. Hyperketonaemia does, however, occur with adrenaline (epinephrine) and noradrenaline (norepinephrine), even in the presence of mildly elevated insulin concentrations. These catecholamines may assume particular importance in mobilization of lipid fuels in milder forms of stress, when insulin secretion is normal or mildly increased. In severe stress, when there is catecholamine-induced suppression in insulin secretion, lipolytic and hyperketonaemic effects of all the catabolic hormones may be manifest. Starvation in humans also results in diminished insulin secretion and increased catabolic hormone secretion. The relative importance of individual hormones in lipid mobilization during starvation is uncertain, although glucagon, growth hormone, noradrenaline and, possibly, dopamine may all play a part.
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PMID:Some hormonal influences on glucose and ketone body metabolism in normal human subjects. 612 46

Recent studies have suggested that the tridecapeptide, neurotensin, may be an endogenous satiety factor. The present study was undertaken to examine the effects of neurotensin on multiple paradigms known to stimulate feeding. Following a 30 hour starvation period, neurotensin suppressed feeding at the 20 microgram and 10 microgram dose, but not at the 1 microgram dose when compared to saline controls. Norepinephrine (20 micrograms ICV) induced feeding was suppressed at the 20 microgram neurotensin dose but not at the 10 microgram or 1 microgram dose. In contrast, neurotensin did not suppress muscimol induced feeding at any of the doses. Insulin induced feeding (10 units SC) also was not suppressed by neurotensin. Neurotensin suppressed dynorphin induced feeding at the 20 microgram and 10 microgram but not at the 1 microgram dose. Neurotensin suppressed spontaneous feeding (p less than 0.01) in vagotomized rats (2.5 +/- 0.3 g/2 hr) when compared with saline controls (4.2 +/- 0.5 g/2 hr) suggesting that an intact vagus is not necessary for neurotensin's anorectic effect. We conclude that neurotensin may play a role in short-term appetite regulation by a complex interaction with monoamines and neuropeptides, particularly norepinephrine and the kappa opiate agonist, dynorphin.
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PMID:Effect of centrally administered neurotensin on multiple feeding paradigms. 613 39

1. Tubule fragments were isolated from renal cortex of fed rats and glucose formation was measured after incubation with 5 mM-sodium lactate. 20 Compound D-600 (10-100 microM) decreased gluconeogenesis from lactate. This inhibition of the process by compound D-600 increased with increasing extracellular Ca2+ concentration, was overridden by noradrenaline and diminished by starvation for 24 h. 3. Inhibition of lactate-supported gluconeogenesis by compound D-600 was not prevented by the alpha 1-adrenoceptor antagonist thymoxamine. 4. Compound D-600 had little effect on gluconeogenesis from 2-oxoglutarate and increased gluconeogenesis from succinate. 5. Compound D-600 opposed stimulation of gluconeogenesis by noradrenaline or oxymetazoline (a selective alpha-adrenoceptor agonist) in a manner suggesting that compound D-600 is an alpha-adrenoceptor blocker. Oxymetazoline was more sensitive than noradrenaline to blockade by both compound D-600 and by the conventional alpha-adrenoceptor antagonist phentolamine. Noradrenaline became more sensitive to blockade by compound D-600 when extracellular Ca2+ was decreased. 6. Compound D-600 did not block stimulation of gluconeogenesis by angiotensin or cyclic AMP.
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PMID:Effect of compound D-600 (methoxyverapamil) on gluconeogenesis and on acceleration of the process by alpha-adrenergic stimuli in rat kidney tubules. 625 65

Activation of lipolysis by cyclic AMP in conditions with accelerated lipid mobilization was examined in subcutaneous adipose tissue incubated in vitro. In (a) 16 obese patients before and during therapeutic starvation, (b) 18 diabetics before and after antidiabetic treatment and (c) 11 hyperthyroid patients before and after anti-thyroid treatment, a positive correlation was found between stimulation of basal cyclic AMP accumulation and stimulation of basal glycerol release using either isopropyl noradrenaline or noradrenaline (r = 0.6-0.9). During antidiabetic treatment stimulation of lipolysis increased in relation to that of cyclic AMP accumulation (F = 10.1, p less than 0.01), whereas during antithyroid therapy there was a decrease (F = 95.2, p less than 0.01). Starvation did not alter the relationship between lipolysis and cyclic AMP in hypogastric adipose tissue whereas in femoral tissue stimulation of lipolysis decreased in relation to that of cyclic AMP accumulation (F = 9.6, p less than 0.01). It is concluded that the amount of cyclic AMP needed to promote lipolysis is increased during starvation and in diabetes mellitus but is decreased in hyperthyroidism. From the studies during starvation it appears that regional differences in the post-receptor activation of lipolysis exist in human adipose tissue.
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PMID:Post receptor activation of lipolysis in starvation, diabetes mellitus and hyperthyroidism. 626 39

Glucose is the principal energy substrate for the brain and studies have shown that the brain is able to increase glucose availability in the face of glucose starvation (neuroglycopaenia). The mechanisms, believed to be hypothalamic, that may be involved in a brain/blood glucose control system have not yet been identified. We have used novel techniques for assessing brain monoamine neuronal activity to investigate its relationship to blood glucose concentrations in the rat. We describe here two important relationships which emerge from these studies. One is that activation of hypothalamic noradrenaline (NA) activity following stress is associated with concurrent increases in plasma glucose concentrations. This relationship is linear and independent of the adrenal or pituitary glands. The second is an inverse relationship between plasma glucose concentration and hypothalamic NA neuronal activity--high blood glucose levels significantly inhibited the hypothalamic NA activity responses to stress, alpha 2-adrenergic blockade and adrenalectomy. Thus glucose (or a metabolite of it) seems to provide a negative feedback signal sensed by hypothalamic NA neuronal systems which, in turn, appear to stimulate liver glucose output by a neural mechanism.
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PMID:Relationships between brain noradrenergic activity and blood glucose. 632 3

The effect of a 24 hr starvation period on islet lysosomal enzyme activities and the in vivo insulin response to glucose, glibenclamide and L-isopropyl-noradrenaline (L-IPNA) was studied in mice. It was observed that fasting induced a significant decrease of islet acid amyloglucosidase activity, whereas the activities of acid phosphatase, beta-N-acetyl-glucosaminidase, and beta-glucuronidase in islet tissue were unaffected by the fasting period studied. Starvation markedly reduced the acute insulin response to a maximal dose of glucose or glibenclamide. However, the insulin response to a maximal dose of L-IPNA was of similar magnitude in both fed and fasted animals. Pretreatment of fasted mice with purified fungal acid amyloglucosidase could restore the impaired insulin response to glucose to the normal level seen in fed mice. It is suggested that islet acid amyloglucosidase activity is of importance for glucose-stimulated insulin secretion, and that reduced levels of islet amyloglucosidase may contribute to the impairment of glucose-induced insulin release seen after fasting.
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PMID:Effect of fasting on islet lysosomal enzyme activities and the in vivo insulin response to different secretagogues. 640 43


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