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

Branched chain amino acids were administered intragastrically in a septic-fractured rat model to determine the degree and mechanism of their protein-sparing ability. The septic injury model was first shown to produce a metabolic response characterized by hyperglycemia, reduced ketonemia and increased nitrogen loss. Branched chain amino acids were then administered either alone or as 25% or 50% (w/w) of a complete crystalline amino acid solution. L-(U-14C)-tyrosine was added to the diet to estimate protein synthesis in individual tissues. Branched chain amino acids, when given alone, spared total body nitrogen as compared with fasting by increasing the fractional synthesis of both mixed liver and muscle protein. Although the two complete amino acid mixtures produced similar nitrogen preservation and muscle synthesis in the septic animals, the crystalline amino acid diet containing 50% branched chain amino acids resulted in the greatest preservation of total liver nitrogen and the highest fractional synthetic rate. The effect of branched chain amino acids would not appear to be explained by their nitrogen content alone, and in starvation with injury and infection, increased intakes may have potential benefit. Clinical trials in starved, injured man appear to be indicated.
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PMID:Branched chain amino acid administration and metabolism during starvation, injury, and infection. 11 63

The sensitivity to alloxan was investigated by blood and urine glucose determination and light and electron microscopic study of the endocrine pancreas in groups of mice differing from each other with respect to food ingestion and treatment before alloxan administration. Because of differences in occurrence of glucosuria, degree and duration of hyperglycemia, and severity of structural lesions, it was concluded that starvation increases the alloxan sensitivity and that pre-treatment with 1.25-dihydroxycholecalciferol (DHCC) or parathormone (PTH), but not with Ca2+, enhances the alloxan effect. The serum-calcium concentration determined 10 minutes after pre-treatment was significantly increased in the group given Ca2+, but not in the groups injected with DHCC or PTH. Starved mice injected with DHCC or PTH 10 minutes before alloxan administration exhibited a pronounced second hyperglycemia of long duration, and extensive, selective B-cell necrosis. Starvation and increased serum concentration of DHCC and PTH are believed, directly or indirectly, to induce B-cell alterations which increase the alloxan sensitivity.
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PMID:Effects of 1.25-dihydroxycholecalciferol, parathormone and Ca2+ on the pancreatic B-cell sensitivity to alloxan. 33 60

Long-term hyperinsulinemia and improved glucose tolerance were produced postoperatively by intravenous feeding with glucose or sorbitol. Raised immuno-reactive insulin (IRI) values persisted eight hours after carbohydrate infusions although the basal plasma glucose concentrations had returned to control values. Plasma glucose curves were normal at this time but were associated with an increased IRI response. These findings suggest that insulin secretion is modified by glucose not only in the short term but also by a separate effect acting over many hours. The combination of starvation and low dose glucose infusion to simulate the hyperglycemia of operation also produced high IRI values but these were associated with a rapid fall in the plasma glucose curve. Starvation alone reduced basal values of plasma glucose and IRI, and the IRI response to glucose infusion was also reduced, despite the plasma glucose curve being at a higher level. It is suggested that the high values of IRI reported in the postoperative period are mediated by a long-term effect of the small but sustained rise in basal plasma glucose. This specific role of glucose in the long-term potentiation of insulin secretion make it the carbohydrate of choice for the intravenous feeding in postoperative patients.
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PMID:Plasma insulin and surgery. II. Later changes and the effect of intravenous carbohydrates. 41 64

Detailed studies of hepatic metabolism of lipemic BHE and nonlipemic Wistar rats were conducted. Hepatic lipogenic capacity was varied through the use of starvation or meal feeding. Livers were clamped in precooled copper plates and used for the assay of glycolytic, gluconeogenic, and lipogenic metabolites. Redox and phosphorylation states were calculated. Mitochondrial metabolism was evaluated through studies of the oxygen consumption of isolated mitochondria and through the study of the activities of the alpha-glycerophosphate and malate aspartate shuttles and ATPase. BHE rats have higher phosphorylation states, higher redox ratios, and lower shuttle activities and oxygen consumption by isolated mitochondria than their Wistar cohorts. The differences in oxidative phosphorylation, redox and phosphorylation states, and in the various shuttle activities suggest that BHE liver cells are geared towards lipogenesis at the expense of oxidative phosphorylation. It appears that the activity of the shuttles is controlled in part by phosphorylation state which in turn appears to affect respiration. We theorize from these data that genetically determined differences in the structure and function of the mitochondrial membrane (and perhaps the cell membrane as well) may affect the communication (via metabolites and adenine nucleotides) between the cytosol and mitochondria. Subtle differences in the exchange of metabolites and/or adenine nucleotides across the mitochondrial membrane could thus explain the lipogenic tendency of the liver of the BHE rat and the subsequent development of maturity onset hyperlipemia and hyperglycemia in this strain of rat.
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PMID:Studies on the control of lipogenesis: strain differences in hepatic metabolism. 43 Feb 26

Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having "alcoholic ketoacidosis" because they had ketonuria or ketonemia with little or no glucosuria. Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L. Fifteen of this group were not diabetic, while six were later found to have mild postprandial hyperglycemia without glycosuria. Three patients who had continued to drink until shortly before admission, though at first suspected of having alcoholic ketosis, were found to have predominant lactic acidosis, with minor elevations of plasma 3-hydroxybutyrate. In contrast to previously reported patients with "alcoholic ketoacidosis", severe acidemia was uncommon in this series. Indeed, seven patients were alkalemic, because of coexisting respiratory or metabolic alkalosis. Most patients had eaten poorly for several days (and usually longer) and had allegedly decreased their alcohol intake during that period. That history, and the usual rapid clearing of ketosis simply by treatment with solutions of glucose and NaCl, suggested that acute starvation was an important factor in the pathogenesis of this disorder. Four patients were treated with insulin and four with NaHCO3 solutions. In retrospect, the need for either of these treatments was not clear. Two of the twenty-four patients died, one from circulatory failure secondary to hemorrhage and the other from pulmonary edema, but no patient died because of ketoacidosis per se.
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PMID:Alcoholic detosis. 80 36

The responses of hepatic glycogen synthase and phosphorylase to fasting and refeeding were assessed as part of an investigation into possible sites of insulin resistance in gold thioglucose (GTG) obese mice. The active forms glycogen synthase and phosphorylase (synthase I and phosphorylase a) and the total activity of these enzymes were estimated in lean and GTG mice over 48 h of food deprivation, and for 120 min after glucose gavage (1 g/kg wt). In lean mice there was a maximal reduction in hepatic glycogen content after 12 h of starvation and the activity of phosphorylase a decreased from 23.8 +/- 1.9 to 6.8 +/- 0.7 mumol/g protein/min. These changes were accompanied by an increase in the activity of synthase I (from 0.14 +/- 0.01 to 0.46 +/- 0.04 mumol/g protein/min). In obese mice, similar changes in enzyme activity occurred after 48 h of starvation. These changes were accompanied by a significant reduction in the hyperinsulinemia and hyperglycemia of the GTG mice. After glucose gavage in both lean and obese mice, the activity of synthase I further increased over the first 30 min and declined thereafter. The activity of phosphorylase a increased progressively after refeeding. Results from this study suggest that despite increased hepatic glycogen deposition, the responses of glycogen synthase and phosphorylase, in livers of obese mice, to fasting and refeeding are similar to those of control mice even in the presence of insulin resistance.
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PMID:The effects of fasting and refeeding on liver glycogen synthase and phosphorylase in obese and lean mice. 160 90

In order to study mechanisms in ruminants responsible for glucocorticoid-induced hyperglycemia the effects of a single intravenous dose of a glucocorticoid on energy metabolism were investigated by measuring plasma levels of glucose, lactate, free fatty acids (FFA), 3-hydroxybutyrate (3-HOB) and acetoacetate (AcAc). Experiments were performed on four castrated male African pygmy goats at two metabolic states: "fed" with a single daily meal of hey and "fasted" with starvation for 3 days. The untreated goats served as their own control. The glucocorticoid application to fed animals resulted in an increase in glucose level (+43%) lasting more than 11 h and an irregular increase of lactate. The concentration of 3-HOB was increased especially before feeding (+64%). In contrast, FFA were decreased (-27%) the second day after glucocorticoid application. In fasted goats the glucocorticoid also caused an increase in glucose level (+25%). The effect was smaller than in fed animals. Concentrations of FFA, 3-HOB and AcAc were 10, 20 and 35% lower than those of untreated goats. With regard to the antiketotic use of glucocorticoids the decrease of plasma levels of FFA and ketone bodies in starving animals is of special importance. Obviously the animals were able to use glucose again as a main energy source instead of FFA.
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PMID:[The effect of glucocorticoid on the glucose metabolism of pigmy goats. 1. Selected metabolites of energy metabolism]. 211 Apr

In the present study glucose kinetic parameters like pool size, distribution volume and rates of total entry and irreversible loss were determined in four castrated male African pygmy goats during hyperglycemia induced by an intravenous glucocorticoid injection (0.25 mg dexamethasone = DXM per kg body weight). Experiments were done at two different metabolic states, "fed" once daily and "fasted" after three days of starvation. The use of [U-14C]- together with [2-3H]- or [6-3H]-glucose made it possible to show changes in rates of gluconeogenesis, phosphorylation and specific recycling of glucose-C (e.g. lactate/alanine). During glucocorticoid induced hyperglycemia (+45%) in fed animals de novo synthesis of glucose (+5%) and lactate/alanine recycling increased (+4%). Rates of irreversible loss for all applied tracers in fasted animals formed only two thirds of the values of fed animals. During hyperglycemia (+40%) after DXM-injection de novo synthesis of glucose (+8%) and lactate/alanine recycling also increased (+27%). Furthermore the rate of phosphorylation of glucose decreased in fasted pygmy goats. The increase in availability of glucose both in fed and fasted animals is due to an increase in gluconeogenesis. In fasted animals additionally a decrease in the rate of phosphorylation and therefore of the peripheral glucose turnover has to be considered.
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PMID:[The effect of glucocorticoids on glucose metabolism in pygmy goats. 2. Glucose turnover and recycling]. 212 56

It was the aim of the present study to examine, at different stages of the obese-hyperglycemic syndrome, rates of islet-cell DNA replication in endogenous pancreatic and grafted islets of such mice. For this purpose obese-hyperglycemic mice were given an islet transplant prepared from lean mice under the kidney capsule. Two weeks later the animals were given an IP injection of 3H-thymidine one hour before being killed. Autoradiography of pancreas and kidney sections indicated the highest labeling index (LI) for the endogenous islet cells in the youngest obese mice (6 weeks old), which was more than fivefold higher than that of lean, normoglycemic controls. The LI, however, decreased extensively with age. The transplanted islets had LI, which were higher and constant during the most intense period of the syndrome, but again there was a decrease in the oldest mice. By isolating and transplanting islets of the oldest obese mice (greater than 12 months) into younger obese mice, it was possible to revive the high cell replicatory activity of the ob/ob islets. Starvation for three days was found to markedly decrease the rate of islet cell DNA replication. Adrenalectomy of obese-hyperglycemic mice resulted in a decrease of the serum glucose and insulin concentrations; concomitantly, there was a decrease of LI of both transplanted and endogenous islets. Thus, it seems as if the attenuation of the hyperglycemia is most probably responsible for the decline of the islet cell replication with increasing age in obese-hyperglycemic mice.
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PMID:DNA replication in transplanted and endogenous pancreatic islets of obese-hyperglycemic mice at different stages of the syndrome. 250 79

Though children with febrile convulsions only have seizures in the early stage of a febrile illness and not later, these seizures have been attributed to the fever. We studied the serum electrolyte and metabolite profiles in the later stage to see if there were fuel responses resulting in electrophysiological changes which prevented further seizure activity. On admission there was intracellular glucose starvation, as evidenced by increased ketones and lactate, and the possibility of the failure of some electrolyte pumps, as suggested by hyperuricaemia (energy crisis) and decreased serum Na+, Cl- and Ca2+. However, there was adaptive hyperglycemia and decreased serum K+. It seems likely that the hyperglycemia, induced the uptake of K+ by neurones, enabling their repolarization and hyperpolarization, which prevented further seizure activity, while Cl- influx short-circuited depolarizing currents produced by Na+ influx. Studies during recovery showed a gradual return of the metabolic and electrolyte aberrations to normality, suggesting that the provision of energy through adaptation to the stress, enabled recovery of the aforementioned pumps.
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PMID:Hyperpolarization and short-circuiting as mechanisms of seizure prevention following febrile convulsions. 277 93


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