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 379 records · Page 21Linked to original sources
PubMed1987

Fatty acid metabolism in symptomatic patients with mitral valve prolapse but without coronary artery disease--comparison with 201Tl myocardial perfusion scintigraphy.

Using 123I-omega-heptadecanoic acid (HDA) and 201Tl, respectively, myocardial fatty acid metabolism and perfusion were studied in 51 symptomatic patients with mitral valve prolapse (MVP) as diagnosed by ventriculography, and no evidence of coronary artery disease. Twelve subjects with normal coronary arteries and normal ventriculogram served as a control group for the evaluation of elimination kinetics of HDA. In the control group, the mean elimination half-life was 26.1 +/- 3.6 min, whereas the patients with MVP had a mean value of 25.0 +/- 6.4 min. In patients with MVP, a high incidence concerning abnormalities of accumulation and/or elimination of HDA occurred, namely accumulation defects in 31% and both prolonged and shortened elimination half-lives in 16% and 29%, respectively. Myocardial perfusion scintigraphy using 201Tl showed abnormalities in 76%. Correlations were found between decreased uptake of HDA and prolonged elimination half-life as well as defects by 201Tl, presumably due to ischemia based on small-vessel disease or abnormalities of cellular metabolism.

Adult↗
PubMed2002

Differences in fatty acid metabolic disorder between ischemic myocardium and doxorubicin-induced myocardial damage: assessment using BMIPP dynamic SPECT with analysis by the Rutland method.

UNLABELLED: Dynamic myocardial SPECT data acquired with 15-(123)I-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) were analyzed by the Rutland method. The relative time-activity curves generated from dynamic SPECT in normal control subjects were compared with similar curves from patients with established ischemic heart disease (IHD) and doxorubicin-induced myocardial damage (DxMD). Comparison of such time-activity curves may provide some indirect information concerning qualitative differences in BMIPP metabolism. METHODS: Thirteen patients with various malignancies who received doxorubicin, 16 patients with IHD, and 15 normal control subjects were examined. Immediately after the bolus injection of BMIPP, dynamic data acquisition with a 3-head SPECT system was started and continued for 15 min. Using the time-activity curves of the myocardium as the output function (Mo(t)) and the time-activity curves of the left ventricular cavity as the input function (B(t)), the Rutland equation was calculated: Mo(t)/B(t) = F + K integral B(t)dt/B(t), where F is the blood - background subtraction factor and K is the uptake constant. The duration of the linear portion in this equation and the K values were evaluated. RESULTS: Mo(t)/B(t) was plotted against integral B(t)dt/B(t). Mo(t)/B(t) showed a good linear correlation with integral B(t)dt/B(t) from 30 s to 230 +/- 57 s in normal control subjects. The duration of this linearity was prolonged to 317 +/- 79 s in DxMD (P = 0.0014) and shortened to 182 +/- 58 s in IHD (P = 0.039). The mean K value was 0.0740 +/- 0.0184 in normal control subjects, significantly higher than the K values of 0.0599 +/- 0.0148 in DxMD patients (P = 0.026) and 0.0497 +/- 0.0189 (P = 0.0020) in IHD patients. CONCLUSION: Analysis of BMIPP dynamic SPECT data by the Rutland method is useful for detecting qualitative differences in BMIPP metabolism in various types of myocardial damage. It is speculated that the fatty acid metabolic disorder is characterized by a delay in metabolism in DxMD and by increased backdiffusion in IHD.

Aged↗
PubMed2001

Stimulatory effects of leptin and muscle contraction on fatty acid metabolism are not additive.

Leptin has been shown to acutely stimulate fatty acid oxidation and triacylglycerol hydrolysis in skeletal muscle. These effects are similar to those induced by muscle contraction alone. Several studies have demonstrated that, during aerobic exercise, plasma leptin concentrations are well maintained; however, none has examined whether the stimulatory effects of leptin and contraction on muscle lipid metabolism are additive. This is the first study to examine the direct effect of leptin on lipid and carbohydrate (CHO) metabolism in isolated oxidative muscle over a range of contraction intensities. We examined the effect of leptin (10 microg/ml) on the synthesis and degradation of muscle lipid pools [phospholipid (PL), diacylglycerol (DG), triacylglycerol (TG)] and palmitate oxidation in isolated resting and contracting (2, 8, and 20 tetani/min) soleus muscles. At rest, leptin increased fatty acid oxidation (+ 40%, P < 0.05) and TG hydrolysis (+ 47%, P < 0.05), while blunting TG esterification (-20%, P < 0.05). Glucose oxidation was unaffected at rest in the presence of leptin. During tetanic contraction, fatty acid oxidation (+20-114%, P < 0.05) and TG esterification (+ 19-33%, P < 0.05) as well as net TG utilization (+ 23%, P < 0.05) were all significantly increased. However, leptin was without further effect on any of these parameters during contraction. Net utilization of intramuscular glycogen, as well as glucose oxidation, was unaffected during contraction by leptin. The findings of the present study indicate that leptin has an important influence on lipid metabolism in resting muscle, but not during contraction.

Animals↗
PubMed2004

The role of uncoupling protein 3 in fatty acid metabolism: protection against lipotoxicity?

The physiological function of the mitochondrial uncoupling protein (UCP), UCP3, is still under debate. There is, however, ample evidence to indicate that, in contrast to UCP1, the primary function of UCP3 is not the dissipation of energy. Rather, several lines of evidence suggest that UCP3 is associated with cellular fatty acid metabolism. The highest levels of expression of UCP3 have been found in type 2 glycolytic muscle fibres, and fasting and high-fat diets up regulate UCP3. This up-regulation is most pronounced in muscle with a low fat oxidative capacity. Acute exercise also up regulates UCP3, and this effect has been shown to be a result of the exercise-induced increase in plasma fatty acid levels. In contrast, regular physical activity, which increases fat oxidative capacity, reduces UCP3 content. Based on these data it has been postulated that UCP3 functions to export those fatty acids that cannot be oxidized from the mitochondrial matrix, in order to prevent fatty acid accumulation inside the matrix. Several experiments have been conducted to test this hypothesis. Blocking carnitine palmitoyltransferase 1, thereby reducing fat oxidative capacity, rapidly induces UCP3. High-fat diets, which increase the mitochondrial supply of fatty acids, also up regulate UCP. However, feeding a similar amount of medium-chain fatty acids, which can be oxidized inside the mitochondrial matrix and therefore does not need to be exported from the matrix, does not affect UCP3 protein levels. In addition, UCP3 is increased in patients with defective beta-oxidation and is reduced after restoring oxidative capacity. In conclusion, it is suggested that UCP3 has an important physiological function in facilitating outward transport from the mitochondrial matrix of fatty acid anions that cannot be oxidized, thereby protecting against lipid-induced mitochondrial damage.

Anions↗
PubMed2001

Growth reduction in glioma cells after treatment with tetradecylthioacetic acid: changes in fatty acid metabolism and oxidative status.

During aerobic metabolism, a small amount of partially reduced oxygen is produced, yielding reactive oxygen species (ROS). Peroxisomes and mitochondria are major contributors to cellular ROS production, which is normally balanced by consumption by antioxidants. The fatty acid analogue tetradecylthioacetic acid (TTA) promotes mitochondrial and peroxisomal proliferation, and may induce oxidative stress and change the growth potential of cancer cells. In the present study, we found that TTA reduced [(3)H]thymidine incorporation in the glioma cell lines BT4Cn (rat), D54Mg (human), and GaMg (human) in a dose- and time-dependent manner. The 50% inhibitory TTA doses were approximately 125 microM for BT4Cn and D54Mg cells and 40 microM for GaMg cells after 4 days. alpha-Tochopherol counteracted this inhibition in GaMg cells. TTA enhanced the oxidation of [1-(14)C]palmitic acid, which could be explained by stimulation of enzymes involved in peroxisomal (fatty acyl-CoA oxidase) and/or mitochondrial (carnitine palmitoyltransferase) fatty acid oxidation. The glutathione content and the activities of glutathione peroxidase, glutathione reductase, and glutathione S-transferase were differentially affected. Increased malondialdehyde (MDA) production was seen in TTA-treated GaMg and D54Mg cells, but not in BT4Cn cells, in vitro. In BT4Cn tumor tissue from TTA-treated rats, MDA was increased while the alpha-tocopherol content tended to decrease. TTA increased the level of cytosolic cytochrome c in BT4Cn cells, which suggests induction of apoptotic cascades. Although several mechanisms are likely to be involved in the TTA-mediated effects on growth, we propose that modulation of cellular redox conditions caused by changes in fatty acid metabolism may be of vital importance.

Animals↗
PubMed1995

N-3 and n-6 fatty acid metabolism in undifferentiated and differentiated human intestine cell line (Caco-2).

Metabolism of n-6 and n-3 fatty acids in the undifferentiated and differentiated human adenocarcinoma colon cell line (Caco-2) was studied. In cells incubated with either 18:2n-6 or 18:3n-3, no significant amounts of long chain n-6 and n-3 metabolites were found. Incubation with either 18:3n-6 or 18:4n-3 raised significantly the levels of 20:3n-6 and 20:4n-3, respectively. In the undifferentiated cells, significant proportions of 20:3n-6 and 20:4n-3 were further delta 5-desaturated to form 20:4n-6 and 20:5n-3, respectively. Incubation with either 20:4n-6 or 20:5n-3 raised the levels of their direct elongation products, 22:4n-6 and 22:5n-3, respectively. Incubation with 22:4n-6 or 22:5n-3 increased the levels of 20:4n-6 and 20:5n-6. These results suggest that delta 6-desaturation in the Caco-2 cells is less active in comparison with elongation, delta 5-desaturation and retro-conversion. These enzymes were modulated by the state of differentiation, and appeared to be non-specific to n-3 and n-6 fatty acids. When cells were incubated with 18:3n-6 and 18:4n-3 concomitantly, the levels of incorporation of total n-6 fatty acids into cellular lipids were greater than those of the n-3 fatty acids, whereas the ratios of 20+22 carbon metabolites to 18-carbon precursor favored n-3 over n-6 fatty acids. These results suggest that n-3 and n-6 fatty acids were not metabolized identically in Caco-2 cells.

Caco-2 Cells↗
PubMed2005

In vivo imaging of hepatic fatty acid metabolism in patients with nonalcoholic steatohepatitis using semiquantative (123)I-BMIPP liver scan.

Recent progress of studies in NASH displays multi-disciplinary characters of the pathogeneses. Despite these advances, the strategic use of imaging modalities such as CT, US, and MRI, remains a relatively low priority in clinical situations, because these can only visualize the presence of fatty infiltration to the hepatic parenchyma, impossible to figure out the dynamic function of NASH liver. Morphological alteration such as CT value, MR signal intensity and echo-grade do not distinguish NASH from simple fatty liver. In this presentation, from a radiologic viewpoint, we show the feasibility of in vivo fatty acid imaging with (123)I-beta-methyl-p-iodophenyl-pentadecanoic acid (BMIPP). BMIPP is an (123)I labeled fatty acid analog for imaging damaged myocardium, using conventional nuclear imaging equipment. Under normal conditions, the energy source for myocardial utilization is dependent on the beta-oxidation of fatty acids. For energy production in ischemic myocardium, the drastic switch from reduced beta-oxidation of fatty acids to glucose metabolism is well known. BMIPP can detect the area of reduced fatty acids metabolism on myocardial imaging and the data can be converted into semiquantitative analysis. Therefore, we speculate that the use of BMIPP to in vivo hepatic imaging in NASH could highlight a lot of matters of NASH. Details of this presentation include: (1) Hepatic imaging with BMIPP; (2) Clearance of BMIPP from NASH liver; (3) semiquantitative analysis of hepatic BMIPP clearance and clinical features of NASH; (4) Profiles of NASH categorized by BMIPP imaging and (5) Preliminary data of BMIPP clearance in patients with Tamoxifen-induced NASH. The core of our stance in this presentation is searching for valuable advice on clinical use of BMIPP in patients with NASH from specialists in the field of HEPATOLOGY.

Journal Article↗
PubMed2006

Acyl carrier protein/SpoT interaction, the switch linking SpoT-dependent stress response to fatty acid metabolism.

Bacteria respond to nutritional stresses by producing an intracellular alarmone, guanosine 5'-(tri)diphosphate, 3'-diphosphate [(p)ppGpp], which triggers the stringent response resulting in growth arrest and expression of resistance genes. In Escherichia coli, upon fatty acid or carbon starvation, SpoT enzyme activity switches from (p)ppGpp degradation to (p)ppGpp synthesis, but the signal and mechanism for this response remain totally unknown. Here, we characterize for the first time a physical interaction between SpoT and acyl carrier protein (ACP) using affinity co-purifications and two-hybrid in E. coli. ACP, as a central cofactor in fatty acid synthesis, may be an ideal candidate as a mediator signalling starvation to SpoT. Accordingly, we show that the ACP/SpoT interaction is specific of SpoT and ACP functions because ACP does not interact with the homologous RelA protein and because SpoT does not interact with a non-functional ACP. Using truncated SpoT fusion proteins, we demonstrate further that ACP binds the central TGS domain of SpoT, consistent with a role in regulation. The behaviours of SpoT point mutants that do not interact with ACP reveal modifications of the balance between the two opposite SpoT catalytic activities thereby changing (p)ppGpp levels. More importantly, these mutants fail to trigger (p)ppGpp accumulation in response to fatty acid synthesis inhibition, supporting the hypothesis that the ACP/SpoT interaction may be involved in SpoT-dependent stress response. This leads us to propose a model in which ACP carries information describing the status of cellular fatty acid metabolism, which in turn can trigger the conformational switch in SpoT leading to (p)ppGpp accumulation.

Acyl Carrier Protein↗
PubMed2006

Alterations in intestinal fatty acid metabolism in inflammatory bowel disease.

Inflammatory bowel disease (IBD) constitutes a severe intestinal disorder in developed countries with increasing incidence worldwide. Upcoming evidence indicates an important role of intestinal epithelial barrier function in the development of IBD. Fatty acids exert nutritional and protective effects on enterocytes, serve as activators of transcription and constitute precursors of inflammatory mediators. The aim of this study was to investigate differential regulation of genes involved in fatty acid uptake and endogenous fatty acid biosynthesis in IBD. Mucosal biopsy specimens from non-affected regions of the intestine were subjected to DNA microarray analysis. Gene array analysis revealed a variety of genes involved in fatty acid uptake and synthesis to be differentially expressed in ileum and colon of selected IBD patients. To verify these results, real-time RT-PCR was performed for selected regulated candidate genes in larger IBD sample numbers. In single biopsy analysis long chain acyl-CoA synthetase (ACSL) 1 and 4 were upregulated in IBD (P<0.05), while a significant decrease in fatty acid synthase expression was found in ileum and colon of ulcerative colitis patients (P<0.001). Expression of the transcription factor liver X receptor (LXR) which was previously shown to induce fatty acid synthase gene expression was not altered on mRNA level in IBD. However, in cell culture experiments using the human intestinal cell line LS174T induction of fatty acid synthase by the LXR ligand T0901317 was inhibited by TNFalpha. Moreover, these experiments indicated a decrease of LXR protein levels by TNFalpha treatment. These data suggest that the decrease of fatty acid synthase expression in ulcerative colitis patients could be at least partially due to a loss of LXR expression and function in the presence of pro-inflammatory cytokines. Observed alterations in expression of genes of fatty acid metabolism may contribute to the pathophysiology of ulcerative colitis.

Animals↗
PubMed2000

Effects of protein-energy malnutrition and human immunodeficiency virus-1 infection on essential fatty acid metabolism in children.

This report summarizes data on the availability of essential fatty acids (EFAs) and their long-chain polyunsaturated fatty acid (LCPUFA) metabolites in protein-energy malnutrition (PEM), in human immunodeficiency virus-1 (HIV-1) infection for which less information is available, and the combination of both PEM and HIV-1. The contribution of different EFAs and LCPUFAs to the fatty-acid composition of plasma and erythrocyte membrane lipids was found to be reduced in children with PEM in comparison with well-nourished children. In addition to limited dietary EFA supply, reduced bioconversion of EFAs to their respective LCPUFA metabolites and/or peroxidative degradation of LCPUFAs may contribute to the reduction of LCPUFA status in malnourished children. Restoration of normal energy, protein, and EFA intakes does not appear to readily correct abnormalities of plasma and erythrocyte membrane LCPUFA values. Enhanced dietary supply of LCPUFAs and/or improved supply of antioxidant vitamins may represent novel therapeutic modalities in severe PEM. With and without PEM, HIV infection was related to altered availability of various EFAs and LCPUFAs in HIV-seropositive children. The plasma total lipid fatty-acid profiles seen in well-nourished children with HIV infection were compatible with an HIV infection-related enhancement of the metabolic activity of the conversion of EFAs to their respective LCPUFA metabolites. However, the plasma phospholipid EFA and LCPUFA profiles seen in severely malnourished children with HIV infection more closely resembled those seen in children with PEM but without HIV infection than in those in children with HIV infection but no PEM. Metabolic studies using stable isotope-labeled fatty acids may contribute to better understanding of the HIV-related changes in EFA metabolism and clearly are needed before therapeutic conclusions can be drawn.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder.

Attention-deficit hyperactivity disorder (ADHD) is the term used to describe children who are inattentive, impulsive, and hyperactive. The cause is unknown and is thought to be multifactorial. Based on the work of others, we hypothesized that some children with ADHD have altered fatty acid metabolism. The present study found that 53 subjects with ADHD had significantly lower concentrations of key fatty acids in the plasma polar lipids (20:4n-6, 20:5n-3, and 22:6n-3) and in red blood cell total lipids (20:4n-6 and 22:4n-6) than did the 43 control subjects. Also, a subgroup of 21 subjects with ADHD exhibiting many symptoms of essential fatty acid (EFA) deficiency had significantly lower plasma concentrations of 20:4n-6 and 22:6n-3 than did 32 subjects with ADHD with few EFA-deficiency symptoms. The data are discussed with respect to cause, but the precise reason for lower fatty acid concentrations in some children with ADHD is not clear.

Attention Deficit Disorder with Hyperactivity↗
PubMed1988

Choice of infusion-sampling mode for tracer studies of free fatty acid metabolism.

To determine the preferred infusion-sampling mode for isotopic studies of free fatty acid (FFA) metabolism, tracer [( 14C]palmitate) was infused into the left ventricle of five anesthetized dogs, and tracee ([3H]palmitate) was infused into three separate peripheral veins of each dog. The [14C]palmitate specific activity (SA) was lower in mixed venous than arterial blood, and [3H]palmitate SA was equal in both sites. The actual infusion rate of [3H]palmitate [2.15 +/- 0.31 X 10(5) disintegrations/min (dpm).kg-1.min-1] could be accurately predicted (2.14 +/- 0.32 X 10(5) dpm.kg-1.min-1) using the known [14C]palmitate infusion rate and the arterial plasma [14C]-to-[3H]palmitate ratio. In contrast, the mixed venous [14C]-to-[3H]palmitate ratio resulted in overestimates (P less than 0.05) of the actual [3H]palmitate infusion rate. In summary, venous tracer infusion with arterial blood sampling for FFA tracer studies provides the most accurate estimates of tracee rate of appearance.

Animals↗
PubMedDate not supplied

[Study on regulation of long-chain fatty acid metabolism with the use of computer analysis of complete bacterial genomes].

One of the main trends in the prokaryote genomics is the comparative analysis of metabolic pathways. This method can be used for the analysis of experimentally studied systems of co-regulated genes, as well as genes with unknown regulatory signals. In this study we apply the comparative analysis of regulatory signals to the genes of the enzymes for fatty acid metabolism from Escherichia coli, Haemophilus influenzae, Vibrio cholerae, Yersinia pestis. Transcription of these genes is regulated by the FadR protein. We describe the FadR regulation of the long-chain fatty acid oxidation and partially that of the fatty acid biosynthesis. We also demonstrate that the gene yafH encoding acyl-CoA dehydrogenase is identical to the gene fadE, previously identified by genetic techniques.

Acyl-CoA Dehydrogenase↗
PubMed1994

Patency of the infarct-related coronary artery--a pertinent factor in late recovery of myocardial fatty acid metabolism among patients receiving thrombolytic therapy?

The decrease in mortality among patients receiving thrombolytic therapy for myocardial infarction is greater than would be expected from the improvement in left ventricular contractile function alone; thus some additional advantage of recanalization of the infarct-related coronary artery probably exists. Changes in the post-infarction myocardial metabolic state with respect to artery patency have not been studied with a gamma camera previously. A single-photon emission tomography scan using the fatty acid analogue para-123I-iodophenylpentadecanoic acid was performed at rest before hospital discharge on nine patients with first anterior myocardial infarction. All patients had received intravenous thrombolytic therapy at the beginning of the insult. The semiquantitative analysis of the left ventricle included a total of 44 segments in each patient. The test was repeated 3 months later, with the patients divided into two groups: six patients had an angiographically patent left anterior descending coronary artery (group A), and three an occluded artery (group B). In group A the number of myocardial segments with abnormal (< 70% of maximum) fatty acid uptake was initially 20.2 +/- 4.7 (mean +/- SD) and was reduced to 11.3 +/- 6.1 during the follow-up (95% confidence interval of the decrease 16.0-1.7 segments). In group B the number of these aberrant segments was fairly constant (21.7 +/- 13.1, initial test, and 21.3 +/- 13.3, retest). Our preliminary results suggest that even when thrombolytic therapy fails to prevent myocardial infarction, myocardial fatty acid metabolism has a better change of recovering if the relevant coronary artery has regained its patency.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1991

Demonstration of disturbed free fatty acid metabolism of myocardium in patients with non-insulin-dependent diabetes mellitus as measured with iodine-123-heptadecanoic acid.

Myocardial free fatty acid metabolism and left ventricular function were evaluated in 15 middle-aged patients with non-insulin-dependent diabetes mellitus (NIDDM) and in 8 healthy control subjects. The study subjects had no evidence of coronary heart disease on the basis of clinical history, exercise ECG or myocardial perfusion scintigraphy. During peak exercise, iodine-123 hepatadecanoic acid (HDA) was intravenously injected. Myocardial activity distribution of 123I-HDA was measured 10, 30, and 50 min after exercise using single-photon emission tomography (SPET); and then further corrected by free 123I-iodine. Venous blood samples were drawn for detecting the plasma activity of 123I. The net extraction of 123I-HDA into the myocardium was obtained by dividing the corrected tissue 123I concentration by the integral of the plasma time activity curve. The net extraction was 0.40 +/- 0.06 min-1 (mean +/- SD) patients with NIDDM and 0.38 +/- 0.06 min-1 in control subjects (P greater than 0.1), respectively. The faster elimination rate of 123I-HDA was found in patients with NIDDM (0.029 +/- 0.008 min-1) than in control subjects (0.022 +/- 0.004 min-1; P less than 0.01). There was no statistically significant difference in left ventricular ejection fraction (LVEF) at rest between patients with NIDDM (53 +/- 9%) and control subjects (56 +/- 2%), whereas the increase of LVEF during exercise remained lower in patients with NIDDM (3.4 +/- 8.2%) than in control subjects (11.8 +/- 5.8%; P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus, Type 2↗