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

The anti-lipolytic effect of the adenosine analogue N6-L-phenylisopropyladenosine was studied with rat adipocytes incubated with a high concentration of adenosine deaminase (0.5 unit/ml, approx. 2.5 micrograms/ml) and concentrations of noradrenaline that were equieffective in different physiological states. These studies were performed to compare the fed and starved (24h) states and to compare a hypothyroid state (induced by feeding propylthiouracil + a low-iodine diet) with the euthyroid state. Starvation increased sensitivity of the cells to the lipolytic action of noradrenaline, while decreasing sensitivity to the antilipolytic action of phenylisopropyladenosine. Hypothyroidism resulted in decreased sensitivity to noradrenaline and increased sensitivity to phenylisopropyladenosine. Studies of the binding of [3H]phenylisopropyladenosine to adipocyte plasma membranes indicated heterogeneity of binding sites or negative co-operativity in the binding. Starvation did not change [3H]phenylisopropyladenosine binding to membranes, whereas hypothyroidism caused an unexpected decrease in both the number and affinity of the binding sites. These observations are discussed in terms of the dual regulation of adipose-tissue lipolysis by lipolytic and anti-lipolytic agents.
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PMID:Changes in the anti-lipolytic action and binding to plasma membranes of N6-L-phenylisopropyladenosine in adipocytes from starved and hypothyroid rats. 649 45

Exhaustive graded exercise leads to changes of hormones, carbohydrate, and lipid metabolism in normal controls and obese patients after prolonged starvation. Concomitant with a large increase of plasma catecholamines, insulin concentration is reduced and blood glucose levels slowly increase. More glucose is made available by glycogenolysis and gluconeogenesis than can be oxidized in the mitochondria. Lactate associated metabolic acidosis appears. Starving obese patients in the basal state have reduced blood glucose concentrations, but their initial values for free glycerol, free fatty acids, and ketone bodies are much higher than in normal controls. This is caused by the starvation induced lipolysis. With exhaustive exercise adrenaline, noradrenaline, and free glycerol increase. In contrast, free fatty acids and ketone bodies decrease, because they are consumed as fuel. Prolonged starvation changes basal values of hormones and metabolites, but it does not change the quality of exercise-induced shifts in these values when compared with those of the normal controls.
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PMID:Hormonal and metabolic changes in starving obese patients during exhaustive physical exercise. 667 70

The antilipolytic effect of insulin in vitro was investigated in conditions known to be associated with resistance to the effect of insulin on glucose metabolism. Human subcutaneous adipose tissue was obtained from 14 obese subjects before and during starvation for 7 days, 12 untreated non-insulin dependent diabetics (NIDDM), 6 untreated insulin dependent diabetics (IDDM), and 10 nonobese control subjects. The tissue was incubated with and without insulin in concentration ranging from 1-10,000 microunits/ml. Responsiveness (maximum effect) and sensitivity to insulin were determined under basal induction conditions, since insulin had a bimodal effect on noradrenaline stimulated lipolysis. Under normal conditions both insulin sensitivity and insulin responsiveness were positively correlated with the basal rate of lipolysis. In obesity, IDDM and NIDDM there were no change in insulin sensitivity or in insulin responsiveness. When the obese subjects were divided into one hyperinsulinemic group (6 individuals) and one group with normal fasting serum insulin levels (7 individuals) a similar antilipolytic effect of insulin was observed in the two groups. During starvation there was a 20-fold increase in insulin sensitivity (p less than 0.01) but no change in insulin responsiveness in femoral fat and only a decrease in responsiveness (p less than 0.01) in abdominal fat. The present data supports the view that antilipolysis in human fat cells is not involved in the insulin resistance seen in obesity, starvation, diabetes and hyperinsulinemia.
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PMID:The antilipolytic effect of insulin in human adipose tissue in obesity, diabetes mellitus, hyperinsulinemia, and starvation. 702 6

The effect of starvation was studied in male Wistar rats. After only 2 days of food deprivation, LH concentrations in serum are greatly suppressed, while a significant increase in plasma corticosterone occurs after 5 days' starvation. The noradrenaline and dopamine turnover in the basal hypothalamus is decreased after 2 days. The catecholamine turnover is also reduced in the preoptic area, and in the median eminence. Injection of the catecholamine precursor L-dopa (100 mg/kg) can prevent the increase of plasma corticosterone, but not the decrease of LH. The alpha-agonist clonidine (150 micrograms/kg), but neither the beta-agonist salbutamol (0.5 mg/kg), nor the dopamine agonist apomorphine (1.0 mg/kg) can prevent the starvation induced corticosterone increase. The decrease of plasma LH is not influenced by the dopamine or noradrenaline agonists. From these data, it appears that a decreased activity of noradrenergic neurons may be responsible for the corticosterone increase in the plasma of starved rats.
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PMID:Catecholamine turnover in the brain and the regulation of luteinizing hormone and corticosterone in starved male rats. 711 89

Changes in lipolysis was monitored by measuring the release of non-esterified fatty acids and glycerol under basal conditions and after stimulation with L-noradrenaline in rat adipose tissue in the course of continuous irradiation with daily gamma exposure doses of 0.57 Gy (60R) for 50 days. As compared with the control animals, lipolysis in the irradiated rats was lower on days 3-14, and higher on day 21-25-32 and at the end of the screening period (day 50) of continuous irradiation. The changes in lipolysis in the course of irradiation reflected individual stages of the general adaptation syndrome (Selye 1950). Many changes were modified by the effect of non-specific factors due to the experimental field and the starvation prior to the analysis. Changes in lipolysis were connected with changes in the mobilization of fatty acids and the concentrations of NEFA in white adipose tissue with changes in serum lipids predominantly in the period of 21-25 days of continuous irradiation.
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PMID:Changes in lipolysis in rat adipose tissue during continuous irradiation. 741 24

The relative stability against a decrease in adrenergic stimulation of the uncoupling protein (UCP) incorporated into different mitochondrial fractions was investigated in brown-fat-cell cultures. Cultures were initiated with undifferentiated cells from young mice and were acutely stimulated with noradrenaline at confluence (day 7). Cells were harvested just after the finish of the 24 h stimulation treatment or 24 h later, and three mitochondrial fractions were isolated by differential centrifugation: the M1 fraction (1000 g), the M3 fraction (3000 g) and the M15 fraction (15,000 g). The results obtained in vitro indicate that removal of adrenergic stimulation determines a selective loss of UCP from the lightest mitochondrial fractions (M3 and M15). Similar results were obtained in a situation in vivo (24 h starvation in mice) which is known to lead to a decreased noradrenaline input to brown adipose tissue, with decreased UCP levels. Thus brown adipocytes possess different mitochondrial subpopulations, which exhibit characteristic changes in their UCP turnover in response to thermogenic signals.
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PMID:Selective loss of the uncoupling protein from light versus heavy mitochondria of brown adipocytes after a decrease in noradrenergic stimulation in vivo and in vitro. 757 72

The effect of fasting for 12, 36 and 72 h was studied in twenty-nine healthy subjects (seventeen women and twelve men). Measurements were made of cardiovascular variables, metabolic rate, respiratory exchange ratio, plasma metabolites, insulin, thyroid hormones and catecholamines. During starvation there were no significant changes in blood pressure, whilst heart rate (beats/min) increased at 36 h and remained elevated after 72 h (12 h 62.5 (SE 1.8), 36 h 68.0 (SE 1.9), 72 h 69.2 (SE 1.8); P < 0.001). Forearm blood flow (FBF) increased progressively from 3.32 (SE 0.20) to 6.21 (SE 0.46) ml/100 ml per min (P < 0.001). Resting metabolic rate (kJ/min) was significantly increased after 36 h of starvation (12 h 4.60 (SE 0.14), 36 h 4.88 (SE 0.13), P < 0.001), but was not significantly different from the 12 h value after 72 h (72 h 4.72 (SE 0.15) P = 0.06). The respiratory exchange ratio fell progressively from 0.80 to 0.76 to 0.72 (P < 0.001). Blood glucose fell, whilst plasma glycerol and beta-hydroxybutyrate rose and plasma lactate did not change. Plasma insulin and free triiodothyronine fell during starvation. Plasma adrenaline and noradrenaline were unchanged at 36 h, but were significantly increased after 72 h. Both sexes showed a similar pattern of response to starvation, although absolute values of blood pressure, forearm blood flow, metabolic rate and plasma catecholamines were higher in men than women. Acute starvation produces profound cardiovascular and metabolic changes which are not explained by the accompanying hormonal changes.
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PMID:The cardiovascular, metabolic and hormonal changes accompanying acute starvation in men and women. 817 72

Norepinephrine and its metabolites were studied in various body fluids (plasma, urine and cerebrospinal fluid) of patients with anorexia nervosa, bulimia nervosa and healthy young women. The reaction of plasma norepinephrine to different stimuli like orthostatic challenge, test meals, standardized exercise, mental challenge tests etc. were studied. All results indicate a reduced noradrenergic activity in the central and peripheral nervous system of patients with eating disorders. The clinical consequences of these changes are hypotension, bradicardia, hypothermia and depression. Evidence is presented that the reduced activity of the sympathetic nervous system is caused by starvation (anorexia nervosa) or intermittent dieting (bulimia nervosa).
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PMID:Central and peripheral noradrenalin regulation in eating disorders. 873 14

When faced with stress, an organism calls upon several mechanisms to maintain biological homeostasis. The cardiovascular system is the first to respond usually with an increase in arterial pressure and tachycardia. Therefore we investigated the central and peripheral sympathetic responses to acute and chronic starvation in Wistar rats. The noradrenaline (NA) turnover rate was determined in different catecholaminergic nuclei (A1, A2, A5, A6) as well as the arterial blood pressure and heart rate modifications. During acute starvation (3 days of starvation), the NA turnover was increased in the A1 and rostral A2 nuclei as well as in ventricles and kidneys and decreased in the A6 nucleus. During chronic starvation (4 consecutive cycles of 3 days of starvation plus 1 day of feeding), the NA turnover was increased in the A5 and caudal A2 nuclei as well as in ventricles and atria and decreased in the A1 nucleus and kidneys. The arterial blood pressure revealed a gradual decrease during the first 3 days of fasting but the heart rate was not modified. We conclude that starvation should be considered as an unusual state of stress because of the absence of locus coeruleus response (A6 nucleus) despite its well-defined role in stress reactions. One of the manifestations of these central and peripheral noradrenergic changes is the change in blood pressure during the starvation-feeding cycles.
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PMID:Effects of acute and chronic starvation on central and peripheral noradrenaline turnover, blood pressure and heart rate in the rat. 1022 76

This investigation reports the possible role of the endocannabinoid anandamide on modulating the behavioral and neurochemical consequences of semi-starvation. We studied the effect of very low dose anandamide (0.001 mg/kg) administration on food intake, cognitive function and catecholaminergic and serotonergic pathways in two murine brain areas concerned with appetite (hypothalamus) and learning (hippocampus), and the peripheral corticosterone response to the stress of 40% diet restriction. Anandamide-treated mice consumed 44% more food (P<0.05) during 1 week of 2.5-h feeding each day. In the hypothalamus, there were significantly increased concentrations of norepinephrine (P<0.01), dopamine (P<0.05) and 5-hydroxytryptamine (5-HT) (P<0.001). In the hippocampus, anandamide increased significantly norepinephrine and dopamine, but decreased 5-HT (all at P<0.001). Diet restriction was accompanied in both areas by a significant decrease in all neurotransmitter concentrations that were partially restored by anandamide for dopamine and 5-HT, but not for norepinephrine. In animals on diet restriction, anandamide significantly improved impaired maze performance. Norepinephrine turnover and plasma corticosterone levels were also raised significantly by anandamide. The fact that low dose anandamide improved food intake, cognitive function and reversed some of the neurotransmitter changes caused by diet restriction, might have implications for the treatment of cachexia associated with acquired immunodeficiency syndrome (AIDS) and cancer, for mood changes sometimes associated with dieting, and in the extreme case, of patients with anorexia.
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PMID:Low dose anandamide affects food intake, cognitive function, neurotransmitter and corticosterone levels in diet-restricted mice. 1076 68


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