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Results for “FATTY ACID METABOLISM”

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PubMed1989

Effects of L-carnitine administration on short-chain fatty acid (acetic acid) and long-chain fatty acid metabolism during hemodialysis.

The purpose of the study is to investigate the effects of L-carnitine on the exogenous acetate metabolism during hemodialysis together with the triglyceride and free fatty acid metabolism. Sixteen chronic renal failure patients on acetate dialysis were orally administered 1,200 mg of L-carnitine chloride per day for 12 weeks. Plasma triglyceride concentrations at 30 and 60 min following initiation of hemodialysis were significantly lower than before hemodialysis, while the plasma concentrations of free fatty acid at the same points into hemodialysis were significantly higher than before hemodialysis, whether L-carnitine chloride was being given or not. This is attributed to the enhanced degradation of triglyceride and the increased generation of the free fatty acid with heparin administration during hemodialysis. The L-carnitine chloride treatment did not affect the plasma triglyceride concentrations at 30 and 60 min into hemodialysis, whereas the free fatty acid concentrations at the same points into hemodialysis were significantly lower after L-carnitine chloride administration commenced than before it. This is attributed to the fact that fatty acid oxidation was enhanced following the L-carnitine chloride treatment. Compared to before the drug administration, the whole body clearance of exogenous acetate was significantly increased after the drug was given, and the plasma acetate level during hemodialysis fell accordingly. This is attributed to the fact that with L-carnitine chloride administration, the amount of accumulated acyl-CoA in the cytosol decreased and consequently the citrate cycle function increased.

Acetates↗

PubMedDate not supplied

[Fatty acid metabolic and perfusion abnormalities in hypertrophied myocardium assessed by dual tracer tomography using thallium-201 and iodine-123-beta-methylpentadecanoic acid].

Fatty acid metabolic and perfusion abnormalities associated with cardiac hypertrophy were investigated using dual tracer tomography with thallium and a cardiac metabolic tracer, 15-(p-iodophenyl)-3-R, S-methylpentadecanoic acid (BMIPP), in eight patients with hypertrophic cardiomyopathy (HCM) and in three with hypertension (HT). Thallium and BMIPP uptakes were scored and analyzed in 143 segments (13/heart) by comparison with the left ventricular wall thickness measured by two-dimensional echocardiography. Complete agreement of both scores in HT patients was significantly higher than that in HCM patients (64% vs 24%, p < 0.001), while a lower BMIPP uptake compared to that of thallium (mismatching) was observed more frequently in HCM than in HT patients (65% vs 31%, p < 0.001). The wall thickness significantly (p < 0.005) correlated with BMIPP uptake score. HCM patients showed a low BMIPP uptake in 22 hypertrophic segments (59%) and 15 non-hypertrophic segments (41%), and reduced BMIPP uptake in 29% hypertrophic segments, while HT patients showed just five segments with decreased BMIPP uptake of which 4 were non-hypertrophic and only one hypertrophic. The left ventricular ejection fraction assessed by radionuclide ventriculography was normal and no regional wall motion abnormality was detected in any patient by echocardiographic and scintigraphic studies. Metabolic abnormalities detected by the iodine-123-beta-methyl fatty acid analog in hypertrophic cardiomyopathy may be independent of thallium myocardial perfusion, regional wall motion, or the magnitude of cardiac hypertrophy, suggesting that fatty acid imaging may be useful in investigating the pathogenesis and subclinical abnormality of hypertrophic cardiomyopathy, and differentiation from secondary, induced cardiac hypertrophy.

Adult↗

PubMed1991

Modulation of coronavirus-mediated cell fusion by homeostatic control of cholesterol and fatty acid metabolism.

Cellular susceptibility to fusion mediated by murine coronavirus (mouse hepatitis virus, MHV strain A59) was separated into lipid-dependent and lipid-independent mechanisms with the use of subclones and selected mutants of mouse L-2 fibroblasts. Fusion-resistant L-2 cell mutants had similar cholesterol and fatty acid composition as did their fusion-susceptible parent subclone, and were presumably deficient in a genetically mutable non-lipid, host cell factor (e.g., fusion protein receptor). On the other hand, cellular sensitivity to virus fusion, which is known to be influenced by cell cholesterol content [Daya et al., 1988], was shown further to be modulated by homeostatic alterations in fatty acid metabolism. Cholesterol supplementation of mouse L-2 fibroblasts or of peritoneal macrophages from MHV-susceptible mice elevated susceptibility to viral fusion. Increased fusion susceptibility occurred in cholesterol-supplemented L-2 cells in the absence of any detectable alterations in host cell fatty acid composition, thus demonstrating fusion enhancement by cholesterol alone. L-2 cells cloned by limiting dilution in normal (not cholesterol-supplemented) medium were found to be heterogeneous in cholesterol content. Interestingly, high cholesterol-containing subclones had increased levels of C-18:0, C-18:2, C-20:4, and C-22:6 and markedly reduced levels of C-18:1 fatty acids when compared to low cholesterol-containing subclones. High cholesterol-containing subclones did not show enhanced susceptibility to viral fusion, suggesting that homeostatic alteration of fatty acid metabolism compensated for the increased cholesterol levels and countered the normally fusion-enhancing effect of cholesterol alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Measurement of myocardial fatty acid metabolism: kinetics of iodine-123 heptadecanoic acid in normal dog hearts.

To define the potential of iodine-123 heptadecanoic acid (IHA) for the noninvasive assessment of myocardial fatty acid metabolism with gamma camera imaging, the influence of myocardial oxygen consumption (MVO2) and blood flow (MBF) on extraction and half-times of IHA were investigated in dogs. Following IHA injection into the left circumflex coronary artery, extraction fraction and half-times were derived from the peak and slope of the IHA time activity curve, which consisted of a vascular, early, and late phase. Single-pass extraction fraction of IHA averaged 0.53 +/- 0.11 s.d. at control and was not influenced by MVO2 and MBF. The half-time of the early phase (T = 9.3 min +/- 2.8 s.d. in controls) as well as the ratio between the size of the early and late phase increased with MVO2 (r = 0.82, r = 0.87, respectively). Thus, early phase intracellular turnover of IHA increased, yet clearance of 123I activity was slowed by augmented cardiac work. Preliminary data of HPLC and electrophoretic analysis of myocardial arterial and venous blood samples over time indicate that the early phase is characterized by a decreasing washout of IHA and a relative increase of radioiodine washout. The half-time of the late phase (T = 245 min +/- 156 s.d. at control) was not related to MVO2 and MBF. In conclusion, myocardial fatty acid metabolism cannot be measured from the half-time of the early phase but might be analyzed from the ratio between the size of the early and late phase when using IHA.

Animals↗

PubMed2004

Perspectives on alcohol consumption: liver polyunsaturated fatty acids and essential fatty acid metabolism.

In this article, subjects diagnosed with alcoholic liver disease are shown to have lower concentrations of several polyunsaturated fatty acids (PUFAs), including 18:2n6, 18:3n6, 20:3n6, 18:3n3, 22:5n3, and 22:6n3, but not 20:4n6 and 22:4n6, nor 22:5n6, in the total lipid extracts of their livers compared with findings for specimens obtained from patients diagnosed with primary biliary cirrhosis and from control subjects. Findings of studies in animals have demonstrated that prolonged alcohol consumption reduces liver polyunsaturate content. However, the effect of ethanol on the elongation/desaturation of essential fatty acids is complex, as in vitro study results indicate that the direction of the effect of alcohol may be related to the dose of alcohol. Findings of studies in hepatocyte cell culture indicate that ethanol increased delta-5 and delta-6 desaturase activities throughout a broad concentration range. In contrast, lower liver desaturase activity has been reported in animals consuming high concentrations of alcohol (36%-40% energy) over a period of several months. Findings from in vivo isotope tracers studies in nonhuman primates and felines indicate that prolonged periods of moderate (mean consumption 2.6 g kg(-1) d(-1) and 1.2 g kg(-1) d(-1), respectively) alcohol consumption had no effect on the uptake of either linoleic (18:2n6) or alpha-linolenic (18:3n3) acids into the plasma and lead to an increased incorporation of these deuterated precursors into 20:4n6 and 22:6n3. Thus, this likely reflects a stimulated, rather than an inhibited, production of long-chain PUFAs. In numerous studies in various species, investigators have documented that alcohol consumption can increase the level of lipid peroxidation in tissues, and sustained periods of ethanol-induced peroxidation can deplete tissues of PUFAs. A hypothesis to rationalize the long-term effects of alcohol consumption on liver PUFA concentration that takes into consideration the effect of ethanol on essential fatty acid metabolism is presented.

Alcohol Drinking↗

PubMed2005

Characterization of carnitine and fatty acid metabolism in the long-chain acyl-CoA dehydrogenase-deficient mouse.

In the present paper, we describe a novel method which enables the analysis of tissue acylcarnitines and carnitine biosynthesis intermediates in the same sample. This method was used to investigate the carnitine and fatty acid metabolism in wild-type and LCAD-/- (long-chain acyl-CoA dehydrogenase-deficient) mice. In agreement with previous results in plasma and bile, we found accumulation of the characteristic C14:1-acylcarnitine in all investigated tissues from LCAD-/- mice. Surprisingly, quantitatively relevant levels of 3-hydroxyacylcarnitines were found to be present in heart, muscle and brain in wild-type mice, suggesting that, in these tissues, long-chain 3-hydroxyacyl-CoA dehydrogenase is rate-limiting for mitochondrial beta-oxidation. The 3-hydroxyacylcarnitines were absent in LCAD-/- tissues, indicating that, in this situation, the beta-oxidation flux is limited by the LCAD deficiency. A profound deficiency of acetylcarnitine was observed in LCAD-/- hearts, which most likely corresponds with low cardiac levels of acetyl-CoA. Since there was no carnitine deficiency and only a marginal elevation of potentially cardiotoxic acylcarnitines, we conclude from these data that the cardiomyopathy in the LCAD-/- mouse is caused primarily by a severe energy deficiency in the heart, stressing the important role of LCAD in cardiac fatty acid metabolism in the mouse.

Acyl-CoA Dehydrogenase, Long-Chain↗

PubMed1998

Regulation of n-3 and n-6 fatty acid metabolism in retinal and cerebral microvascular endothelial cells by high glucose.

The present study was undertaken to determine whether polyunsaturated fatty acid metabolism is affected by high glucose levels in cerebral and retinal microvascular endothelial cells. The metabolism of [3-14C]22:5n-3 and [1-14C]18:2n-6 was studied in cells previously cultured for 5 days in normal (5 mM) or high (30 mM) glucose medium. After incubation of retinal endothelial cells with [3-14C]22:5n-3 in the high glucose condition, the formation of labeled 24:6n-3 and 22:6n-3 was increased, and that of labeled 24:5n-3 was decreased, compared with the normal glucose condition. The changes were found for fatty acids esterified in cellular lipids and those released into the medium. After incubation with [1-14C]18:2n-6, levels of all elongation/desaturation products were increased at the expense of the precursor in retinal endothelial cells cultured in high glucose medium. The changes were primarily found for esterified fatty acids, with the release of n-6 fatty acids being minor in both glucose concentrations. By contrast, high glucose levels did not affect the metabolism of [3-14C]22:5n-3 and [1-14C]18:2n-6 in cerebral endothelial cells. The changes in metabolic activity of retinal endothelial cells were not reflected in the fatty acid composition. The present data suggest that high glucose can increase the desaturation process in retinal but not cerebral endothelial cells. This may produce some lipid abnormalities in retinal microvasculature and contribute to altered vascular function observed in diabetic retinopathy.

Animals↗

PubMed2004

Glucose and fatty acid metabolism in McA-RH7777 hepatoma cells vs. rat primary hepatocytes: responsiveness to nutrient availability.

The overabundance of dietary fats and simple carbohydrates contributes significantly to obesity and metabolic disorders associated with obesity. The liver balances glucose and lipid distribution, and disruption of this balance plays a key role in these metabolic syndromes. We investigated (1) how hepatocytes balance glucose and fatty acid metabolism when one or both nutrients are supplied in abundance and (2) whether rat hepatoma cells (McA-RH7777) reflect nutrient partitioning in a similar manner as compared with primary hepatocytes. Increasing media palmitate concentration increased fatty acid uptake, triglyceride synthesis and beta-oxidation. However, hepatoma cells had a 2-fold higher fatty acid uptake and a 2-fold lower fatty acid oxidation as compared with primary hepatocytes. McA-RH7777 cells did not synthesize significant amounts of glycogen and preferentially metabolized the glucose into lipids or into oxidation. In primary hepatocytes, the glucose was mostly spared from oxidation and instead partitioned into both de novo glycogen and lipid synthesis. Overall, lipid production was rapidly induced in response to either glucose or fatty acid excess and this may be one of the earliest indicators of metabolic syndrome development associated with nutrient excess.

Animals↗

PubMed2002

Adipose tissue and fatty acid metabolism in humans.

It is now clear that there are major regional differences in adipose tissue function as regards the uptake and release of fatty acids. Visceral adiposity is a good predictor of abnormal regulation of adipose tissue fuel export, but it is not the source of excess systemic FFA in humans. Regional differences in adipose tissue uptake of fatty acids may be an important determinant of body fat distribution, which in turn appears to predict abnormalities of fatty acid metabolism.

Adipose Tissue↗

PubMed2004

Assessment of myocardial perfusion and fatty acid metabolism in a patient with Churg-Strauss syndrome associated with eosinophilic heart disease.

Churg-Strauss syndrome is characterized by asthma, eosinophilia and systemic necrotizing vasculitis; cardiac involvement (ie, eosinophilic heart disease) is the major cause of morbidity and mortality, although there are no reports of an association between left ventricular dysfunction because of eosinophilic heart disease and myocardial blood flow or myocardial fatty acid metabolism. A patient presented with Churg-Strauss syndrome associated with eosinophilic heart disease that had progressed to dilated cardiomyopathy. Coronary angiography, thallium-201 ((201)Tl) and iodine-123 beta-methyl-iodophenyl pentadecanoic acid ((123)I BMIPP) myocardial single photon emission computed tomography (SPECT) were performed to evaluate left ventricular dysfunction. Although coronary angiography was normal and (201)Tl SPECT showed no apparent image defect, (123)I BMIPP SPECT showed diffuse decreased accumulation, excepting the apex. The left ventricular dysfunction in patients with eosinophilic heart disease is associated with impaired myocardial fatty acid metabolism rather than with impaired myocardial blood flow.

Aged↗

PubMed1999

Essential fatty acid metabolism in long term primary cultures of rat cardiomyocytes: a beneficial effect of n-6:n-3 fatty acids supplementation.

In long term (21 days) primary cultures of neonatal rat cardiomyocytes, utilized as a model of in vitro senescence, we investigated the dual effect of the time length in culture and of the supplementation with n-6:n-3 fatty acid mixtures on linoleic (LA) and alpha-linolenic acid (ALA) metabolism. Cardiomyocytes were divided into groups receiving: (1) control medium; (2) control medium plus n-3 fatty acids; (3) and (4) control medium plus n-6 and n-3 fatty acids in the ratio 1:2 or 2:1, respectively. In control cells. senescence caused a reduction in the conversion of LA and ALA, and the decrease in their metabolites was bypassed by the different supplementations. The fatty acid composition of cardiomyocyte lipids was therefore affected by both senescence and supplementation, as evidenced by the n-6:n-3 fatty acid ratio and the unsaturation index (U.I.) in cellular lipids. The final result of ageing in culture and of fatty acid supplementations was in all the groups of cells but one (n-6:n-3, 2:1) an unbalance in the n-6:n-3 fatty acid ratio. All the supplementations were able to counteract the decrease in the U.I. observed with senescence, but only the n-6:n-3 (2:1) was able to do so by increasing the cellular content of the fatty acids which are precursors of anti-aggregation eicosanoids without altering the n-6:n-3 fatty acid ratio.

Animals↗

PubMed2005

Desensitization of cyclic GMP-mediated regulation of fatty acid metabolism in hepatocytes from ethanol-fed rats.

The mechanisms by which ethanol causes accumulation of hepatic triacylglycerols are complex. It has been proposed that nitric oxide/cyclic GMP signaling pathway may be involved in regulation of fatty acid metabolism in the liver. Here, we investigated if this mechanism may have a role in adaptation to ethanol consumption. Hepatocytes were isolated from rats fed with an ethanol-containing liquid diet and pair-fed control rats, and incubated with a range of concentrations of 8-bromo-cyclic GMP. In both types of cells, this cyclic GMP analog inhibited in parallel fatty acid synthesis de novo and acetyl-CoA carboxylase activity. Addition of 8-bromo-cyclic GMP also decreased the rate of palmitate esterification to triacylglycerols and phospholipids, whereas palmitate oxidation was increased. However, in all these metabolic effects, hepatocytes from ethanol-fed rats were significantly less sensitive to the addition of 8-bromo-cyclic GMP. In order to know if this may be a more general mechanism of adaptation to ethanol, we also studied the effects on glucose metabolism. Similarly, hepatocytes from ethanol-fed rats showed a decreased sensitivity in the inhibition by 8-bromo-cyclic GMP of glycogen synthesis, fatty acid synthesis and the synthesis of glycerol backbone of hepatic triacylglycerols. These data suggest that ethanol consumption induces a desensitization of the regulatory effects mediated by cyclic GMP in fatty acid metabolism, contributing to triacylglycerol accumulation in the liver.

Acetyl-CoA Carboxylase↗

PubMed2004

Species differences in the physiological activity of dietary lignan (sesamin and episesamin) in affecting hepatic fatty acid metabolism.

The effect of sesame (Sesamum orientale) lignan preparation containing equivalent amounts of sesamin and episesamin on hepatic fatty acid metabolism was compared in rats, mice and hamsters. Animals were fed on either a diet free of lignan or a diet containing 2 g lignan/kg for 15 d. The lignan preparation greatly increased hepatic activity and the mRNA levels of enzymes involved in fatty acid oxidation, while it strongly down-regulated those of enzymes involved in lipogenesis in rats. In contrast, lignan did not modify these variables in mice and hamsters. Changes observed, if any, were more attenuated in these mice and hamsters than in rats. Sesamin and episesamin concentrations in serum and liver of animals fed on lignan-containing diets were significantly greater (P<0.05) in rats than in mice and hamsters. Moreover, sesamin:episesamin values in tissues were far from that expected from the value in the lignan preparation given to the animals and were dependent on the animal species. Liver microsomes from each animal species degraded sesamin and episesamin in the presence of NADPH. The combined value of sesamin and episesamin degradation rates was lower in rats than in mice and hamsters. In addition, there was considerable diversity in the specificity of the enzyme reaction toward sesamin and episesamin among animal species. The differences in the amounts of lignan remaining in the tissues may account for the species dependence of the physiological activity of sesame lignan in affecting hepatic fatty acid oxidation and synthesis.

Animals↗

PubMed1988

Age-related changes of long-chain fatty acid metabolism in rat liver.

Palmitate oxidation activity and the activities of several enzymes involved in long-chain fatty acid metabolism were examined in the liver of young adult (2-month-old) and senescent (32-month-old) female rats. Palmitate oxidation activity in rat liver mitochondria showed age-related decrease, as judged by the rates of both 14CO2 production and formation of radioactive acid-soluble products from [1-14C]palmitate. In addition, long-chain acyl-coenzyme A synthetase activity was found to be decreased in liver mitochondria and increased in liver microsomes in senescent rats. These results suggest that, in the rat liver, preferential channeling of long-chain fatty acids through the triacylglycerol synthetic pathway may increase with age, and as a result, energy production by their oxidation may decrease.

Aging↗

PubMed1976

Effect of glucose utilization inhibitor isolated from the serum and urine of patients with chronic renal failure on the free fatty acid metabolism in rat kidney cortex slices.

The authors studied interference by the inhibitor of glucose utilization with free fatty acid (FFA) metabolism in rat kidney cortex slices. They found that FFA uptake by the kidneys, their incorporation into triglycerides (TG) and oxidation to 14CO2 were lower when the inhibitor was present in the incubation medium. The findings show that the inhibitor, as well as inhibiting glucose utilization in various tissues, interferes directly with fat metabolism.

Animals↗

PubMed1995

Brain uptake and metabolism of [1-11C]octanoate in rats: pharmacokinetic basis for its application as a radiopharmaceutical for studying brain fatty acid metabolism.

The uptake of octanoate in rat brain and its metabolism were investigated by means of intravenously injecting [1-11C] or [1-14C]octanoate as a tracer. The radioactivity in the cerebrum was increased by an injection of [1-11C]octanoate, and reached its peak level (0.33% ID/g) in about 2 to 5 min, and then decreased slowly. The cerebrum-to-blood ratio of the radioactivity increased with time over a period of 30 min. At 30 sec, [1-11C]octanoate that remained unchanged in the cerebrum accounted for only 8% of the total radioactivity, in spite of there being about 90% in the blood. By means of an injection of [1-14C]octanoate, more than 70% of the total radioactivity in the cerebrum was found to be attributable to radiolabeled glutamate and glutamine at each time point measured between 30 sec and 30 min. The results show that [1-11C]octanoate enters rat brain easily and is trapped in the cerebrum, probably in the form of glutamate and glutamine, and the usefulness of [1-11C]octanoate as a radiopharmaceutical for studying brain fatty acid metabolism by positron emission tomography is therefore suggested.

Animals↗

PubMed1992

[Phase 3 study of beta-methyl-p-(123I)-iodophenyl-pentadecanoic acid, a myocardial imaging agent for evaluating fatty acid metabolism--a multi-center trial].

A multi-center trial of beta-methyl-p-(123I)-iodophenyl-pentadecanoic acid (123I-BMIPP) was performed to assess its clinical usefulness in the evaluation of myocardial fatty acid metabolism in 587 patients with various heart diseases. 123I-BMIPP showed relatively decreased uptake compared with 201Tl in the myocardial lesions of 62% of patients with ischemic heart disease (IHD), 39% of those with cardiomyopathy and 32% of those with other heart diseases. In case of myocardial infarction, less uptake of 123I-BMIPP (Type B) than 201Tl was more frequently seen in patients with successful recanalization than in those without recanalization. The patients with matched distribution of the two tracers (Type E) increased in the direct proportion to the interval between the onset of myocardial infarction and the radionuclide studies. The uptake of 123I-BMIPP correlated well with myocardial viability evaluated by 201Tl exercise-redistribution studies. Type B was frequently seen in the areas with 201Tl redistribution, while Type E was seen in the fixed defect areas. In the other heart diseases studied, Type E was observed in approximately 60% of patients with dilated or secondary cardiomyopathies. Type B was seen in about 45% of patients with valvular heart diseases and myocarditis. Various types of mismatch between the two tracers were demonstrated in hypertrophic cardiomyopathy and hypertensive heart disease. It is concluded that 123I-BMIPP is a safe and useful agent for the diagnosis of various heart diseases, since it reflects myocardial fatty acid metabolism.

Adolescent↗

PubMed1985

Multiple disturbances of free fatty acid metabolism in noninsulin-dependent diabetes. Effect of oral hypoglycemic therapy.

To assess the mechanisms for the elevation of free fatty acids in noninsulin-dependent diabetes, free fatty acid metabolism and lipid and carbohydrate oxidation were compared in 14 obese diabetic Pima Indians and in 13 age-, sex-, and weight-matched nondiabetics. The studies were repeated in 10 of the diabetics after 1 mo of oral hypoglycemic therapy. Fasting plasma glucose concentrations were elevated in diabetics (242 +/- 14 vs. 97 +/- 3 mg/dl, P less than 0.01) and decreased to 142 +/- 12 (P less than 0.01) after therapy. Fasting free fatty acid concentrations were elevated in diabetics (477 +/- 26 vs. 390 +/- 39 mumol/liter, P less than 0.01) and declined to normal values after therapy (336 +/- 32, P less than 0.01). Although free fatty acid transport rate was correlated with obesity (r = 0.75, P less than 0.001), the transport of free fatty acid was not higher in diabetics than in nondiabetics and did not change after therapy. On the other hand, the fractional catabolic rate for free fatty acid was significantly lower in untreated diabetics (0.55 +/- 0.04 vs. 0.71 +/- 0.06 min-1, P less than 0.05); it increased after therapy to 0.80 +/- 0.09 min-1, P less than 0.05, and was inversely correlated with fasting glucose (r = -0.52, P less than 0.01). In diabetics after therapy, lipid oxidation rates fell significantly (from 1.35 +/- 0.06 to 1.05 +/- 0.01 mg/min per kg fat-free mass, P less than 0.01), whereas carbohydrate oxidation increased (from 1.21 +/- 0.10 to 1.73 +/- 0.13 mg/min per kg fat-free mass, P less than 0.01); changes in lipid and carbohydrate oxidation were correlated (r = 0.72, P less than 0.02), and in all subjects lipid oxidation accounted for only approximately 40% of free fatty acid transport. The data suggest that in noninsulin-dependent diabetics, although free fatty acid production may be elevated because of obesity, the elevations in plasma free fatty acid concentrations are also a result of reduced removal, and fractional clearance of free fatty acid appears to be closely related to diabetic control. Furthermore, the increase in fractional clearance rate, despite a marked decrease in lipid oxidation, suggests that the clearance defect in the diabetics is due to an impairment in reesterification, which is restored after therapy.

Adult↗