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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

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. 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

This study was designed to ascertain whether the overall availability of whole-body lipids and nitrogen is a limiting factor for survival in tumor-bearing mice suffering from anorexia and cachexia. Three-month-old nongrowing mice (C57BL/6J) were given s.c. transplants of a methylcholanthrene-induced sarcoma. Freely fed, starved, and pair-fed animals were used. Body and lipid composition, tumor growth, and survival time were measured. Freely fed sarcoma-bearing mice died with profoundly altered body composition. This was not explained by the anorexia assessed in pair-feeding experiments. Starvation had caused a more severe depletion in body composition in both tumor-bearing and nontumor-bearing animals than the tumor alone did in freely fed tumor-bearing mice. Freely fed tumor-bearing animals had normal proportions of whole-body triglycerides, cholesterol, and polar lipids, but they lost palmitic acid quantitatively more than any other fatty acid. It is unlikely that any single fatty acid became limiting during tumor growth. The results show that the overall availability of lipids, nitrogen, and glucose precursors is not a limiting factor for survival in experimental tumor cachexia. Other factors considered to be more likely as determining factors for the death of tumor-bearing animals are discussed.
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PMID:Role of whole-body lipids and nitrogen as limiting factors for survival in tumor-bearing mice with anorexia and cachexia. 657 17

The conversion of radioactive C6-C16-monocarboxylic acids to urinary adipic, suberic, sebacic and 3-hydroxybutyric acids was investigated in vivo in unstarved, starved and diabetic ketotic rats. Hexanoic, octanoic and decanoic acids were converted to C6-, C6-C8- and C6-C10-dicarboxylic acids, respectively, in fed and 72-h-starved rats. Lauric acid was converted to C6-C8-dicarboxylic acids in starved rats but not in unstarved rats. Decanoic and lauric acids were converted to relatively high amounts of C6-C8-dicarboxylic acids compared with myristic acid in myristic acid in ketotic diabetic rats, while radioactivity from [1-14C]-and [16-(14)] palmitic acid was not incorporated into C6-C8-dicarboxylic acids in diabetic ketotic rats. C6-C12-monocarboxylic acids in hydrolysed rat adipose tissue wee determined by gas-liquid chromatography-mass spectrometry (selected ion monitoring). Decanoic and lauric acids were found in amounts of 7.6-9.1 and 85.9-137.5 micrometers/100 mg tissue, respectively, whereas the amounts of hexanoic and octanoic acids were negligible. It is concluded that the biological origin of the C6-C8-dicarboxylic aciduria seen in ketotic rats are C10-C14-monocarboxylic acids, which are initially omega-oxidised solely or partly as free acids and subsequently beta-oxidised to adipic and suberic acids. The in vitro omega-oxidation of C6-C16-monocarboxylic acids to corresponding dicarboxylic acids in the 100,000 Xg supernatant fraction of rat liver homogenate was measured by selected ion monitoring. 0.09, 0.14, 16.1, 5.8, 7.0 and -6.9% of, respectively, hexanoic, octanoic, decanoic, lauric, myristic and palmitic acid were omega-oxidised to dicarboxylic acids of corresponding chain lengths after 90 min of incubation, when correction for the production of dicarboxylic acids in control assays was made. An in vitro production of C12-C16-dicarboxylic acids was detected in all assays ()including control assays), probably formed from"endogenous' monocarboxylic acids preexistent in the homogenate. Ths "endogenous' production of dicarboxylic acids was inhibited by C10-C16-monocarboxylic acids, where palmitic acid had the strongest effect. In fact, palmitic acid inhibited its own omega-oxidation when added in concentrations above 0.6 mM. Starvation of rats for 72 h did not alter the "endogenous' in vitro production of hexadecanedioic acid.
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PMID:The biological origin of ketotic dicarboxylic aciduria. In vivo and in vitro investigations of the omega-oxidation of C6-C16-monocarboxylic acids in unstarved, starved and diabetic rats. 679 96

Cell growth of Saccharomyces cerevisiae ATCC 12341 inhibited by the antibiotic cerulenin, a specific inhibitor of fatty acid synthesis, was restored by oleic acid (18 : 1) to give saturated fatty acid-starved cells, which could not grow when again transferred into a fresh synthetic medium containing the antibiotic and oleic acid. The growth of the saturated fatty acid-starved cells was restored when they were transferred into a medium supplemented with myristic acid (14 : 0), pentadecanoic acid (15 : 0), and palmitic acid (16 : 0) in the presence of cerulenin and oleic acid. Cellular saturated fatty acid content in the growth-restored cells was also restored to about two-thirds of that of the normal yeast cells. The DNA, RNA, and cell wall synthetic capabilities of the saturated fatty acid-starved cells were almost normal, but the L-leucine uptake and cytochrome pattern were severely impaired. These impairments were reversed on supplying palmitic acid. The decrease of L-leucine uptake of the yeasts was also caused by the addition of cerulenin alone. However, since the decrease occurred later than the inhibition of fatty acid synthesis, it was considered to be a secondary effect. These results, obtained by using the saturated fatty acid-starved cells, indicate that the membranes of S. cerevisiae require certain amounts of saturated fatty acid and that the membrane functions (energy metabolism, transport, and so on) are impaired by starvation of saturated fatty acids.
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PMID:Saturated fatty acid-starved cells of Saccharomyces cerevisiae grown in the presence of cerulenin and oleic acid. 701 49

The aim of the present study was to investigate the hepatic regulation and beta-oxidation of long-chain fatty acids in peroxisomes and mitochondria, after 3-thia- tetradecylthioacetic acid (C14-S-acetic acid) treatment. When palmitoyl-CoA and palmitoyl-L-carnitine were used as substrates, hepatic formation of acid-soluble products was significantly increased in C14-S-acetic acid treated rats. Administration of C14-S-acetic acid resulted in increased enzyme activity and mRNA levels of hepatic mitochondrial carnitine palmitoyltransferase (CPT)-II. CPT-II activity correlated with both palmitoyl-CoA and palmitoyl-L-carnitine oxidation in rats treated with different chain-length 3-thia fatty acids. CPT-I activity and mRNA levels were, however, marginally affected. The hepatic CPT-II activity was mainly localized in the mitochondrial fraction, whereas the CPT-I activity was enriched in the mitochondrial, peroxisomal, and microsomal fractions. In C14-S-acetic acid-treated rats, the specific activity of peroxisomal and microsomal CPT-I increased, whereas the mitochondrial activity tended to decrease. C14-S-Acetyl-CoA inhibited CPT-I activity in vitro. The sensitivity of CPT-I to malonyl-CoA was unchanged, and the hepatic malonyl-CoA concentration increased after C14-S-acetic acid treatment. The mRNA levels of acetyl-CoA carboxylase increased. In hepatocytes cultured from palmitic acid- and C14-S-acetic acid-treated rats, the CPT-I inhibitor etomoxir inhibited the formation of acid-soluble products 91 and 21%, respectively. In contrast to 3-thia fatty acid treatment, eicosapentaenoic acid treatment and starvation increased the mitochondrial CPT-I activity and reduced its malonyl-CoA sensitivity. Palmitoyl-L-carnitine oxidation and CPT-II activity were, however, unchanged after either EPA treatment or starvation. The results from this study open the possibility that the rate control of mitochondrial beta-oxidation under mitochondrion and peroxisome proliferation is distributed between an enzyme or enzymes of the pathway beyond the CPT-I site after 3-thia fatty acid treatment. It is suggested that fatty acids are partly oxidized in the peroxisomes before entering the mitochondria as acylcarnitines for further oxidation.
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PMID:3-Thia fatty acid treatment, in contrast to eicosapentaenoic acid and starvation, induces gene expression of carnitine palmitoyltransferase-II in rat liver. 1038 Jan 16

beta-Ketoacyl-acyl carrier protein (ACP) synthase III (KAS III, also called acetoacetyl-ACP synthase) encoded by the fabH gene is thought to catalyze the first elongation reaction (Claisen condensation) of type II fatty acid synthesis in bacteria and plant plastids. However, direct in vivo evidence that KAS III catalyzes an essential reaction is lacking, because no mutant organism deficient in this activity has been isolated. We report the first bacterial strain lacking KAS III, a fabH mutant constructed in the Gram-positive bacterium Lactococcus lactis subspecies lactis IL1403. The mutant strain carries an in-frame deletion of the KAS III active site region and was isolated by gene replacement using a medium supplemented with a source of saturated and unsaturated long-chain fatty acids. The mutant strain is devoid of KAS III activity and fails to grow in the absence of supplementation with exogenous long-chain fatty acids demonstrating that KAS III plays an essential role in cellular metabolism. However, the L. lactis fabH deletion mutant requires only long-chain unsaturated fatty acids for growth, a source of long-chain saturated fatty acids is not required. Because both saturated and unsaturated fatty acids are required for growth when fatty acid synthesis is blocked by biotin starvation (which prevents the synthesis of malonyl-CoA), another pathway for saturated fatty acid synthesis must remain in the fabH deletion strain. Indeed, incorporation of [1-14C]acetate into fatty acids in vivo showed that the fabH mutant retained about 10% of the fatty acid synthetic ability of the wild-type strain and that this residual synthetic capacity was preferentially diverted to the saturated branch of the pathway. Moreover, mass spectrometry showed that the fabH mutant retained low levels of palmitic acid upon fatty acid starvation. Derivatives of the fabH deletion mutant strain were isolated that were octanoic acid auxotrophs consistent with biochemical studies indicating that the major role of FabH is production of short-chain fatty acid primers. We also confirmed the essentiality of FabH in Escherichia coli by use of a plasmid-based gene insertion/deletion system. Together these results provide the first genetic evidence demonstrating that FabH conducts the major condensation reaction in the initiation of type II fatty acid biosynthesis in both Gram-positive and Gram-negative bacteria.
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PMID:Beta-ketoacyl-acyl carrier protein synthase III (FabH) is essential for bacterial fatty acid synthesis. 1452 10

At conditions of low iron availability, Neisseria meningitidis produces a family of FrpC-like, type I-secreted RTX proteins of unknown role in meningococcal lifestyle. It is shown here that iron starvation also induces production of FrpD, the other protein expressed from a gene located immediately upstream of the frpC gene in a predicted iron-regulated frpDC operon. We found that FrpD is highly conserved in a set of meningococcal strains representative of all serogroups and does not exhibit any similarity to known sequences of other organisms. Subcellular localization and [3H]palmitic acid labeling in Escherichia coli revealed that FrpD is synthesized with a type II signal peptide for export across the cytoplasmic membrane and is, upon processing to a lipoprotein, sorted to the outer bacterial membrane. Furthermore, the biological function of FrpD appears to be linked to that of the RTX protein FrpC, because FrpD was found to bind the amino-proximal portion of FrpC (first 300 residues) with very high affinity (apparent Kd approximately 0.2 nM). These results suggest that FrpD represents an rtx loci-encoded accessory lipoprotein that could be involved in anchoring of the secreted RTX protein to the outer bacterial membrane.
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PMID:The Neisseria meningitidis outer membrane lipoprotein FrpD binds the RTX protein FrpC. 1552 36


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