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Results for “FATTY ACIDS”

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At least 91 records · Page 5Linked to original sources
PubMed2003

Physiologic melatonin concentration, omega-3 fatty acids, and conjugated linoleic acid inhibit fatty acid transport in rodent hind limb skeletal muscle in vivo.

Melatonin (MLT), the circadian neurohormone secreted by the pineal gland in mammals during darkness, eicosapentanoic acid (EPA), and conjugated linoleic acid (CLA) have established regulatory roles in cancer growth. Investigations in our laboratory have indicated that these agents inhibit fatty acid (FA) transport by tumors and several sub-types of white adipose tissue via inhibitory G protein-coupled receptor mechanisms. Skeletal muscle constitutes over 45% of human body mass and plays an important role in cancer cachexia and obesity-related diseases. Since fatty acid oxidation is a major source of energy for this tissue, we tested the hypothesis that physiologic MLT levels, EPA, or CLA injected intravenously, inhibit FA uptake in rat skeletal muscle in vivo. We used a surgical technique for catheterizing the femoral vein in rats that allows rapid blood collection from the entire hind limb, while ensuring continuous blood flow to the tissue. Blood acid/gas tensions and hematocrit were monitored and remained constant during the course of each experiment. The MLT, EPA, and CLA inhibited FA uptake by the tissue and lowered cAMP values. Glucose uptake and glycerol production in the hind limb were not affected. These investigations suggest a novel role for MLT, omega-3 FAs, and CLA in the regulation of FA transport and fat metabolism in skeletal muscle.

Animals↗
PubMed1977

Pulmonary fatty acid synthesis. II. Amino acids as fatty acid precursors in rat lung.

The incorporation of various 14C-labeled amino acids into CO2 and lipids by rat lung slices was examined. Alanine, valine, leucine, isoleucine, aspartate, and glutamate were oxidized by lung tissue, whereas glycine and phenylalanine were not oxidized. Carbon originating from alanine, leucine, and glutamate was incorporated into pulmonary fatty acids by a mechanism indicative of de novo synthesis. Experiments with specifically labeled [14C]aspartate and [14C]glutamate revealed that the complete citrate-malate cycle described by Patel et al. (25) is of minor importance in pulmonary lipogenesis due to the extremely low activity of NADP-malate dehydrogenase. Glucose and pyruvate were also actively incorporated into fatty acids, and it is suggested that citrate in pulmonary tissue, as in other tissues, plays an important role in the transport of acetyl units from the mitochondria to the cell cytosol during lipogenesis from various carbohydrate and amino acid substrates.

ATP Citrate (pro-S)-Lyase↗
PubMed2003

Cuticular lipids of the booklouse, Liposcelis bostrychophila: hydrocarbons, aldehydes, fatty acids, and fatty acid amides.

The booklouse, Liposcelis bostrychophila, is an increasingly common pest of stored food products worldwide. We report here the cuticular lipid composition of this pest (the first report of the hydrocarbons of any member of the Order Psocoptera and the first report of fatty acid amides as cuticular components for any insect). No unsaturated hydrocarbons were present. A homologous series of n-alkanes (C21-C34), monomethyl alkanes (3-, 4-, 5-, 7-, 9-, 11-, 12-, 13- and 15-methyl-) with a carbon chain range of C28-C42, and dimethyl alkanes (3, 7-; 9, 13-; 11, 15-; 13, 17-; 9, 21-; 11, 19-; and 13, 21-) with a carbon number range of C31-C41 were identified. The relative abundances of these hydrocarbons were low, comprising approximately 0.0125% of total biomass. The amides were a homologous series (C16-C22 in chain length), with the major amide being stearoyl amide. In addition to the amides, free fatty acids (C16:1, C16:0, C18:2, C18:1, and C18:0 in chain length) and three straight chain aldehydes (C15, C16, and C17:1 in chain length) also occurred as cuticular components. These findings are discussed in terms of the chemical and physiological ecology of this species.

Aldehydes↗
PubMed2002

Differential effect of insulin on saturated and unsaturated fatty acids.

Fatty acids fulfill important roles in physiology. The plasma concentrations of fatty acids are principally regulated by insulin, which suppresses the release of fatty acids from lipid stores, and catecholamines, which increase their release from lipid stores. Although insulin regulates the concentration of plasma free fatty acids (FFAs), little is known about the relative effects of insulin on the saturated compared with the unsaturated plasma fatty acids. In the current study, we specifically measured the plasma concentration of 3 saturated and 4 unsaturated fatty acids along with an estimate of lipolytic activity using a stable isotope of glycerol during a 3-hour, 1-step, euglycemic clamp study in humans. The data showed the expected decline in plasma fatty acids from 0.26 +/- 0.02 to 0.06 +/- 0.01 micromol/mL. Saturated fatty acids were reduced from 0.12 +/- 0.01 to 0.05 +/- 0.005 micromol/mL and unsaturated fatty acids were reduced from 0.11 +/- 0.01 to 0.01 +/- 0.001 micromol/mL after 3 hours of insulin infusion. At baseline, the ratio of saturated to unsaturated fatty acid was 55:45, which increased to 82:18 by the end of study. The changes in fatty acids were evident within 1 hour. Whole body lipolytic rates were measured with deuterated glycerol and decreased from 1.48 +/- 0.56 micromol x kg(-1) x min(-1) to 0.75 +/- 0.34 micromol x kg(-1) x min(-1). Baseline postabsorptive plasma fatty acid concentrations were significantly correlated to insulin sensitivity (M value) as measured during the euglycemic clamp. There were no significant differences between the more insulin-sensitive subjects when compared with the more insulin-resistant subjects with respect to the relative decreases in saturated and unsaturated fatty acids during insulin infusion. These data demonstrate a sustained differential effect of insulin on the plasma fatty acid profile.

Adolescent↗
PubMed2001

A new concept of cellular uptake and intracellular trafficking of long-chain fatty acids.

Fatty acids are the main structural and energy sources of the human body. Within the organism, they are presented to cells as fatty acid:albumin complexes. Dissociation from albumin represents the first step of the cellular uptake process, involving membrane proteins with high affinity for fatty acids, e.g., fatty acid translocase (FAT/CD 36) or the membrane fatty acid-binding protein (FABPpm). According to the thus created transmembrane concentration gradient, uncharged fatty acids can flip-flop from the outer leaflet across the phospholipid bilayer. At the cytosolic surface of the plasma membrane, fatty acids can associate with the cytosolic FABP (FABP(c)) or with caveolin-1. Caveolins are constituents of caveolae, which are proposed to serve as lipid delivery vehicles for subcellular organelles. It is not known whether protein (FABP(c))- and lipid (caveolae)-mediated intracellular trafficking of fatty acids operates in conjunction or in parallel. Channeling fatty acids to the different metabolic pathways requires activation to acyl-CoA. For this process, the family of fatty acid transport proteins (FATP 1-5/6) might be relevant because they have been shown to possess acyl-CoA synthetase activity. Their variable N-terminal signaling sequences suggest that they might be targeted to specific organelles by anchoring in the phospholipid bilayer of the different subcellular membranes. At the highly conserved cytosolic AMP-binding site of FATP, fatty acids are activated to acyl-CoA for subsequent metabolic disposition by specific organelles. Overall, fatty acid uptake represents a continuous flow involving the following: dissociation from albumin by membrane proteins with high affinity for fatty acids; passive flip-flop across the phospholipid bilayer; binding to FABP(C) and caveolin-1 at the cytosolic plasma membrane; and intracellular trafficking via FABP(c) and/or caveolae to sites of metabolic disposition. The uptake process is terminated after activation to acyl-CoA by the members of the FATP family targeted intracellularly to different organelles.

Animals↗
PubMed1980

Mechanism of chain length determination in biosynthesis of milk fatty acids.

Fatty acid synthetases isolated from all mammalian tissues synthesize predominately palmitic acid. However, in vivo the mammary gland fatty acid synthetases of some species are responsible for the synthesis of medium chain fatty acids. The objective of this presentation is to outline the mechanism which regulates the product specificity of fatty acid synthetases in general and to illustrate how this control is modified in the mammary gland. Fatty acid synthetases isolated from mammalian tissues are composed of two similar, probably identical, polypeptides, each carrying as many as seven enzyme components. Thioesterase I, the component which functions to terminate growth of acyl chains on the multienzyme, is located at one terminus of each polyfunctional polypeptide and can be detached by limited proteolysis with trypsin. By studying separately the kinetics of chain elongation by the core of the trypsinized complex and of chain termination by the isolated thioesterase I component, it has been possible to establish that the specificities of the elongation and termination reactions account for the synthesis of predominantly the carbon-16 fatty acid by purified fatty acid synthetases. Mammary glands of some species contain an additonal enzyme, thioesterase II, which can modify the product specificity of fatty acid synthetase by hydrolyzing medium chain acyl moieties from thioester linkage to the 4'phosphopantetheine of the multienzyme. At all stages of development of rat mammary gland, the amount of theoesterase II present correlates well with the proportion of medium chain fatty acids synthesized by the gland. This mammary gland-specific thioesterase appears responsible for the ability of this tissue to synthesize medium chain fatty acids characteristic of milk fat.

Animals↗
PubMed1990

Influence of dietary linoleic acid and trans fatty acids on the fatty acid profile of cardiolipins in rats.

Cardiolipins (CL) have unique fatty acid profiles with generally high levels of polyunsaturated fatty acids, primarily 18:2n-6, and low levels of saturated fatty acids. In order to study the effect of dietary fatty acid isomers on the fatty acid composition of cardiolipins, rats were fed partially hydrogenated marine oils (HMO), rich in 16:1, 18:1, 20:1, and 22:1 isomeric fatty acids, supplemented with linoleic acid at levels ranging from 1.9% to 14.5% of total fat. Although the dietary fats contained 33% trans fatty acids, the levels of trans fatty acids in CL were below 2.5% in all organs. The fatty acid profiles of cardiolipins of liver, heart, kidney and testes showed different responses to dietary linoleic acid level. In liver, the contents of 18:2 reflected the dietary levels. In heart and kidney, the levels of 18:2 also paralleled increasing dietary levels, but in all groups fed HMO, levels of 18:2 were considerably higher than in the reference group fed palm oil. In testes, the 18:2 levels were unaffected by the dietary level of 18:2 and HMO.

Animals↗
PubMedDate not supplied

Coronary vasodilation by fatty acids.

Fatty acids increase the coronary flow rate of rat hearts, perfused according to the Langendorff technique. Long-chain and medium-chain fatty acids are more effective vasodilators than short-chain fatty acids. The vasodilatation by fatty acids does not proceed through the intermediate formation of the vasodilator adenosine, nor by stimulation of adenylcyclase activity. Since at low Ca2+ concentrations fatty acids not only stimulate the coronary flow rate but also cardiac contractility, it is suggested that especially the lipophilic fatty acids have calcium ionophoric properties leading to increased Ca2+ removal from smooth muscle cytosol and hence to vasodilatation. Preliminary experiments, moreover, indicate that both medium- and long-chain fatty acids, like prostaglandin E1 and Ca2+, inhibit membrane ATPase(s) of aorta smooth muscle cells, suggesting increased Ca2+ binding to vascular smooth muscle cell membranes.

Adenosine↗