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PubMed1996

Fatty acid metabolic imaging with 123I-BMIPP for the diagnosis of coronary artery disease: application to patients with diabetes mellitus and hyperlipidaemia.

The aim of this study was to assess the relation of plasma substrate concentration to 123I-beta-methyliodophenyl-pentadecanoic acid (123I-BMIPP) kinetics in the myocardium and to test the application of 123I-BMIPP imaging to patients with diabetes mellitus (DM) and/or hyperlipidemia (HL). 123I-BMIPP imaging was performed on 78 patients with suspected coronary artery disease, 22 with HL, 11 with DM, 12 with HL and DM, and 33 with neither HL or DM. Significant coronary stenosis (defined as > or = 50% of luminal diameter) was documented in 49 patients. After an overnight fast, blood samples were drawn for blood glucose, insulin, cholesterol, triglycerides and free fatty acid levels. Then, 148 MBq 123I-BMIPP was injected intravenously and flushed rapidly with saline. Data were obtained for 60s in a standard anterior projection in list mode, at a rate of 1 frame per second. Myocardial single photon emission tomographic (SPET) images were obtained 20 min and 4 h post-injection. The myocardial uptake of 123I-BMIPP was calculated using the Ishii-MacIntyre method. Regional accumulation of 123I-BMIPP was scored semi-quantitatively from 0 (normal) to 4 (no activity), and the sum of regional scores in each patient was defined as the total defect score (TDS). Myocardial uptake and clearance of 123I-BMIPP had no relation to the levels of blood glucose, insulin, cholesterol, triglycerides or free fatty acids. Myocardial uptake and clearance of 123I-BMIPP, TDS and the sensitivity of detecting significant coronary stenosis were not significantly different between the four groups of patients. We conclude that 123I-BMIPP can be used to detect impaired fatty acid metabolism in patients with diabetes mellitus and/or hyperlipidaemia.

Biological Transport, Active↗
PubMed2003

Changes of peroxisomal fatty acid metabolism during cold acclimatization in hibernating jerboa (Jaculus orientalis).

Jerboa (Jaculus orientalis) is a deep hibernator originating from sub-desert highlands and represents an excellent model to help to understand the incidence of seasonal variations of food intake and of body as well as environmental temperatures on lipid metabolism. In jerboa, hibernation processes are characterized by changes in the size of mitochondria, the number of peroxisomes in liver and in the expression of enzymes linked to fatty acid metabolism. In liver and kidney, cold acclimatization shows an opposite effect on the activities of the mitochondrial acyl-CoA dehydrogenase (-50%) and the peroxisomal acyl-CoA oxidase (AOX) (+50%), while in brown and white adipose tissues, both activities are decreased down to 85%. These enzymes activities are subject to a strong induction in brown and in white adipose tissue (3.4- to 7.5-fold, respectively) during the hibernation period which is characterized by a low body temperature (around 10 degrees C) and by starvation. Expression level of AOX mRNA and protein are increased during both pre-hibernation and hibernation periods. Unexpectedly, treatment with ciprofibrate, a hypolipemic agent, deeply affects lipolysis in brown adipose tissue by increasing acyl-CoA dehydrogenase activity (3.4-fold), both AOX activity and mRNA levels (2.8- and 3.8-fold, respectively) during pre-hibernation. Therefore, during pre-hibernation acclimatization, there is a negative regulation of fatty acid degradation allowing to accumulate a lipid stock which is later degraded during the hibernation period (starvation) due to a positive regulation of enzymes providing the required energy for animal survival.

Acclimatization↗
PubMed1988

Systemic triglyceride storage disease with normal carnitine: a putative defect in long-chain fatty acid metabolism.

A 45-year-old Japanese man presented with lipid storage myopathy, fatty liver, cardiomyopathy, vacuolated leukocytes (Jordans' anomaly) and perceptive deafness. His parents were consanguineous and his younger sister was also affected. Histopathological and biochemical studies revealed an abnormal accumulation of triglyceride in muscle, liver, leukocytes, gastrointestinal endothelial cells and cultured skin fibroblasts. On electron microscopy, the vacuoles lacked limiting membranes and were adjacent to the mitochondria. Total and free carnitines in muscle were normal levels. Production rate of 14CO2 or acid-soluble [14C]metabolites from [1-14C]palmitate in the patient's cells was decreased to about 50% of that in control cells, whereas that from [1-14C]butyrate was normal. Long-chain fatty acyl esterase activities in the patient's leukocytes were normal at both pH 4.0 and pH 8.0. Despite the strong suggestion of an impaired metabolism of long-chain fatty acids, there were no evidences of abnormalities in carnitine metabolism or uptake of fatty acids into cells. The disorder is clinically different from defects in carnitine metabolism, defects in the carnitine-acylcarnitine translocase system or in mitochondrial beta-oxidation enzymes. Although the underlying metabolic defect has not been elucidated, this disease seems to be an autosomal-recessively inherited disorder of systemic triglyceride storage, probably due to an impaired regulation of lipolysis and triacylglycerol synthesis.

Carnitine↗
PubMedDate not supplied

Clinical aspects of essential fatty acid metabolism: Jonathan Rhoads Lecture.

The clinical implications of the metabolism of the 2 essential fatty acids, linoleic and alpha-linolenic acid, are most clearly related to the membrane phospholipid concentrations of their elongation and desaturation products, arachidonic, eicosapentaenoic, and docosahexaenoic acid. Levels of these very long chain polyunsaturated fatty acids can be altered by diet, prematurity, and disease which can affect growth (nutritional repletion) and the intensity and character of systemic inflammation as well as cognitive and visual function in infants.

Adult↗
PubMed2003

A null mutation in H-FABP only partially inhibits skeletal muscle fatty acid metabolism.

The low-molecular-mass, cytosolic heart-type fatty acid-binding protein (H-FABP) is thought to be required for shuttling FA through the cytosol. Therefore, we examined the effects of an H-FABP-null mutation on FA and carbohydrate metabolism in isolated soleus muscle at rest and during a period of increased metabolic demand (30-min contraction). There were lower concentrations of creatine phosphate (-41%), ATP (-22%), glycogen (-34%), and lactate (-31%) (P < 0.05) in H-FABP-null soleus muscles, but no differences in citrate synthase and beta-3-hydroxyacyl-CoA dehydrogenase activities or in the intramuscular triacylglycerol (TAG) depots. There was a 43% increase in subsarcolemmal mitochondria in H-FABP-null solei. FA transport was reduced by 30% despite normal content of sarcolemmal long-chain fatty acid transporters fatty acid translocase/CD36 and plasma membrane-associated FABP transport proteins. Compared with wild-type soleus muscles, the H-FABP-null muscles at rest hydrolyzed less TAG (-22%), esterified less TAG (-49%), and oxidized less palmitate (-71%). The H-FABP-null soleus muscles retained a substantial capacity to increase FA metabolism during contraction (TAG esterification by +72%, CO2 production by +120%), although these rates remained lower (TAG esterification -26% and CO2 production -64%) than in contracting wild-type soleus muscles. Glycogen utilization during 30 min of contraction did not differ, whereas glucose oxidation was lower at rest (-24%) and during contraction (-32%) in H-FABP-null solei. Although these studies demonstrate that the absence of H-FABP alters rates of FA metabolism, it is also apparent that glucose oxidation is downregulated. The substantial increase in FA metabolism in contracting H-FABP-null muscle may indicate that other FABPs are also present, a possibility that we were not able to completely eliminate.

Animals↗
PubMed1979

Regulation of hepatic free fatty acid metabolism by glucagon and insulin.

The roles of glucagon and insulin in the direct short-term regulation of hepatic free fatty acid (FFA) metabolism were studied in hepatocytes isolated from fed, fasted, and streptozotocin-induced diabetic rats. In fed animals, the principal metabolic product of palmitate metabolism was triglyceride, whereas ketones were the major product in fasted and diabetic animals. Glucagon at physiological concentrations increased ketogenesis and decreased triglyceride synthesis from palmitate in hepatocytes from fed rats at FFA concentrations 1.0 mM or less. Insulin had no effect on FFA metabolism when present as the sole hormone, but could antagonize the actions of submaximal concentrations of glucagon. The metabolism of palmitate in fasted or diabetic hepatocytes was unaffected by either hormone. Ketogenesis from octanoate was also unaffected by hormone addition in all cell types. These data are consistent with a locus of hormonal regulation at a step prior to beta-oxidation of fatty acid. Glucagon and insulin may modulate FFA metabolism by both intrahepatic and extrahepatic mechanisms.

Animals↗
PubMed1992

Nonessential fatty acids in formula fat blends influence essential fatty acid metabolism and composition in plasma and organ lipid classes in piglets.

The n-6 and n-3 fatty acid status of developing organs is the cumulative result of the diet lipid composition and many complex events of lipid metabolism. Little information is available, however, on the potential effects of the saturated fatty acid chain length (8:0-16:0) or oleic acid (18:1) content of the diet on the subsequent metabolism of the essential fatty acids 18:2n-6 and 18:3n-3 and their elongated/desaturated products. The effects of feeding piglets formulas with fat blends containing either coconut oil (12:0 + 14:0) or medium chain triglycerides (MCT, 8:0 + 10:0) but similar levels of 18:1, 18:2n-6 and 18:3n-3, or MCT with high or low 18:1 but constant 18:2n-6 and 18:3n-3 on the fatty acid composition of plasma, liver and kidney triglycerides, phospholipids and cholesteryl esters, and of brain total lipid, were studied. Diet-induced changes in the fatty acid composition of lipid classes were generally similar for plasma, liver and kidney. Dietary 18:1 content was reflected in tissue lipids and was inversely associated with levels of 18:2n-6. Lower percentage of 18:2n-6, however, was not associated with lower levels of its elongated/desaturated product 20:4n-6 but was associated with higher levels of 22:6n-3. Feeding coconut oil vs. MCT resulted in lower 18:1 levels in all lipids, and higher percentages of 20:4n-6 in tissue phospholipid. Increasing the dietary n-6/n-3 ratio from 5 to 8 significantly increased tissue percentage of 18:2n-6 and decreased phospholipid 22:6n-3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Isotope tracer measures of meal fatty acid metabolism: reproducibility and effects of the menstrual cycle.

Oxidation and adipose tissue uptake of dietary fat can be measured by adding fatty acid tracers to meals. These studies were conducted to measure between-study variability of these types of experiments and assess whether dietary fatty acids are handled differently in the follicular vs. luteal phase of the menstrual cycle. Healthy normal-weight men (n = 12) and women (n = 12) participated in these studies, which were block randomized to control for study order, isotope ([3H]triolein vs. [14C]triolein), and menstrual cycle. Energy expenditure (indirect calorimetry), meal fatty acid oxidation, and meal fatty acid uptake into upper body and lower body subcutaneous fat (biopsies) 24 h after the experimental meal were measured. A greater portion of meal fatty acids was stored in upper body subcutaneous adipose tissue (24 +/- 2 vs. 16 +/- 2%, P < 0.005) and lower body fat (12 +/- 1 vs. 7 +/- 1%, P < 0.005) in women than in men. Meal fatty acid oxidation (3H2O generation) was greater in men than in women (52 +/- 3 vs. 45 +/- 2%, P = 0.04). Leg adipose tissue uptake of meal fatty acids was 15 +/- 2% in the follicular phase of the menstrual cycle and 10 +/- 1% in the luteal phase (P = NS). Variance in meal fatty acid uptake was somewhat (P = NS) greater in women than in men, although menstrual cycle factors did not contribute significantly. We conclude that leg uptake of dietary fat is slightly more variable in women than in men, but that there are no major effects of menstrual cycle on meal fatty acid disposal.

Abdomen↗
PubMed1993

Polyunsaturated fatty acid metabolism and acetylated low density lipoprotein uptake in J774A.1 cells.

The mechanism of the antiatherogenic activity of n-3 polyunsaturated fatty acids is not well understood. In these studies, we studied the metabolism of unsaturated fatty acids in murine macrophage-like J774A.1 cells. The major metabolic pathway of 18- and 20-carbon chain unsaturated fatty acids in these cells is the sequence of 2-carbon chain elongation, successive two steps of delta 8- and delta 5-desaturation, and additional elongation. Polyunsaturated fatty acids, arachidonic acid [20:4 (n-6)] and eicosapentaenoic acid [20:5 (n-3)], are elongated into 22:4 (n-6) and 22:5 (n-3) fatty acids, respectively. Accumulation of 22:4 (n-6) and 22:5 (n-3) fatty acids shows that J774A.1 cells have an active chain elongation activity, but lack delta 4-desaturase activity. Furthermore, J774A.1 cells demonstrated almost negligible delta 6-desaturase activity. Enrichment of the membrane lipids of J774A.1 cells with polyunsaturated fatty acids, arachidonic acid [(20:4 (n-6)] and eicosapentaenoic acid [(20:5 (n-3)], increased membrane fluidity and decreased the uptake of acetylated low density lipoprotein.

Animals↗
PubMedDate not supplied

Alteration of hepatic fatty acid metabolism after burn injury in pigs.

BACKGROUND: The primary goal of this study was to investigate hepatic fatty acid (FA) metabolism after severe thermal injury. METHODS: Sixteen pigs were divided into control (n = 8) and burn (n = 8, with 40% full thickness total body surface area burned) groups. Catheters were inserted in the right common carotid artery, portal vein, and hepatic vein for blood sampling. Flow probes were placed around the hepatic artery and portal vein for blood flow measurements. Animals were given pain medication and sedated until the tracer study on day 4 after burn. The pigs were infused for 4 hours with U-13C16-palmitate in order to quantify hepatic FA kinetics and oxidation. RESULTS: Liver triglyceride (TG) content was elevated from 162 +/- 16 (control) to 297 +/- 28 micromol TG/g dry liver wt. (p < .05). Hepatic FA uptake and oxidation were similar between the 2 groups, as were malonyl-coenzyme A (CoA) levels and activities of acetyl-CoA carboxylase and adenosine monophosphate (AMP)-activated protein kinase. In contrast, incorporation of plasma-free fatty acids into hepatic TG was elevated (p < .05) and very low density lipoprotein TG (VLDL-TG) secretion was decreased from 0.17 +/- 0.02 (control) to 0.03 +/- 0.01 micromol/kg per minute in burned pigs (p < .05). CONCLUSIONS: The accumulation of hepatic TG in burned animals is due to inhibition of VLDL-TG secretion and to increased synthesis of hepatic TG. Fatty acids are not channeled to TG because of impaired oxidation.

Acetyl-CoA Carboxylase↗
PubMed1992

Effects of cholesterol on viability and (n - 6) fatty acid metabolism in cultured human monocyte-like cells (U937).

Effects of supplementation of growth-promoting cholesterol on metabolism of the cytotoxic (n - 6) polyunsaturated fatty acids in cultured human monocyte-like cells (U937) have been examined. U937 cells were incubated in 5% delipidated fetal bovine serum containing 0 or 38.7 microM cholesterol. The rate of uptake and the distribution of metabolites of (n - 6) fatty acids (such as 18:2(n - 6), 18:3(n - 6), and 20:3(n - 6), and 20:4(n - 6)) were examined by adding radiolabelled fatty acid at a level of 1 microgram/mL (3.3 microM for 20-carbon fatty acids and 3.6 microM for 18-carbon-fatty acids). For assessing the cytotoxicity, (n - 6) fatty acids were added to medium at a concentration of 5 micrograms/mL (16.4 microM for 20-carbon fatty acids and 17.9 microM for 18-carbon fatty acids). Cholesterol supplementation suppressed the uptake of all (n - 6) fatty acids and reduced the cytotoxic effects of 18:2(n - 6), 20:3(n - 6), and 20:4(n - 6), but not 18:3(n - 6). In addition, cholesterol supplementation increased peroxide production and metabolism of (n - 6) fatty acids in U937 cells. Thus, the differential suppressive effect of cholesterol on the cytotoxicity of different fatty acids could not be attributed to an inhibitory effect on fatty acid delta 6- and delta 5-desaturation, or to an antioxidant effect on peroxide formation.

Cell Death↗
PubMedDate not supplied

Myocardial free fatty acid metabolism of the ischemic heart treated by left ventricular assist device.

Three-beta-methyl-iodophenyl-pentadecanoic acid (BMIPP), a newly developed radiographic probe of metabolic processes in tissue free fatty acid (FFA), was applied to a study analyzing the effect of a left ventricular assist device (LVAD) on impaired dog hearts. The radiographic image obtained with BMIPP was compared with 201thallium chloride (TL) imaging, which indicates tissue perfusion. In the myocardial infarction (MI) model, the BMIPP and TL uptake were equally increased with the use of LVAD in the marginal area of the MI. In another model using the reperfused myocardium after ischemia, the BMIPP and TL uptake were increased in the reperfused area by LVAD pumping. On the other hand, BMIPP uptake in the residual myocardium of both models was decreased by LVAD pumping when compared with TL uptake. This discrepancy between these radiographic tracers in the residual myocardium suggests that tissue metabolic processes may be suppressed as result of a decrease in the energy demand by the myocardium caused by LVAD pumping. The results of this study showed that use of LVADs for the impaired heart improved cell function of "stunned" myocardium and also unloaded the excess work from the residual myocardium as judged by FFA metabolism.

Animals↗
PubMed1988

Nucleotide sequence of the fadR gene, a multifunctional regulator of fatty acid metabolism in Escherichia coli.

The Escherichia coli fadR gene is a multifunctional regulator of fatty acid and acetate metabolism. In the present work the nucleotide sequence of the 1.3 kb DNA fragment which encodes FadR has been determined. The coding sequence of the fadR gene is 714 nucleotides long and is preceded by a typical E. coli ribosome binding site and is followed by a sequence predicted to be sufficient for factor-independent chain termination. Primer extension experiments demonstrated that the transcription of the fadR gene initiates with an adenine nucleotide 33 nucleotides upstream from the predicted start of translation. The derived fadR peptide has a calculated molecular weight of 26,972. This is in reasonable agreement with the apparent molecular weight of 29,000 previously estimated on the basis of maxi-cell analysis of plasmid encoded proteins. There is a segment of twenty amino acids within the predicted peptide which resembles the DNA recognition and binding site of many transcriptional regulatory proteins.

Acetates↗
PubMed2003

Case report: unstable angina with flow-fatty acid metabolism mismatch and reverse flow-glucose metabolism mismatch patterns.

A 79-year-old man with unstable angina underwent an emergency coronary angiography, and percutaneous balloon angioplasty was performed for LCX. Left ventriculography showed hypokinesis in the posterior wall, inferior and apical wall immediately after the PCI therapy. The defects on 123I-BMIPP SPECT seen in the inferior, posterior and lateral wall were more extensive than those observed on 99mTc-MIBI SPECT, and a flow-fatty acid metabolism mismatch pattern was observed. The 18F-FDG PET showed reduced uptake in the lateral segment, although 13N-NH3 PET showed normal perfusion, and a reverse flow-glucose metabolism mismatch pattern was observed. Left ventriculography showed significant improve to normal contraction on the 3-month follow up, and there was not significantly reduced uptake in 99mTc-MIBI SPECT, 123I-BMIPP SPECT, 13N-NH3 PET or 18F-FDG PET.

Aged↗
PubMed1983

The control of fatty acid metabolism in liver cells from fed and starved sheep.

Isolated liver cells prepared from starved sheep converted palmitate into ketone bodies at twice the rate seen with cells from fed animals. Carnitine stimulated palmitate oxidation only in liver cells from fed sheep, and completely abolished the difference between fed and starved animals in palmitate oxidation. The rates of palmitate oxidation to CO2 and of octanoate oxidation to ketone bodies and CO2 were not affected by starvation or carnitine. Neither starvation nor carnitine altered the ratio of 3-hydroxybutyrate to acetoacetate or the rate of esterification of [1-14C]palmitate. Propionate, lactate, pyruvate and fructose inhibited ketogenesis from palmitate in cells from fed sheep. Starvation or the addition of carnitine decreased the antiketogenic effectiveness of gluconeogenic precursors. Propionate was the most potent inhibitor of ketogenesis, 0.8 mM producing 50% inhibition. Propionate, lactate, fructose and glycerol increased palmitate esterification under all conditions examined. Lactate, pyruvate and fructose stimulated oxidation of palmitate and octanoate to CO2. Starvation and the addition of gluconeogenic precursors stimulated apparent palmitate utilization by cells. Propionate, lactate and pyruvate decreased cellular long-chain acylcarnitine concentrations. Propionate decreased cell contents of CoA and acyl-CoA. It is suggested that propionate may control hepatic ketogenesis by acting at some point in the beta-oxidation sequence. The results are discussed in relation to the differences in the regulation of hepatic fatty acid metabolism between sheep and rats.

3-Hydroxybutyric Acid↗