PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “FATTY ACID METABOLISM”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed1983

Immunocytochemical localization of fatty acid metabolizing heat-stable and heat-labile enoyl-coenzyme A (CoA) hydratases in liver and renal cortex.

Two enzymes, the heat-stable and the heat-labile enoyl-coenzyme A (CoA) hydratases, involved in the metabolism of fatty acids were localized in liver and renal cortex using specific antibodies, immunofluorescence, and the protein A-gold immunocytochemical technique. The qualitative and quantitative results have demonstrated that the heat-stable enoyl-CoA hydratase is a mitochondrial membrane-associated protein of hepatocytes and of epithelial cells in proximal and distal renal tubules. The hepatic sinusoidal cells, as well as the endothelial and epithelial cells of the glomeruli, fail to demonstrate any specific labeling. The heat-labile enoyl-CoA hydratase, on the other hand, was detected in the peroxisomal matrix of hepatocyte and proximal tubule epithelial cells. Its distribution was identical to that of catalase. The significance of the differential distribution of peroxisomal and mitochondrial enoyl-CoA hydratases is discussed in relation to their function.

Animals↗
PubMed2005

Spontaneous anterograde flow of the infarct artery preserves myocardial perfusion and fatty acid metabolism in patients with anterior acute myocardial infarction.

BACKGROUND: It remains unclear whether spontaneous anterograde flow preserves myocardial fatty acid metabolism in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: The present study comprised 129 patients with a first anterior AMI in whom Thrombolysis in Myocardial Infarction (TIMI) 3 flow was obtained on the final angiogram: 28 patients with spontaneous anterograde flow and 101 patients with total occlusion on the initial angiogram. Thallium-201 (201Tl) and iodine-123-beta-methyl-p-iodophenyl penta-decanoic acid (123I-BMIPP) dual-isotope myocardial single-photon emission computed tomography (SPECT) was performed at 6.5+/-4.2 days after onset. The SPECT image was divided into 17 segments, and each segment was graded with scores between 0 and 4 (0, normal uptake; 4, defective). The sum of each score was defined as the total defect score (TDS). TDS values for 201Tl (9.0 +/-7.4 vs 16.8+/-12.2, p < 0.01) and 123I-BMIPP (19.3+/-11.6 vs 24.1 +/-10.4, p < 0.05) were significantly lower in patients with spontaneous anterograde flow than in those with total occlusion. CONCLUSIONS: These results suggest that spontaneous anterograde flow of the infarct artery preserves not only myocardial perfusion but also fatty acid metabolism in patients with AMI. 123I-BMIPP SPECT image may underestimate the area at risk especially in patients with spontaneous anterograde flow.

Aged↗
PubMed2002

Myocardial sympathetic denervation, fatty acid metabolism, and left ventricular wall motion in vasospastic angina.

UNLABELLED: Although various noninvasive methods have been used to detect vasospasm, none of them are sensitive enough for patients with sporadic attacks. Because abnormal fatty acid metabolism and cardiac adrenergic neuronal damage are observed in ischemic myocardium, (123)I-15-(p-iodophenyl)-3-R,S-methyl pentadecanoic acid (BMIPP) and (123)I-metaiodobenzylguanidine (MIBG) have recently been proposed as useful tracers for detection of myocardial damage. This study investigated the relationships among the coronary vasospastic regions, abnormal left ventricular regional wall motion, fatty acid metabolism, and sympathetic nerve functions and their changes during treatment in patients with vasospastic angina. METHODS: We evaluated 50 patients with vasospastic angina (25 with clinically documented vasospasm [group A] and 25 with vasospasm induced by ergonovine provocation [group B]) and 25 control subjects who had chest pain but had normal coronary arteries without ergonovine provocation of spasm. Sixteen patients in group A were reevaluated 6 mo after medical treatment. The territorial regions of the vasospasm-induced coronary artery, wall motion determined by left ventriculography, and BMIPP and MIBG uptake were compared. RESULTS: Regions exhibiting a positive reaction to the ergonovine provocation were observed in the right coronary artery in 41 patients, the left anterior descending artery in 33, and the left circumflex artery in 21. Provocation occurred in multiple vessels in 29 patients (58%). Reduction of wall motion was observed in 19 patients (38%). Sensitivity and specificity for the identification of vasospastic angina were 86% (43/50 patients) and 88% (22/25 control subjects), respectively, for BMIPP scintigraphy and 100% (50/50 patients) and 56% (14/25 control subjects), respectively, for MIBG scintigraphy. In the region exhibiting a reduction in left ventricular wall motion, BMIPP or MIBG uptake was decreased. The sensitivity and specificity of determination of vasospasm-induced coronary arteries were 71% (67/95 arteries) and 95% (71/75 arteries), respectively, for BMIPP scintigraphy and 96% (91/95 arteries) and 55% (41/75 arteries), respectively, for MIBG scintigraphy. After 6 mo, during treatment, vasospasm was reinduced by ergonovine provocation in 6 patients (group I) and was not reinduced in 10 patients (group II). Improvements of decreased BMIPP and MIBG uptake were lower in group I (25% +/- 4% and 16% +/- 4%, respectively) than in group II (69% +/- 4% and 50% +/- 3%, respectively; both P < 0.01). The regions in which vasospasm was reinduced exhibited decreased BMIPP and MIBG uptake. CONCLUSION: Abnormal fatty acid metabolism and cardiac sympathetic denervation were observed more frequently than were wall motion abnormalities in the vasospastic region in patients with vasospastic angina. BMIPP and MIBG scintigraphy are highly accurate and noninvasive techniques for determining the presence and location of vasospasm.

3-Iodobenzylguanidine↗
PubMed2001

Carnitine affects fatty acid metabolism after cardioplegic arrest in neonatal rabbit hearts.

BACKGROUND: Fatty acid (FA) metabolism and the contribution of carnitine to metabolism after cardioplegic arrest still remain unclear, especially in the neonatal heart where beta-oxidation is not a predominant source of adenosine triphosphate. METHODS: FA metabolism and the effects of carnitine administration were evaluated using a newborn (7-day-old) rabbit blood-perfused Langendorff model subjected to cold cardioplegic arrest. The hearts were divided into five groups; (1) perfused with unmodified diluted blood (n = 9), (2) subjected to 180 minutes of cold cardioplegic arrest and reperfused with the blood (n = 9), (3) subjected to the same ischemia and reperfused with the blood containing 40 microM/L (n = 9), (4) 0.5 mM/L (n = 5), and (5) 5 mM/L of carnitine (n = 5). During reperfusion, FA metabolism was assessed by iodine-123-labeled 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid, a fatty acid. The myocardial time-radioactivity curve was then determined and a mathematical compartment analysis of the external detection was used to elucidate FA metabolism in the cardiac myocyte. RESULTS: Cold cardioplegic arrest resulted in significantly impaired FA metabolism following reperfusion. Compartment analysis suggested that FA activation in the cytosol and beta-oxidation were impaired. Carnitine supplementation in groups 3 and 4 improved FA metabolism during reperfusion. In contrast, supplementation in group 5 had no beneficial effect on FA metabolism. CONCLUSIONS: These results suggest that FA metabolism is impaired after cold cardioplegic arrest and that carnitine supplementation may improve aerobic metabolism in neonates after open heart surgery.

Animals↗
PubMed2003

Effects of temocapril and olmesartan on myocardial sympathetic nervous activity and fatty acid metabolism in rats with chronic beta-adrenergic stimulation.

We investigated the effects of an angiotensin-converting enzyme inhibitor (temocapril) and an angiotensin II type 1 receptor blocker (olmesartan) on changes in myocardial sympathetic nervous activity, fatty acid metabolism and myocardial blood flow using 131I-meta-iodobenzylguanidine, 125I-beta-methyl-iodophenyl pentadecanoic acid and 99mTc-tetrofosmin, respectively, in rats with isoproterenol-induced cardiac hypertrophy. Male Sprague-Dawley rats underwent isoproterenol administration (3 mg/kg per day) for 1 week by osmotic mini-pump. The hearts were excised and analyzed for the uptake of meta-iodobenzylguanidine. Beta-methyl-iodophenyl pentadecanoic acid and tetrofosmin in 11 segments in four groups; sham group (saline), isoproterenol group (isoproterenol alone), angiotensin-converting enzyme inhibitor group (isoproterenol and temocapril), and angiotensin II type 1 receptor blocker group (isoproterenol and olmesartan). Isoproterenol significantly increased the heart weight compared with the sham group, whereas it was significantly blunted in the angiotensin-converting enzyme inhibitor and angiotensin II type 1 receptor blocker groups. The ratio of the percent kilogram dose per gram of meta-iodobenzylguanidine to tetrofosmin, an index of myocardial sympathetic nervous activity, was significantly decreased in the isoproterenol group (0.18 +/- 0.01) compared with the sham group (0.41 +/- 0.03). Importantly, these changes were significantly improved in the angiotensin-converting enzyme inhibitor (0.28 +/- 0.01) and the angiotensin II type 1 receptor blocker groups (0.32 +/- 0.01). The ratio of the percent kilogram dose per gram of beta-methyl-iodophenyl pentadecanoic acid to tetrofosmin, an index of myocardial fatty acid metabolism, was significantly decreased in the isoproterenol group (1.30 +/- 0.03) compared with the sham group (1.60 +/- 0.10). In contrast, there were no significant differences in beta-methyl-iodophenyl pentadecanoic acid to tetrofosmin ratios between the sham and angiotensin-converting enzyme inhibitor groups, or the angiotensin II type 1 receptor blocker group. Cardiac hypertrophy induced by chronic beta-adrenergic stimulation is accompanied by impairment of sympathetic nervous activity and fatty acid metabolism. These abnormalities are effectively prevented by the angiotensin-converting enzyme inhibitor and the angiotensin II type 1 receptor blocker.

Adrenergic Fibers↗
PubMed1990

[Postprandial fatty acid metabolism].

In accordance with metabolic properties in the mucosal and liver cells, the exogenous fatty acids may be classified as short chain (C4 and C6), medium chain (C8 and C10), transitional (C12 and C14) and long chain (C16 upward) fatty acids. The postprandial fatty acid metabolism takes place in two phases. In the first, approximately 8 hour phase, the clearance of chylomicrons and most of the chylomicron remnants as well as the uptake of short and medium chain fatty acids by the liver are completed. Most of the exogenous long chain fatty acids (chylomicron fatty acids) are cleared extrahepatically. However, about 10% of the long chain fatty acids are taken up by the liver, and during the second postprandial phase, lasting about 24 hours, the liver secretes most of these exogenous fatty acids with very low density lipoproteins. The exogenous fatty acids may circulate between the liver and adipose tissue until they are finally metabolized mainly in extrahepatic tissues.

Cholesterol↗
PubMed1999

Abnormal fatty acid metabolism in patients with coronary vasospasm.

Although various noninvasive methods have been used to detect vasospasm, none of them are sensitive enough for patients with sporadic attacks. Since abnormal fatty acid metabolism is observed in ischemic myocardium, 123I-beta-methyl-p-iodophenyl pentadecanoic acid (BMIPP), a radiolabeled fatty acid analog, has recently been proposed as a useful tracer for detecting myocardial damage. The aim of this study was to clarify the clinical implications of decreased myocardial BMIPP uptake in patients with vasospastic angina. We evaluated 53 patients with vasospastic angina (32 with clinically documented vasospasm [Group-A] and 21 with vasospasm induced by ergonovine provocation [Group-B]) and 27 control subjects, 20 in Group-A were re-evaluated 6 months after medical treatment. The territorial regions of vasospasm-induced coronary artery, the wall motion by left ventriculography, and BMIPP uptake were compared. Vasospasm was induced in multiple coronary arteries in 29 (55%) patients. Reduced wall motion and decreased BMIPP uptake were observed in 19 (36%) patients and 47 (89%) patients, respectively. The sensitivity and specificity of determination of vasospasm-induced coronary arteries with BMIPP scintigraphy were 71% (69/97 coronary arteries) and 88% (126/143), respectively. Vasospasm was re-induced by ergonovine provocation in 8 patients (Group-I) and not re-induced in 12 (Group-II) after treatment. In Group-I, improvement of decreased BMIPP uptake was lower than in Group-II (19+/-11 vs. 59+/-22%, mean+/-SD, p < 0.001). The regions in which vasospasm was re-provoked exhibited decreased BMIPP uptake. Abnormal fatty acid metabolism was more often observed than wall motion abnormality in the vasospastic region in patients with vasospastic angina. BMIPP scintigraphy is a highly accurate and non-invasive technique for determining the presence and location of vasospasm.

Adult↗
PubMed1986

Activity of acyl carrier protein isoforms in reactions of plant Fatty Acid metabolism.

Two forms of spinach acyl carrier protein (ACP-I and ACP-II) have recently been characterized and found to be expressed in a tissue-specific manner (JB Ohlrogge, TM Kuo, 1985 J Biol Chem 260: 8032). To examine possible different functions for these ACP isoforms, we have tested purified preparations of spinach leaf ACP-I and ACP-II and Escherichia coli ACP in several in vitro reactions of fatty acid metabolism. Total de novo fatty acid synthesis and malonyl-CoA:ACP transacylase do not appear to discriminate between acyl carrier protein isoforms. In contrast, the K(m) of oleoyl-ACP thioesterase for oleoyl-ACP-II is 10-fold higher than for oleoyl-ACP-I, whereas the K(m) of acyl-ACP glycerol-3-phosphate acyl transferase is 5-fold higher for oleoyl-ACP-I than for oleoyl-ACP-II. A characterization of these reactions and a possible role for ACP isoforms in regulation of fatty acid metabolism in plants are described.

Journal Article↗
PubMed1982

Suspected faulty essential fatty acid metabolism in Sjögren-Larsson syndrome.

The aim of the present study was to examine the fatty acid patterns of plasma phospholipids, cholesteryl esters, triglycerides and free fatty acids in patients with Sjögren-Larsson syndrome in order to detect whether absorption or metabolism is essential fatty acids may be abnormal. The fatty acid patterns were analyzed by gas liquid chromatography. The proportions of 23 fatty acids were calculated. The parameters used for assessment of the essential fatty acid metabolic status were calculated and compared with those from a group of institutionalized mentally retarded patients and from a group of healthy controls. There was no significant difference in either the fatty acid components or parameters used to evaluate the essential fatty acid metabolic study when the mentally retarded and control groups were compared. The relative concentration of linoleic acid (18:2 omega 6) in plasma phospholipids in patients with Sjögren-Larsson syndrome did not differ significantly from that of the healthy or mentally retarded controls, indicating that the Sjögren Larsson syndrome does not involve a dietary essential fatty acid deficiency or a defect in absorption of linoleate. In the phospholipids of Sjörgren-Larsson syndrome patients, the metabolites derived from linoleic acid were found to be significantly lower than in health controls, suggesting the metabolic defect. The total products of delta 6 desaturation were reduced to 3% of that in controls, whereas the products of delta 5 and delta 9 desaturation were not noticeably affected in the patients with Sjögren-Larsson syndrome. All individuals with Sjörgren-Larsson syndrome exhibited decreased products of delta 6 desaturation which also affected subsequent metabolites in the metabolite sequence.

Adolescent↗
PubMed2004

Porcine leptin alters isolated adipocyte glucose and fatty acid metabolism.

This study examined if leptin can acutely affect glucose or fatty acid metabolism in pig adipocytes and whether leptin's actions on lipogenesis are manifested through interaction with insulin or growth hormone. Subcutaneous adipose tissue was obtained from approximately 55 kg crossbred barrows at the USDA abattoir. Isolated adipocytes were prepared using a collagenase procedure. Experiments assessed U-14C-glucose or 1-14C-palmitate metabolism in isolated adipocytes exposed to: basal medium (control), 100 nM insulin, 100 ng/ml porcine growth hormone, 100 ng/ml recombinant porcine leptin, and combinations of these hormones. Treatments were performed in triplicate and the experiment was repeated with adipocytes isolated from five different animals. Cell aliquots (250 microl) were added to 1 ml of incubation medium, then incubated for 2h at 37 degrees C for measurement of glucose and palmitate oxidation or incorporation into lipid. Incubation of isolated adipocytes with insulin increased glucose oxidation rate by 18% (P<0.05), while neither growth hormone nor leptin affected glucose oxidation (P>0.5). Total lipid synthesis from glucose was increased by approximately 25% by 100 nM insulin or insulin+growth hormone (P<0.05). Insulin+leptin reduced the insulin response by 37% (P<0.05). The combination of all three hormones increased total lipid synthesis by 35%, relative to controls (P<0.05), a rate similar to insulin alone. Fatty acid synthesis was elevated by insulin (32%, P<0.05) or growth hormone (13%, P<0.05). Leptin had no effect on fatty acid synthesis (P>0.05). Leptin reduced the esterification rate by 10% (P<0.05). Growth hormone and insulin could overcome leptin's inhibition of palmitate esterification (P>0.05).

Adipocytes↗
PubMed1989

Relation between essential fatty acid metabolism and gastrointestinal symptoms in cystic fibrosis.

Studies in our laboratory have supported the hypothesis, that the basic defect in cystic fibrosis increases the metabolism of essential fatty acids and thereby gradually gives rise to essential fatty acid deficiency, which is a well documented finding in most cases with this disease. Both the increased metabolism--giving high liberation of arachidonic acid and its metabolic products, i.e. different eicosanoids--and the subsequent essential fatty acid deficiency will cause gastrointestinal symptoms and the sequence of this development will mirror the natural history of the disease. Clinical data and results from animal research are discussed in relation to gastrointestinal symptoms and signs of cystic fibrosis.

Cystic Fibrosis↗
PubMed2006

Fatty acid metabolism in adipose tissue, muscle and liver in health and disease.

Fat is the largest energy reserve in mammals. Most tissues are involved in fatty acid metabolism, but three are quantitatively more important than others: adipose tissue, skeletal muscle and liver. Each of these tissues has a store of triacylglycerol that can be hydrolysed (mobilized) in a regulated way to release fatty acids. In the case of adipose tissue, these fatty acids may be released into the circulation for delivery to other tissues, whereas in muscle they are a substrate for oxidation and in liver they are a substrate for re-esterification within the endoplasmic reticulum to make triacylglycerol that will be secreted as very-low-density lipoprotein. These pathways are regulated, most clearly in the case of adipose tissue. Adipose tissue fat storage is stimulated, and fat mobilization suppressed, by insulin, leading to a drive to store energy in the fed state. Muscle fatty acid metabolism is more sensitive to physical activity, during which fatty acid utilization from extracellular and intracellular sources may increase enormously. The uptake of fat by the liver seems to depend mainly upon delivery in the plasma, but the secretion of very-low-density lipoprotein triacylglycerol is suppressed by insulin. There is clearly cooperation amongst the tissues, so that, for instance, adipose tissue fat mobilization increases to meet the demands of skeletal muscle during exercise. When triacylglycerol accumulates excessively in skeletal muscle and liver, sometimes called ectopic fat deposition, then the condition of insulin resistance arises. This may reflect a lack of exercise and an excess of fat intake.

Adipose Tissue↗
PubMed2001

Freeze-thaw effects on metabolic enzymes in wood frog organs.

To determine whether episodes of natural freezing and thawing altered the metabolic makeup of wood frog (Rana sylvatica) organs, the maximal activities of 28 enzymes of intermediary metabolism were assessed in six organs (brain, heart, kidney, liver, skeletal muscle, gut) of control (5 degrees C acclimated), frozen (24 h at -3 degrees C), and thawed (24 h back at 5 degrees C) frogs. The enzymes assessed represented pathways including glycolysis, gluconeo-genesis, amino acid metabolism, fatty acid metabolism, the TCA cycle, and adenylate metabolism. Organ-specific responses seen included (a) the number of enzymes affected by freeze-thaw (1 in gut ranging to 17 in heart), (b) the magnitude and direction of response (most often enzyme activities decreased during freezing and rebounded with thawing but, liver showed freeze-specific increases in several enzymes), and (c) the response to freezing versus thawing (enzyme activities in gut and kidney changed during freezing, whereas most enzymes in skeletal muscle responded to thawing). Overall, the data show that freeze-thaw implements selected changes to the maximal activities of various enzymes of intermediary metabolism and that these may aid organ-specific responses that alter fuel use during freeze-thaw, support cryoprotectant metabolism, and aid organ endurance of freeze-induced ischemia.

Acclimatization↗
PubMed1982

[Effect of clofibric acid on fatty acid metabolism in HLP patients in the 2d half of life].

Ten patients with primary type IIb hyperlipoproteinemia and one hundred patients with primary type IV hyperlipoproteinemia (sixty-seven men and forty-three women aged forty-three to seventy-four) were treated with clofibric acid (Regadrin) for three years. Gas chromatographic analysis of the composition of cholesterol ester and triglyceride fatty acids in serum were done prior to and at four-month intervals during therapy. During treatment of type IIb and type IV hyperlipoproteinemia there was observed a decrease of palmitic, stearic, palmitoleic, oleic, and eicosane-tetraenoic acids as well as an increase of linoleic, linolenic, arachidonic, and eicosane-pentaenoic acids in the triglyceride fraction. These changes manifest themselves most conspicuously in the effect of clofibric acid upon the hepatogenic fatty acid metabolism (increased synthesis or reduced catabolization of polyunsaturated fatty acids and increased oxidation or reduced formation of monounsaturated and saturated fatty acids, increased esterification of polyenic acids). In addition, these is the possibility of selective displacement of saturated and monounsaturated fatty acids of the unsaturated fatty acids fraction as well as specific inhibition of their esterification with glycerol by clofibric acid. Treatment with clofibric acid over a long period of time may well give rise to additional reactions through influences exerted upon the insulin level.

Adult↗