[Effect of heterologous enzyme complexes of fatty acid metabolism on blood lipids in humans].
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Enzymes↗
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Results for “FATTY ACID METABOLISM”
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[Fatty acid metabolism of calves with special reference to linoleic acid. 3. Fatty acid distribution of main lipid fractions in organs and tissues].
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Animals↗
Effect of pancreas transplantation on free fatty acid metabolism in uremic IDDM patients.
To assess the effect of pancreas transplantation on free fatty acid (FFA) and glucose metabolism, we studied seven uremic IDDM patients (HbA1c 9.1%), nine IDDM patients after combined kidney-pancreas transplantation (HbA1c 5.8%), seven patients with chronic uveitis (HbA1c 5.6%), and nine normal control subjects (HbA1c 5.5%) by means of the [3(- 3)H]glucose and [1(-14)C]palmitate infusion techniques combined with indirect calorimetry and euglycemic insulin clamp. In the postabsorptive state, pancreas-transplant patients had similar plasma glucose and FFA concentrations and non-statistically different rates of hepatic glucose production (HGP) and FFA turnover, while demonstrating a reduced rate of FFA oxidation (42 +/- 5 vs. 73 +/- 10 micromol x m-2 x min-1; P < 0.05) compared with control subjects. After 180 min of tracer equilibration, all subjects underwent a low-dose (100 min, 8 mU x m-2 x min-1) followed by a high-dose (100 min, 40 mU x m-2 x min-1) euglycemic insulin infusion. During insulin infusion, pancreas-transplant patients showed a greater inhibition of FFA concentration (609 +/- 76 to 58 +/- 15 micromol/l) compared with healthy subjects (681 +/- 90 to 187 +/- 25 micromol/l; P < 0.01 vs. pancreas-transplant patients). FFA turnover and oxidation rates during both low-dose and high-dose insulin infusions were lower in pancreas-transplant patients compared with healthy subjects (P < 0.03 and P < 0.01, for turnover and oxidation, respectively). Uremic IDDM patients demonstration altered basal and insulin-mediated glucose metabolism. Pancreas transplantation normalized only insulin-mediated glucose oxidation, leaving the stimulation of non-oxidative glucose disposal still markedly defective. In conclusion, patients after pancreas transplantation have normal basal FFA turnover and reduced basal FFA oxidation rates. During hyperinsulinemia, pancreas-transplant patients show a normal inhibition of FFA turnover and FFA oxidation. Insulin-mediated glucose metabolism remained abnormal after pancreas transplantation. Our findings may be related to the effect of chronic immunosuppressive therapy on glucose and FFA metabolism.
Adult↗
Effect of ethanol on glycerolipid and fatty acid metabolism in Hep G2 human-hepatoma cells.
It is well-known that ethanol alters fatty acid and glycerolipid metabolism in liver, but most of the studies have been developed on rats, so little is known about the corresponding effects on human liver. We have chosen the Hep G2 human hepatoma cell line, which appears to be an excellent in vitro model system. Cells were incubated in ethanol containing medium (0-400 mM) for 48 h. Incorporation and metabolism of radioactive substrates (14C(U) glycerol,[1-14C] palmitic acid and [1-14C] eicosatrienoic acid (n-6) were analyzed in cellular and conditioned medium lipids. Cellular growth rate and lipid composition of control and ethanol-treated cells were also studied. The results showed that ethanol inhibited logarithmic cellular growth rate in a concentration dependent manner, without affecting viability. Ethanol (400 mM) did not modify cellular major lipid composition except for an increase of cholesteryl esters, but produced a decrease in the proportions of myristic, palmitic and palmitoleic acids. Ethanol enhanced the incorporation of radioactive fatty acids into cellular glycerolipids but did not alter the rate of incorporation of 14C(U) glycerol. This was attributed to an isotopic solution of the radioactive glycerol as a result of increased alpha-glycerophosphate biosynthesis. Incorporation of radioactive fatty acids and glycerol into conditioned medium glycerolipids were increased in cells incubated in presence of ethanol. The increased incorporation of 14C glycerol into conditioned medium together with a simultaneous diminution in labeling cellular glycerides suggest that there would be a stimulation of the export of these lipid classes to conditioned medium. Conversion of [1-14C] palmitic to oleic acid and eicosatrienoic to arachidonic acid were inhibited in 400 mM ethanol treated cells suggesting an inhibition of delta 9 and delta 5 desaturase activity.
Carcinoma, Hepatocellular↗
Multiple contributions from long-chain fatty acid metabolism in Y-1 and MA-10 cells.
Acute steroidogenesis in either Y-1 or MA-10 cells is sensitive to different effects of fatty acids compare to a chronic stimulation. A 3-h stimulation of StAR expression in both cell types was completely blocked by NDGA and AA861, each functioning as lipoxygenase inhibitors. However, the acute 15-min stimulation in Y-1 cells was inhibited by these agents by distinct mechanisms. The inhibition by NDGA was reversed by arachidonic, linoleic, and oleic acids. The inhibition by AA861 was insensitive to reversal by these acids. StAR expression was not affected by these short-term inhibitor treatments. These more rapid fatty acid reversible effects of NDGA are consistent with previously reported inhibition of mitochondrial Acyl CoA ligase. This may function in cooperation with StAR and PBR in providing fatty acid regulation of mitochondrial cholesterol transport. The acute effect of AA861 supports the involvement of an NDGA-insensitive lipoxygenase in the acute stimulation of mitochondrial cholesterol metabolism. The activity of MA-10 cells during prolonged treatments with cAMP appears to utilize each of these processes, which depend on different metabolism of fatty acids.
Animals↗
[Fatty acid metabolism using C-11 palmitate: (1). Resting study].
Serial dynamic images were obtained at rest following intravenous injection of 185-370 MBq (5-10 mCi) of 11C-palmitate for 40-50 minutes in 3 normal subjects and 6 patients with coronary artery disease. Due to the rapid clearance of activity from the blood, myocardial images were observed within 5 minutes after the injection in each case. The time activity curve of each myocardial region indicates biexponential clearance. The early clearance half time (Te 1/2) was similar in normal myocardium (18.8 +/- 6.0 min), ischemic myocardium (19.3 +/- 5.8 min) and infarcted myocardium (15.5 +/- 6.0 min). The late clearance half time (Tl 1/2) was also similar among these groups (81.4 +/- 36.0, 66.9 +/- 25.7 and 57.8 +/- 37.4, respectively). However, the residual fraction (%E) was slightly lower in the ischemic myocardium (19.6 +/- 11.0%) (p less than 0.05), indicating decreased beta oxidation in the former. Although positron emission tomography using 11C-palmitate may permit assessment of fatty acid metabolism, the parameters in this study were greatly fluctuated at rest among the normal, ischemic and infarcted myocardium. Further investigations under various interventions may be warranted.
Carbon Radioisotopes↗
Effect of insulin on oxidative and nonoxidative pathways of free fatty acid metabolism in human obesity.
The dose-response relationship between the plasma insulin concentration and oxidative and nonoxidative pathways of free fatty acid (FFA) metabolism was examined in 11 obese and 7 lean subjects using a stepwise insulin clamp technique in combination with indirect calorimetry and infusion of [1-14C]palmitate. The fasting plasma FFA concentration was elevated in obese subjects (793 +/- 43 vs. 642 +/- 39 mumol/l; P less than 0.01) and was associated with an increased basal rate of plasma FFA turnover, FFA oxidation, and nonoxidative FFA disposal, i.e., reesterification (all P less than 0.01). Suppression of plasma FFA turnover by physiological increments in plasma insulin was impaired in obese compared with lean subjects. However, plasma FFA turnover expressed per kilogram fat mass was normally suppressed by insulin in obese subjects. Although insulin suppressed plasma FFA oxidation to the same extent in lean and obese subjects, inhibition of total lipid oxidation by insulin was impaired in the obese group. Obese subjects had an enhanced basal rate of nonoxidative FFA disposal, which was suppressed less by physiological increments in plasma insulin compared with lean controls. Therefore, we conclude that 1) lipolysis in uncomplicated obesity is normally sensitive to insulin; the enhanced FFA flux is simply a consequence of the increased fat mass. 2) Nonoxidative FFA disposal expressed per lean body mass is enhanced in obese subjects and correlates with the increase in plasma FFA concentration and fat mass. 3) Enhanced oxidation of intracellular lipids contributes to the enhanced rate of total lipid oxidation in obese subjects.
Fatty Acids, Nonesterified↗
Myocardial perfusion and fatty acid metabolism in patients with tako-tsubo-like left ventricular dysfunction.
OBJECTIVES: We sought to assess myocardial perfusion and metabolism in patients with peculiar transient asynergy, which consisted of basal normokinesia and apical akinesia of the left ventricle (LV) at the same time. BACKGROUND: This asynergy has been widely called "tako-tsubo-like LV dysfunction" in Japan, but little is known about its pathophysiology. METHODS: We performed rest tallium-201 ((201)Tl) and iodine-123-beta-methyl-p-iodophenyl penta-decanoic acid ((123)I-BMIPP) dual-isotope myocardial single-photon emission computed tomography (SPECT) in 14 patients with tako-tsubo-like LV dysfunction. The LV was divided into 17 segments, and each segment was graded with scores between normal uptake (0) and defect (4). We also measured the Thrombolysis in Myocardial Infarction trial (TIMI) frame count in 28 patients and 20 control subjects. RESULTS: Early SPECT (5 +/- 3 days) revealed that the total defect score value with BMIPP was significantly higher than reduced uptake with (201)Tl (p < 0.01). Reduced uptake of BMIPP was observed in parallel with an apical akinetic region and usually involved uptake of (201)Tl. This discrepancy improved gradually during the follow-up period (29 +/- 6 days) (p = 0.36). Compared with control subjects, patients had a TIMI frame count that was significantly higher in all coronary arteries immediately after onset. This higher TIMI frame count decreased but was sustained even after resolution of tako-tsubo-like LV dysfunction. CONCLUSIONS: Our data suggest that myocardial fatty acid metabolism is more severely impaired than myocardial perfusion, in parallel with an apical akinetic region during the early phase, and that impaired multivessel coronary microcirculation is involved, at least in part, in tako-tsubo-like LV dysfunction.
Aged↗
ADD1/SREBP1 promotes adipocyte differentiation and gene expression linked to fatty acid metabolism.
Adipocyte determination and differentiation-dependent factor 1 (ADD1) is a member of the basic helix-loop-helix leucine zipper (bHLH-LZ) family of transcription factors that binds to two distinct DNA sequences and has been associated with both adipocyte development and cholesterol homeostasis (where it has been termed SREBP1). To investigate the biological role of ADD1, we expressed wild-type and dominant negative forms of this protein with retroviral vectors in preadipocytes and nonadipogenic cells. A dominant-negative form of ADD1 with a point mutation in the DNA-binding domain sharply represses the differentiation of 3T3-L1 cells as observed morphologically or by the expression of adipocyte-specific mRNAs. When NIH-3T3 cells ectopically expressing ADD1 are cultured under hormonal conditions not favoring differentiation, they do not overtly differentiate but still activate expression of mRNAs for fatty acid synthase (FAS) and lipoprotein lipase (LPL), two key genes that regulate fatty acid metabolism. Under culture conditions permissive for differentiation including a PPAR activator, 15%-20% of the cells expressing ADD1 undergo adipogenesis while 2%-3% of cells containing a control vector differentiate. Simultaneous expression of ADD1 with PPARgamma increases the transcriptional activity of this adipogenic nuclear hormone receptor, suggesting involvement of ADD1 in this pathway. These data indicate that ADD1 plays an important role in fat cell gene expression and differentiation, and suggest that it may function by augmenting a step in PPARgamma-mediated transcription.
3T3 Cells↗
Pathways of fatty acid metabolism in human platelets.
The metabolic fate of (14)C-labeled fatty acids which have been incubated with human platelets, has been traced. The following has been shown. (a) Intact platelets have a considerable capacity to oxidize fatty acids. (b) When tracer amounts of four of the most common fatty acids in normal plasma were incubated with platelets, each showed a distinctive pattern of uptake among neutral lipids and phospholipids. With regard to the latter, it was shown that these distribution patterns were, in most cases, similar to those of the fatty acids found in natural platelet phospholipids. (c) By increasing the time of incubation or the amount of added oleic acid, the distribution of oleic acid uptake between lecithin and other phosphoglycerides was altered so that a larger share was incorporated into the latter. (d) The effects of added lysolecithin or lysoethanolamine phosphoglycerides on oleic acid incorporation into platelet phosphoglycerides are quite variable. At low concentrations, added lysolecithin functions chiefly as a reaction partner for oleic acid. Added adenosine triphosphate and CoASH augment the incorporation of oleic acid into lecithin over a wide range of added lysolecithin (12.5-500 mumoles/liter). At higher concentrations of added lysolecithin, in the absence of ATP and CoASH, oleic acid incorporation into lecithin is considerably reduced. Also, added lysolecithin and lysoethanolamine phosphoglycerides, in the absence of ATP and CoASH, are able, at certain concentrations, to stimulate oleic acid incorporation into all except the serine phosphoglycerides. (e) Platelets appear to have a de novo pathway for renewal of lecithin.
Adenosine Triphosphate↗
[Simultaneous evaluation of myocardial perfusion and fatty acid metabolism using dynamic SPECT with single injection of 123I-15-(p-iodophenyl)-3-methyl pentadecanoic acid (BMIPP)].
The purpose of this study is to clarify whether dynamic SPECT (DECT) immediately after the injection of 123I-15-(p-iodophenyl)-3-methyl pentadecanoic acid (BMIPP) may represent myocardial perfusion imaging. Ten patients with unstable angina pectoris (UAP), 11 patients with acute myocardial infarction (AMI) and 6 patients with non-ischemic heart disease (NIHD) were studied using BMIPP myocardial scintigraphy with DECT. DECT acquisition was started 2 minutes after the injection of BMIPP, and DECT images were obtained every three minute for 15 minutes with 3-headed gamma camera SPECT system. Additionally, static SPECT images were acquired 30 minutes after the injection of BMIPP. These SPECT images of BMIPP were compared with thallium-201 myocardial perfusion images at rest. In UAP group, early DECT images showed almost the same findings as thallium-201 images in 8 of 10 patients, and SPECT images at 30 minutes after the injection showed reduced accumulation of BMIPP compared with thallium-201 images in all patients. In AMI group, early DECT images showed the same findings as thallium-201 perfusion images in 9 of 11 patients, and SPECT images at 30 minutes after the injection showed reduced accumulation of BMIPP compared with thallium-201 images in 5 of 11 patients. These results indicate that myocardial perfusion can be evaluated in the early image using DECT, in addition to myocardial fatty acid metabolism in the delayed image.
Adult↗
Effects of fasting on muscle mitochondrial energetics and fatty acid metabolism in Ucp3(-/-) and wild-type mice.
Uncoupling protein-3 (UCP3) is a mitochondrial carrier protein of as yet undefined physiological function. To elucidate characteristics of its function, we studied the effects of fasting on resting metabolic rate, respiratory quotient, muscle Ucp3 expression, and mitochondrial proton leak in wild-type and Ucp3(-/-) mice. Also analyzed were the fatty acid compositions of skeletal muscle mitochondria in fed and fasted Ucp3(-/-) and wild-type mice. In wild-type mice, fasting caused significant increases in Ucp3 (4-fold) and Ucp2 (2-fold) mRNA but did not significantly affect mitochondrial proton leak. State 4 oxygen consumption was not affected by fasting in either of the two groups. However, protonmotive force was consistently higher in mitochondria of Ucp3(-/-) animals (P = 0.03), and fasting further augmented protonmotive force in Ucp3(-/-) mice; there was no effect in wild-type mitochondria. Resting metabolic rates decreased with fasting in both groups. Ucp3(-/-) mice had higher respiratory quotients than wild-type mice in fed resting states, indicating impaired fatty acid oxidation. Altogether, results show that the fasting-induced increases in Ucp2 and Ucp3 do not correlate with increased mitochondrial proton leak but support a role for UCP3 in fatty acid metabolism.
Animals↗
Suppression of fatty acid metabolism after exercise stress in patients with no electrocardiographic ST segment shift during balloon angioplasty.
Although ST segment shift is a marker of myocardial ischemia, some patients have no ST segment shift during percutaneous transluminal coronary angioplasty (PTCA). The aim of this study is to investigate myocardial perfusion and metabolism in adaptation for ischemia using 201TI and 123I-BMIPP dual exercise stress myocardial single photon emission computed tomography (SPECT) (dual stress SPECT). In 28 patients with coronary artery disease, dual stress SPECT was performed 3 weeks before PTCA. Early and delayed images were obtained at 5 minutes and at 3 hours after termination of ergometer stress, respectively. During PTCA, 12-lead ECG was recorded, and a significant ST segment shift was defined as more than 1 mm elevation or a depression of the J-point at the first ballooning. No collateral circulation on the coronary angiogram or 201TI filling on the delayed images were observed on any of the target regions of PTCA. Patients were divided into 2 groups: with (Group A: n = 15) and without (Group B: n = 13) significant ST segment shift during PTCA. A redistribution of TI was observed in 14 (93%) of Group A and 10 (77%) of Group B patients. Incidence of BMIPP redistribution was significantly higher in Group B (11 [85%]) than in Group A (3 [20%]) (p < 0.05). Redistribution of BMIPP means suppression of fatty acid metabolism during exercise stress. Augmentation of glucose metabolism is speculated to be an energy source in ischemic preconditioning.
Angioplasty, Balloon, Coronary↗
MUSCULAR DYSTROPHY: A PROBLEM IN POLYUNSATURATED FATTY ACID METABOLISM?
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Fats, Unsaturated↗
[The effect of ketalar on fatty acid metabolism in the myocardium].
The intraperitoneal administration of ketalar in a dose of 50 mg/kg elevated the myocardial levels of triglycerides, reduced non-esterified fatty acids and enhanced uncontrolled mitochondrial respiration during oxidation of caprylate and palmitoylcarnitine. The efficiency of phosphorylation remained unchanged.
Animals↗
Unsaturated fatty acid metabolism in Neurospora.
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Biochemical Phenomena↗
Metabolic response during impending myocardial infarction. I. Relevance of studies of glucose and fatty acid metabolism in animals.
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Anaerobiosis↗
Serial evaluation of fatty acid metabolism in rats with myocardial infarction by pinhole SPECT.
BACKGROUND: Iodine 123-labeled 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) is mainly trapped in the myocardium as triglyceride, depending on the adenosine triphosphate level. Ten percent to 20% of it is metabolized through alpha-oxidation after beta-oxidation; however, the precise mechanism of the regulatory pathways of BMIPP is yet to be clarified. METHODS AND RESULTS: A brief left coronary artery occlusion (10-30 minutes) was performed in 28 male Wistar-Kyoto rats. Dual single photon emission computed tomography images of BMIPP and thallium 201 were obtained 3 days and 24 days after the operation. The activities of 3-hydroxyacyl-coenzyme A dehydrogenase (HAD), citrate synthase (CS), and alpha-glycerol-phosphate dehydrogenase (GPD) were then measured in both ischemic and nonischemic regions. BMIPP and Tl-201 chloride severity scores were also evaluated conventionally. CS and HAD levels were significantly lower in the ischemic region than in the nonischemic region in the chronic group (CS, 102.9 +/- 28.1 vs 138.7 +/- 33.7 micromol/g/min, respectively, P =.0051; HAD, 54.7 +/- 20.1 vs 78.6 +/- 18.7 micromol/g/min, respectively, P =.0031). There was no difference in GPD between the ischemic and nonischemic regions. The BMIPP severity score had closer inverse relations with HAD (acute, r = -0.82; chronic, r = -0.80) and CS (acute, r = -0.87; chronic, r = -0.81), but not with GPD, than did Tl-201 chloride severity score. CONCLUSIONS: BMIPP imaging correlates well with the activities of HAD and CS, suggesting that a decrease in BMIPP uptake reflects deterioration of both fatty acid metabolism and citrate cycle and shows information other than regional myocardial perfusion.
3-Hydroxyacyl CoA Dehydrogenases↗