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

The pattern of substrate uptake by the heart in prolonged starvation, when lipid reserves are approaching depletion, has been examined. The classical Langendorff perfused heart preparation was employed to determine substrate uptakes in male rats fed ad libitum or starved for 7 days. Levels of metabolites in "arterial" and "venous" perfusion media and in heart tissue were determined by fluoroenzymatic assays, with the exception of palmitic acid which was analyzed by gas chromatography. It was found that glucose is the principal fuel of oxidation in perfused hearts of ad libitum-fed rats, whereas palmitate (FFA) is the major fuel of oxidation in perfused hearts of starved rats, followed by lactate, glucose, beta-hydroxybutyrate, pyruvate and alanine. Such changes might be related to some of the alterations in the metabolic pathway (e.g., glycolytic inhibition) in prolonged starvation.
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PMID:Effect of prolonged starvation on substrate uptake in the isolated perfused rat heart. 51 2

A tracer kinetic study with [14C]-1-palmitic acid was carried out to study the influence of acute exposure to cold and starvation on free fatty acid (FFA) metabolism in serum of newborn rabbits. The turnover rate of serum FFA was 10.20 mumol/min in well fed rabbits kept in a thermoneutral environment (normal conditions). Cold exposure as well as starvation either in a cold or thermoneutral environment resulted in a diminution of the turnover rate, being the consequence of a significantly reduced pool of FFA. It was 9.57 mumol under normal conditions. The disappearance rate (1.07 min-1), half time (0.65 min) and turnover time (0.94 min) of well nourished animals was slightly, but mostly not significantly, influenced by cold exposure and starvation. The cold induced increase in serum FFA concentration and the decrease following restoration of thermoneutrality did not run parallel with changes in the absolute turnover rate.
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PMID:[The effect of cold and hunger on the free fatty acid metabolism in the serum of newborn rabbits]. 123 80

Palmitate ability to modify D-[U-14C]glucose incorporation into different lipids ("de novo" synthesis), as well as sugar-stimulation of insulin release and 45Ca2+-fluxes, was investigated in islets of fed and 48-h starved rats. The fatty-acid induced dose-dependent, correlative increments of insulin secretion, 45Ca2+-influx and the "de novo" synthesis of each phospholipid fraction analysed at 20 mmol/l (but not 3 mmol/l) glucose. Omission of calcium reduced drastically (p less than 0.001) insulin release and the "de novo" synthesis of neutral glycerolipids, leaving unaltered that of acidic phospholipids (phosphatidate and phosphoinositides). The increased synthesis of the latter is therefore not the consequence of stimulated secretion. It could initiate or contribute to maintain an increased turnover of islet phosphoinositides, thus generating some mediators of the calcium signalling system (inositol phosphates). Starvation led to a drastic reduction (p less than 0.001) of both insulin secretion, "de novo" synthesis of each lipid fraction, and 45Ca2+-influx in response to glucose and palmitate. The presence of a fatty-acid oxidation inhibitor (2-bromostearate or 2-tetradecylglycidate) prevented the effect of starvation on 45Ca2+-influx, as it has been shown to do on insulin secretion and palmitate incorporation into islet lipids. It is finally suggested that palmitate might amplify the insulin secretory response of islets to glucose, through the stimulation of the "de novo" synthesis of phosphoinositides and the subsequent generation of inositol phosphates, which would contribute to accelerated calcium turnover.
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PMID:Palmitate dependence of insulin secretion, "de novo" phospholipid synthesis and 45Ca2+-turnover in glucose stimulated rat islets. 306 35

The influence of a physiologic range of palmitate concentrations (0, 0.25, 0.5, and 1.0 mmol/L) on glucose ability to modify insulin secretion, (U-14C) palmitate oxidation, and (U-14C) glucose incorporation into lipids has been studied in islets isolated from either fed or 48-hour starved rats. Palmitate potentiated the insulin response of fed islets to glucose in a particular dose-related manner. Glucose stimulated secretion was accompanied by a decreased palmitate oxidation and an increased (U-14C) glucose incorporation into di-, tri-acylglycerols, and predominantly into phospholipids. These metabolic parameters showed also a positive dependence on palmitate concentration. Starvation increased islet capacity to oxidize palmitate, rendered it insensitive to glucose inhibition, and inhibited both (U-14C) glucose incorporation into all lipid fractions and sugar induced insulin release. The stimulation of islet lipid synthesis by glucose seems to be limited by the exogenous supply of fatty acids and their rate of oxidation. As judged from (U-14C) glucose incorporation data, the rate of phospholipid biosynthesis showed a significant and positive correlation with insulin secretion. This metabolic pathway might provide islet cells with some lipid intermediates (diacylglycerol and/or specific phospholipids) that have been considered as possible mediators of the calcium messenger system.
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PMID:Glucose stimulation of insulin secretion in islets of fed and starved rats and its dependence on lipid metabolism. 351 58

1. 0.5mm-Palmitate stimulated incorporation of [U-(14)C]glucose into glyceride glycerol and fatty acids in normal fat cells in a manner dependent upon the glucose concentration. 2. In the presence of insulin the incorporation of 5mm-glucose into glyceride fatty acids was increased by concentrations of palmitate, adrenaline and 6-N-2'-O-dibutyryladenosine 3':5'-cyclic monophosphate up to 0.5mm, 0.5mum and 0.5mm respectively. Higher concentrations of these agents produced progressive decreases in the rate of glucose incorporation into fatty acids. 3. The effects of palmitate and lipolytic agents upon the measured parameters of glucose utilization were similar, suggesting that the effects of lipolytic agents are mediated through increased concentrations of free fatty acids. 4. In fat cells from 24h-starved rats, maximal stimulation of glucose incorporation into fatty acids was achieved with 0.25mm-palmitate. Higher concentrations of palmitate were inhibitory. In fat cells from 72h-starved rats, palmitate only stimulated glucose incorporation into fatty acids at high concentrations of palmitate (1mm and above). 5. The ability of fat cells to incorporate glucose into glyceride glycerol in the presence of palmitate decreased with increasing periods of starvation. 6. It is suggested that low concentrations of free fatty acids stimulate fatty acid synthesis from glucose by increasing the utilization of ATP and cytoplasmic NADH for esterification of these free fatty acids. When esterification of free fatty acids does not keep pace with their provision, inhibition of fatty acid synthesis occurs. Provision of free fatty acids far in excess of the esterification capacity of the cells leads to uncoupling of oxidative phosphorylation and a secondary stimulation of fatty acid synthesis from glucose.
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PMID:The regulation of glyceride synthesis in isolated white-fat cells. The effects of palmitate and lipolytic agents. 434 51

Mycobacterium avium, a facultative pathogen for humans, undergoes a life cycle in which selected small cells elongate and then fragment to form coccobacilli. M. avium cells of uniform size were selected by membrane filtration and tested for growth and division in the presence or absence of palmitic acid. Growth was measured by increased cellular protein, and cell division was determined by increased colony-forming units on agar or, electronically, by increased numbers of particles. Both growth and division rates of M. avium were found to be dependent upon the initial concentration of palmitic acid presented to the cells. The division constant varied from 0.05 to 0.13 when the concentration of palmitic acid ranged from 0 to 175 nmol/ml of medium. With [(14)C]palmitic acid as a tracer, it was found that rapid cell division began upon cessation of fatty acid uptake. During division, new lipid materials were released which contained (14)C derived from [(14)C]palmitic acid. Limited cell division and no fragmentation occurred in fatty acid-starved cultures. During fatty acid starvation, the transparent colony form, considered a pathogen, underwent a transition to the colony form considered a nonpathogen. The possible relationships between the organism's dependence on fatty acid and its ability to infect humans are discussed.
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PMID:Effect of palmitic acid utilization on cell division in Mycobacterium avium. 481 62

1. Measurements were made of milk yield, mammary blood flow and mammary arteriovenous differences during the measurement of substrate entry rate by the isotope dilution method using [U-(14)C]glucose, acetate, palmitate, stearate or oleate in conscious lactating goats after 24 hr starvation.2. As previously reported, in fasting, milk yield fell to 40 +/- 3.4 (S.E.)%, lactose secretion to 31 +/- 3.4%, milk fat secretion to 81 +/- 6.7% and mammary blood flow fell to 53 +/- 7.5% of the values before fasting. Mammary O(2) uptake was only 45 +/- 5% of the mean value in fed animals and there were marked falls in the uptakes of glucose, acetate and triglycerides, a smaller fall in beta-hydroxybutyrate uptake, and a large increase in free fatty acid uptake.3. Glucose was found to enter the circulation of the fasting animal at 1-1.6 mg/min/kg body wt. (entry rate) and it gave rise to 3-5% of the total CO(2). The udder took up 10.7-16.1 mg/min/kg of tissue and 8-10% of mammary CO(2) was derived from glucose, although only 5-10% was oxidized. Mammary uptake accounted for 35-43% of the total glucose entering the circulation.4. In the whole animal acetate entry rate was 1-1.4 mg/min/kg and 9-10% of total CO(2) was derived from it. The udder used 0.8-2.4 mg/min/kg of tissue and 9-13% of mammary CO(2) was derived from acetate, 46-79% of that taken up being oxidized. Mammary uptake accounted for only 2-6% of the total acetate entry rate. Negligible quantities of isotope were found in milk fatty acids and there was a fall in the proportion of milk fatty acids of chain length up to C(14) which in fed animals are synthesized from acetate and beta-hydroxybutyrate.5. Palmitate, stearate and oleate entered the circulation as free fatty acids at 0.94-6.8 mg/min/kg and 6-9% of total CO(2) was derived from each. The udder took up 3.0-5.7 mg/min/kg of tissue and 4-8% of mammary CO(2) was derived from each acid. In the udder 8 and 5.5% of stearate and oleate were oxidized and 25% of palmitate. Mammary uptake of stearate was 31.5% of the total entry rate, palmitate 1%, and oleate 7.5%. Only long chain milk fatty acids were labelled.6. During fasting the mammary R.Q. was 0.85 +/- 0.045 compared with a value in fed animals of 1.24 +/- 0.02, when the udder is synthesizing fatty acids from acetate. The total mammary uptake of lipid precursors was only 74% of the rate of milk fat secretion and there was an 18% shrinkage in empty udder volume, suggesting the use of endogenous mammary tissue substrates.
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PMID:Mammary and whole animal metabolism of glucose and fatty acids in fasting lactating goats. 571 53

1. The rate of entry into the plasma of stearic acid in fed and starved non-pregnant sheep and of palmitic acid in fed and starved pregnant sheep has been measured by a continuous-infusion isotope-dilution method. 2. In non-pregnant sheep the entry rate of stearic acid rose from 0.38mg./min./kg. when fed to 0.69mg./min./kg. after 72hr. starvation. In pregnant sheep, the entry rate of palmitic acid rose from 0.55mg./min./kg. when fed to 0.64mg./min./kg. on starvation. 3. The entry rates of palmitic acid and stearic acid are related to their respective plasma concentrations. 4. At a given plasma concentration the entry rate of palmitic acid in pregnant sheep was greater than that of stearic acid in non-pregnant sheep. 5. There was no detectable conversion of palmitate or stearate into other plasma long-chain fatty acids. There was negligible incorporation of fatty acids into other plasma lipids with the exception of the plasma triglycerides of fed pregnant sheep. 6. Up to 12% of expired carbon dioxide was derived from palmitic acid or stearic acid. The high rate of oxidation of plasma palmitic acid in fed pregnant sheep is noteworthy.
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PMID:Utilization of free fatty acids by starved and pregnant sheep. 600 75

1. Starvation did not affect the rates of glucose utilization or lactate formation by guinea-pig cerebral cortex slices. 2. Palmitate (1mm), butyrate (5mm) or acetoacetate (5mm) did not affect glucose utilization or lactate formation by cerebral cortex slices from guinea pigs starved for 48hr. 3. dl-beta-Hydroxybutyrate (10mm) increased the formation of lactate without affecting glucose utilization by cerebral cortex slices from guinea pigs starved for 48hr. This implies that beta-hydroxybutyrate decreased the rate of glucose oxidation. 4. Metabolism of added ketone bodies can account for 20-40% of observed rates of oxygen consumption. 5. Lactate or pyruvate (5mm) decreased the rates of glucose utilization by guinea-pig cerebral cortex slices.
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PMID:Effects of fatty acids, ketone bodies, lactate and pyruvate on glucose utilization by guinea-pig cerebral cortex slices. 604 93

The hypothesis was made of an increased oxidation of fatty acids (FFA) and a decrease of their esterification rate contributing to the islet secretory defect during starvation. 2-Bromostearate (BrS), a FFA-oxidation inhibitor, was therefore tested on the islet secretion of insulin, glucagon and somatostatin stimulated by glucose or palmitate under fasted or fed conditions. Starvation for 48 h blocked both the glucose-induced stimulation and inhibition of insulin and somatostatin and the glucagon secretion. BrS completely restored the insulin response and stimulated both somatostatin and glucagon-basal release, the latter inhibition by glucose being partially recovered. Palmitate transient stimulation of insulin and somatostatin and inhibition of glucagon release was turned into a sustained increase in all three cases by addition of BrS. The potentiation by BrS of palmitate secretory effects in "fed" islets and of hormone release in "fasted" islets, apparently suggest that inhibition of FFA-oxidation may play a role in the regulation of islet secretion.
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PMID:Starvation-induced secretory changes of insulin, somatostatin, and glucagon and their modification by 2-bromostearate. 614 16


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