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

Starvation did not cause increase of hormone-sensitive lipase in rat epididymal adipose tissue. Adrenaline did not activate lipase in the fat cells, although it accelerated the release of free fatty acids from the cells. The results suggest that the mechanism of the stimulation of lipolysis by adrenaline is different from that in the cyclic AMP theory. Adrenaline-sensitive fat globules were prepared by hypotonic treatment of fat cells. Lipolysis in the fat globules was stimulated by adrenaline. It was shown that adrenaline-induced lipolysis in the fat globules was not due to activation of lipase but to initiation of a reaction between lipase and triglyceride. It is well known that calcium ions are essential for ACTH-induced lipolysis and that the hormone stimulates calcium uptake into adipose tissue. It was demonstrated that calcium ions accelerated formation of a complex between fat and lipase. The mechanism of the actions of adrenaline and ACTH are discussed on the basis of these results.
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PMID:Mechanism of actions of adrenaline and ACTH in fat mobilization. 17 4

The response of intact and bursectomized chicks to stressful stimuli has been examined. The stressors imposed were: a. fast-acting ACTH adminstration; b. immersion in cold water; c. starvation. In Bursa-intact chicks the results were as follows: 1. Plasma corticosterone was increased by all stimuli. 2. Adrenal corticosterone was decreased by ACTH treatment while it was increased by immersion in cold water and by starvation. 3. Plasma glucose was increased by ACTH administration and cold water immersion and decreased by starvation of the birds. 4. Adrenal ascorbic acid concentration was not influenced by all stimuli. 5. Adrenal weights were found to be increased by ACTH and starvation treatments only. 6. Bursa weights were increased by ACTH administration. 7. A very low concentration of corticosterone was found in the Bursa of Fabricius. Bursectomized chicks differed from the intact ones in the following: 1. Plasma and adrenal corticosterone concentrations were not increased by starvation. 2. Plasma glucose increased moderately with ACTH administration. 3. Adrenal ascorbic acid was depleted by all stimuli but was not related to the corticosterone level in the adrenals and blood plasma.
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PMID:Effects of stress on the corticosterone content of the blood plasma and adrenal gland of intact and bursectomized Gallus domesticus. 18 May 4

The activity and regulation of rat adrenal delta-aminolevulinic acid synthetase (EC 2.3.1.37) has been studied. The activity of delta-aminolevulinic acid synthetase in rat adrenal homogenates is comparable to the activity found in rat hepatic homogenates when untreated animals are employed. Starvation of rats for 24 and 48 hours increased adrenal delta-aminolevulinic acid synthetase activity without altering the hepatic enzyme. The treatment of rats with ACTH gel also increased adrenal delta-aminolevulinic acid synthetase activity. The effect of starvation on rat adrenal delta-aminolevulinic acid synthetase activity appears to be mediated by ACTH and can be prevented by the administration of dexamethasone. Adrenal delta-aminolevulinic acid synthetase appears to be refractory to induction by agents which induce the hepatic enzyme. These results suggest that the adrenal enzyme may be uniquely controlled by neural and endocrine influences which differ from the factors which regulate the activity of the hepatic enzyme.
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PMID:Studies on heme synthesis in the rat adrenal. 18 76

Metabolic and endocrine studies on a 7-year-old boy who presented with hypoglycaemic convulsions are reported in detail, proving the diagnosis of isolated ACTH deficiency--a rare cause of hypoglycaemia in childhood. Adrenaline secretion during insulin-induced hypoglycaemia was reduced. Low blood alanine levels occurred during starvation-induced hypoglycaemia, together with raised total blood ketone bodies; blood glucose did not increase adequately after oral alanine at this time. Hypoglycaemia in isolated ACTH deficiency appears to be due to a combination of impaired alanine mobilisation and a decreased rate of gluconeogenesis.
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PMID:Isolated ACTH deficiency. Metabolic and endocrine studies in a 7-year-old boy. 21 Jul 21

Changes in concentrations of metabolites of the main nutrients in the blood plasma, caused by weaning and by different body weight gains, by starvation, exogenous adrenaline and ASTH administration were studied in 141 weaned piglets of the Large White breed at an age of 26 to 69 days. After weaning, the total protein level showed a faster decrease in the intensively growing piglets than in those with lower growth rates. This rapid decrease was induced by adrenaline. The post-weaning levels of glucose decreased irrespective of the growth rate of the piglets. Adrenaline caused hyperglycaemia and, after 48 hours of starvation, hypoglycaemia. Urea levels significantly increased after weaning. During starvation they remained unchanged, even under exposure to hormonal effects. Cholesterol concentration decreased after weaning, after ACTH and adrenaline administration also showed a decrease. The concentration of non-esterified fatty acids decreased after weaning, the decrease being more pronounced in the piglets with less intensive growth. The action of adrenaline, ACTH, together with an increased level of glucocorticoids, increased the concentration of these acids even in the state of starvation. It is assumed that early piglet weaning implies great metabolic changes which need not impair growth if their character is transient. The author evaluates the suitability of the starter used and parameters chosen for the determination of the metabolic profile of pigs.
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PMID:[Effects of different growth rates in weaned piglets, starvation and hormonal action, on various metabolic parameters in the blood plasma]. 22 71

1. Regulation of gluconeogenic substrate supply and modulation of the gluconeogenic pathway in the liver are both important in the control of gluconeogenesis by glucocorticoids. 2. Adrenal deficiency decreases the release of gluconeogenic and other amino acids from skeletal muscle during starvation. The effect is reversed by glucocorticoid replacement. The changes in amino acid release are accompanied by similar alterations in tissue amino acid levels and are not explained by alterations in net protein breakdown. Glucocorticoids do not alter protein catabolism and cause a small inhibition of protein synthesis. The biochemical alterations underlying the changes in amino acid metabolism induced by these steroids remain to be elucidated. Glucocorticoids may also regulate the supply of gluconeogenic substrates through permissive effects on the lipolytic action of catecholamines and other hormones in adipose tissue and on the glycogenolytic action of catecholamines on skeletal muscle. 3. Glucocorticoids are required for the increases in gluconeogenesis in starvation and diabetes. Part of their action is exerted directly on the liver and appears to involve modulation of P-enlopyruvate carboxykinase levels. Glucocorticoids increase the synthesis of this enzyme apparently through effects at the level of transcription. 4. Glucocorticoids exert permissive effects on the stimulation of gluconeogenesis in the liver by glucagon and epinephrine. The steroids are not required for cAMP generation or protein kinase activation by these hormones, but appear to act by maintaining the responsiveness of certain enzymes to the effects of the cAMP and alpha-adrenergic systems. It is proposed that this involves the maintenance of a normal intracellular ionic environment.
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PMID:Regulation of gluconeogenesis by glucocorticoids. 38 91

4 children with ketotic hypoglycemia (KH) showed during a fasting period over 24 hours significant higher decreases of serum alanine levels than normal controls. Insulin induced hypoglycemia was followed by only minimal increase of urine epinephrine secretion, while all controls showed more than 6 times higher increases. 2-desoxy-glucose-tests were pathological in all cases with KH. One can speculate, that there is a connection between the reduced availability of alanine and the adrenal medullary hyporesponsiveness. Epinephrine stimulates glycogenolysis in muscle cells. Lack of epinephrine reduces pyruvate production and subsequently alanine synthesis. Alanine however is essential for gluconeogenesis in liver cells especially during starvation. After some days administration of diazoxide the 2-desoxy-glucose-test was normalised in all patients. This observation could probably be of some interest in therapy of KH.
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PMID:[Pathogenesis of ketotic hypoglycemia (author's transl)]. 41 97

Experiments show the influence of progressive starvation upon the synthetic and metabolic activity of monoaminergic function in the brain and the adrenal gland of young rats of two different ages. Brain and adrenal monoamine oxidase (MAO) showed a tendency to decline with the prolongation of the starvation interval. After 60 h of starvation, MAO activity was irreversibly decreased, even with 24 h of feeding, in the two age groups. Cerebral catechol-O-methyltransferase (COMT) activity was very slightly affected in response to the starvation in the older group, but the younger group showed an increased level of enzyme activity, and refeeding after 60 h of starvation of the young rats produced further increases. 60 h of starvation produced an increase in COMT activity of the adrenal gland of the older rats whereas the younger group did not show any marked change. Adrenal phenylethanolamine-N-methyltransferase (PNMT) declined after 24 and 48 h of starvation in the older rats, but the younger rats showed progressive increases after similar intervals of starvation. After 60 h of starvation, PNMT in the adrenal gland of the old rats increased significantly when compared to the control value, but the younger rats did not show any important change. Adrenal stores of adrenaline rose progressively up to 60 h of starvation in the old rats whereas the younger group responded in a contrary manner. Adrenal noradrenaline followed a similar pattern of evolution in both groups up to 60 h of starvation (when the results are expressed per milligram of adrenal protein), and refeeding had very little influence on the effects of starvation. The effects of starvation upon adrenal and cerebral MAO activity were verified with two different substrates. The results provide evidence that the metabolism of monoamines by oxidative deamination can be markedly affected by starvation, and this can be irreversible even after 24 h of feeding of starved rats. COMT activity augments when MAO activity declines.
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PMID:Influence of progressive starvation upon brain and adrenal monoaminergic activity in developing rats of two different ages. 47 96

The mechanism and cellular targets of mononuclear cell depletion were investigated in strains of mice susceptible or resistant to lethal infection with a virulent street rabies virus (SRV). Significant depletion was evident in the thymus of all infected animals at approximately 5 days postinfection and subsequently involved the spleen and lymph nodes in mice developing clinical signs of rabies. Immunofluorescent analyses of lymphocyte subsets in depleted spleens revealed that cell losses were non-selective since the relative proportions of K+, Thy-1+, Lyt-1+, and Lyt-2+ cells remained unchanged. Diminished expression of I-A membrane glycoproteins on spleen lymphocytes was noted, however, perhaps reflecting reduced availability of I-A-inducing lymphokines. Adrenal hormone toxicity was identified as the cause of mononuclear cell depletion in that mice adrenalectomized before SRV infection showed no evidence of lymphoid depletion. The failure of adrenalectomy to alter anti-rabies antibody responses or SRV lethality also indicates that involution of the lymphoid system is a consequence and not a cause of genetically controlled host susceptibility to SRV. The mechanism of adrenal gland stimulation in rabies-infected mice appears to involve a virus-induced dysfunction in the pituitary gland rather than a stress response to paralysis-induced starvation, based on results of kinetic studies on weight loss, appetite depression, and paralysis in these animals and previous reports of pituitary infection during rabies disease. The relationship of these observations to current theories on rabies virus pathogenicity is discussed.
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PMID:Murine susceptibility to street rabies virus is unrelated to induction of host lymphoid depletion. 232 81

Lactose synthesis and fatty acid synthesis in intact lactating-rat mammary gland were measured simultaneously by incorporation of [U-14C]glucose and of both [U-14C]glucose and 3H2O respectively. Both processes were almost abolished by overnight starvation. Self-re-feeding caused recovery of lipogenesis to 100% of normal by 2 h and to 170% by 5 h. Lactose synthesis recovered to 80% of normal by 5 h. Food intubated to starved rats caused partial recovery in 3 h, standard diet favouring lactose synthesis and sugars favouring lipogenesis. Casein and starch were ineffective. Olive oil intubated to fed rats suppressed lipogenesis greatly and lactose synthesis slightly. Paraffin oil or water partly mimicked these effects. Adrenaline (subcutaneous) decreased lipogenesis from glucose, whereas insulin (subcutaneous) caused hypoglycaemia associated with loss of lactose synthesis but unchanged fatty acid synthesis. Streptozotocin and 2-bromo-alpha-ergocryptine (CB-154) impaired lipogenesis but not lactose synthesis. The results are interpreted in terms of competition for intracellular glucose by biosynthetic pathways for lactose and fat, and the possible implications for variations in milk composition are discussed.
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PMID:Lactose and fatty acid synthesis in lactating-rat mammary gland. Effects of starvation, re-feeding, and administration of insulin, adrenaline, streptozotocin and 2-bromo-alpha-ergocryptine. 623 23


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