Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.3.99.3 (acyl-CoA dehydrogenase)
 1,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the effects of unweighting on the structural and metabolic adaptations of a non-postural muscle, deltoideus muscle biopsies were taken in seven male healthy subjects, before and after a 37 day bedrest. Myofibrillar ATPase histochemistry demonstrated no change in fibre type distributions (I, IIA, IIB), in fibre cross-sectional areas nor in capillary supply. No difference was noted in enzyme activities of oxidative metabolism (citrate synthase, 3-hydroxy-acyl-CoA dehydrogenase), and glycolysis (hexokinase, lactate dehydrogenase). Electron microscopy showed a decrease in the volume density of lipids but no change in mitochondrial volume density and distribution. The results indicate that bedrest induces no major morphological and biochemical changes in deltoideus muscle, contrary to what was previously reported in vastus lateralis muscle. This lack of changes is probably related to an unaltered deltoideus muscle use.
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PMID:Effects of bedrest on deltoideus muscle morphology and enzymes. 955 Feb 25

The objectives of this study were to determine the effects of 10 consecutive days of moderate-intensity training on 1) the muscular metabolic response to exercise at 100% of the pre-training maximum rate of oxygen consumption (VO2max); and 2) mitochondrial enzyme markers (citrate synthase, CS; succinate dehydrogenase, SDH; 3-hydroxy-acyl-CoA dehydrogenase, HAD) of oxidative capacity in middle gluteal muscle. Six mature, unfit Thoroughbred horses completed both incremental (for determination of VO2max) and high-intensity exercise protocols before (HI1) and after (HI2) training. Training consisted of 10 consecutive days of running at 55% VO2max for 60 min per day (13-14 km/day). For the HI, horses completed a 10 min warm-up, followed by exercise at 100% of pre-training VO2max (mean speed 9.8 m/s) until fatigue. Training resulted in an 8.9% increases in VO2max (Pre: 142 +/- 4 ml/kg bwt/min; Post: 155 +/- 4 ml/kg bwt/min) and a 24% increase in run time to fatigue during HI. Whereas VO2 during HI was not altered by training, peak values for VCO2 and R were significantly lower following training. Compared to HI1, there was a 45% reduction in the net rate of muscle glycogenolysis during HI2. Peak (end exercise) values for plasma and muscle lactate concentrations decreased by 22 and 23%, respectively, after training. Training also attenuated the exercise-associated increase in plasma norepinephrine, but there was no effect on plasma epinephrine concentrations. Maximal activities of CS, SDH, and HAD were unaltered by training. We conclude that 10 days of moderate-intensity exercise results in decreases in muscle glycogenolysis and anaerobic metabolism during high-intensity exercise at the same absolute workload. Furthermore, development of measurable increases in mitochondrial oxidative potential may not be required for expression of these metabolic adaptations in early training.
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PMID:Muscular and metabolic responses to moderate-intensity short-term training. 1065 74

Muscle contraction causes an increase in activity of 5'-AMP-activated protein kinase (AMPK). This study was designed to determine whether chronic chemical activation of AMPK will increase mitochondrial enzymes, GLUT-4, and hexokinase in different types of skeletal muscle of resting rats. In acute studies, rats were subcutaneously injected with either 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR; 1 mg/g body wt) in 0.9% NaCl or with 0.9% NaCl alone and were then anesthetized for collection and freezing of tissues. AMPK activity increased in the superficial, white region of the quadriceps and in soleus muscles but not in the deep, red region of the quadriceps muscle. Acetyl-CoA carboxylase (ACC) activity, a target for AMPK, decreased in all three muscle types in response to AICAR injection but was lowest in the white quadriceps. In rats given daily, 1 mg/g body wt, subcutaneous injections of AICAR for 4 wk, activities of citrate synthase, succinate dehydrogenase, and malate dehydrogenase were increased in white quadriceps and soleus but not in red quadriceps. Cytochrome c and delta-aminolevulinic acid synthase levels were increased in white, but not red, quadriceps. Carnitine palmitoyl-transferase and hydroxy-acyl-CoA dehydrogenase were not significantly increased. Hexokinase was markedly increased in all three muscles, and GLUT-4 was increased in red and white quadriceps. These results suggest that chronic AMPK activation may mediate the effects of muscle contraction on some, but not all, biochemical adaptations of muscle to endurance exercise training.
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PMID:Activation of AMP-activated protein kinase increases mitochondrial enzymes in skeletal muscle. 1084 39

The hypothesis tested was that dietary fat, when compared with an isoenergetic amount of non-structural carbohydrates, stimulates lipolysis in adipose tissue and also stimulates the fatty-acid oxidative capacity in skeletal muscle from horses. Six adult horses were fed a high-fat, glucose or starch containing diet according to a 3 x 3 Latin square design with feeding periods of three weeks. The diets were formulated so that the intake of soybean oil versus either glucose or corn starch were the only variables. In accordance with previous work, whole plasma triacylglycerol (TAG) concentration decreased significantly by 58% following fat supplementation. This fat effect was accompanied by a 247% increase in lipoprotein lipase (LPL) activity in post-heparin plasma. The dietary variables did neither significantly affect the basal in vitro lipolytic rate nor the lipolytic rate after adding noradrenaline. There was no significant diet effect on the activities of hexokinase and phosphofructokinase as indicators of glycolytic flux and citrate synthase and 3-hydroxy-acyl-CoA dehydrogenase as indicators of fatty-acid oxidative capacity. The concentrations of muscle glycogen and TAG were not affected by fat supplementation. It is concluded that our hypothesis is not supported by the present results.
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PMID:Lipid metabolism in equines fed a fat-rich diet. 1088 8

The aim of this study was to evaluate the changes in aerobic and anaerobic metabolism produced by a newly devised short training programme. Five young male volunteers trained daily for 2 weeks on a cycle ergometer. Sessions consisted of 15-s all-out repetitions with 45-s rest periods, plus 30-s all-out repetitions with 12-min rest periods. The number of repetitions was gradually increased up to a maximum of seven. Biopsy samples of the vastus lateralis muscle were taken before and after training. Performance changes were evaluated by two tests, a 30-s all-out test and a maximal progressive test. Significant increases in phosphocreatine (31%) and glycogen (32%) were found at the end of training. In addition, a significant increase was observed in the muscle activity of creatine kinase (44%), phosphofructokinase (106%), lactate dehydrogenase (45%), 3-hydroxy-acyl-CoA dehydrogenase (60%) and citrate synthase (38%). After training, performance of the 30-s all-out test did not increase significantly, while in the maximal progressive test, the maximum oxygen consumption increased from mean (SD) 57.3 (2.6) ml x min(-1) x kg(-1) to 63.8 (3.0) ml min(-1) x kg(-1), and the maximum load from 300 (11) W to 330 (21) W; all changes were significant. In conclusion, this new protocol, which utilises short durations, high loads and long recovery periods, seems to be an effective programme for improving the enzymatic activities of the energetic pathways in a short period of time.
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PMID:A short training programme for the rapid improvement of both aerobic and anaerobic metabolism. 1098 4

The influence of training on GLUT4 expression in slow- and fast-twitch skeletal muscle fibres was studied in male endurance-trained athletes and control subjects. The trained state was ensured by elevated maximal oxygen uptake (29%), as well as citrate synthase (60%) and 3-hydroxy-acyl-CoA dehydrogenase (38%) activities in muscle biopsy samples of the vastus lateralis. GLUT4 densities in slow- and fast-twitch fibres were measured by the use of a newly developed, sensitive method combining immunohistochemistry with morphometry, and no effect of training was found. GLUT4 density was higher in slow-twitch fibres compared to fast-twitch fibres (P<0.05) when biopsy samples from untrained subjects were examined. In athletes GLUT4 density was identical in slow- and fast-twitch fibres. Slow-twitch fibre diameters were 10% larger in the athletes (P<0.01), and slow-twitch fibre fractions were 140% of the fraction in the control group. Thus, GLUT4 originating from slow-twitch fibres was increased by 30% (P<0.02) in athletes. We conclude that long-lasting endurance training increases slow-twitch fibre GLUT4 expression by means of an elevated slow-twitch fibre mass in human skeletal muscle.
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PMID:The GLUT4 density in slow fibres is not increased in athletes. How does training increase the GLUT4 pool originating from slow fibres? 1171 44

The metabolic active form of free fatty acids, long-chain acyl-coenzyme A (lc-acyl-CoA), binds to its 10-kDa binding protein with high affinity. In the present study, we investigated the content of lc-acyl-CoA binding protein (ACBP) in different skeletal muscle fibre types. Soleus had the highest expression of ACBP (0.33+/-0.02 microg mg protein(-1)) and the content was as high as in heart muscle. The content in mixed gastrocnemius (0.27+/-0.02 microg mg protein(-1)), extensor digitorum longus (0.21+/-0.01 microg mg protein(-1)) and white gastrocnemius (0.16+/-0.01 microg mg protein(-1)) were lower than in soleus and differed from each other ( P<0.05). The ACBP content correlated positively with the fraction of myosin heavy chain I in the skeletal muscles (Spearman rank correlation rho=0.90; P<0.0001), and negatively with the myosin heavy chain IIB fraction ( rho=-0.92; P<0.0001). The content of ACBP also correlated with 3-hydroxy-acyl-CoA dehydrogenase (HAD) and citrate synthase (CS). Five weeks of endurance training increased HAD and CS activities in soleus and mixed gastrocnemius but did not affect the ACBP content. These findings demonstrate that ACBP expression is fibre-type specific in skeletal muscles and correlates with beta-oxidative potential. Training-induced increase in oxidative capacity was not paralleled by an increase in ACBP content.
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PMID:Acyl-coenzyme A binding protein expression is fibre-type specific in rat skeletal muscle but not affected by moderate endurance training. 1181 Feb 7

Accumulation of acyl-CoA is hypothesized to be involved in development of insulin resistance. Acyl-CoA binds to acyl-CoA binding protein (ACBP) with high affinity, and therefore knowledge about ACBP concentration is important for interpreting acyl-CoA data. In the present study, we used a sandwich enzyme-linked immunosorbent assay to quantify ACBP concentration in different muscle fiber types. Furthermore, ACBP concentration was compared in muscles from lean and obese Zucker rats. Expression of ACBP was highest in the slow-twitch oxidative soleus muscle and lowest in the fast-twitch glycolytic white gastrocnemius (0.46 +/- 0.02 and 0.16 +/- 0.005 microg/mg protein, respectively). Expression of ACBP was soleus > red gastrocnemius > extensor digitorum longus > white gastrocnemius. Similar fiber type differences were found for carnitine palmitoyl transferase (CPT)-1, and a correlation was observed between ACBP and CPT-1. Muscles from obese Zucker rats had twice the triglyceride content, had approximately twice the long-chain acyl CoA content, and were severely insulin resistant. ACBP concentration was approximately 30% higher in all muscles from obese rats. Activities of CPT-1 and 3-hydroxy-acyl-CoA dehydrogenase were increased in muscles from obese rats, whereas citrate synthase activity was similar. In conclusion, ACBP expression is fiber type-specific with the highest concentration in oxidative muscles and the lowest in glycolytic muscles. The 90% increase in the concentration of acyl-CoA in obese Zucker muscle compared with only a 30% increase in the concentration of ACBP supports the hypothesis that an increased concentration of free acyl-CoA is involved in the development of insulin resistance.
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PMID:Acyl-CoA binding protein expression is fiber type- specific and elevated in muscles from the obese insulin-resistant Zucker rat. 1181 54

In a previous report, we observed an altered proportion of fiber types and a reduction of capillary per fiber ratio in extensor digitorus longus (EDL) and soleus (SOL) muscles of deoxicorticosterone acetate (DOCA)-salt hypertensive rats when compared with controls. The aim of the present study was to ascertain various carbohydrate and lipid enzyme activities and substrates that may be involved in the morphological changes reported. In the SOL muscle of hypertensive rats, glucose, glycogen and triglycerides (TG) levels were increased, citrate synthase (CS) and beta-hydroxy-acyl-CoA dehydrogenase (HAD) activities were reduced, while hexokinase (HK) and lipoprotein lipase (LPL), LPL mass, lactate and free fatty acids (FFA) levels were unchanged. In EDL muscles of hypertensive rats, glycogen levels and LPL mass were higher than in controls, while CS, HAD, HK, and LPL activities and glucose, lactate, FFA and TG levels were unmodified. Serum levels of insulin, TG, cholesterol and FFA were increased while glucose levels were decreased and high-density lipoprotein-cholesterol levels were similar in hypertensive rats when compared with controls. In conclusion, hypertensive rats showed increased glycogen in both EDL and SOL muscles, with hyperinsulinemia and reduced glycemia. Hyperinsulinemia might have been a compensatory response to insulin resistance. The oxidative capacity of SOL muscle was reduced indicating that glucose uptake was conduced via non-oxidative metabolism. TG, FFA and cholesterol were increased in serum and TG in SOL muscle.
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PMID:Metabolic changes in DOCA-salt hypertensive rats. 1191 12

The aim of the present study was to relate changes in muscle oxidative capacity and free fatty acid flux in response to oil supplementation to fuel utilisation during subsequent exercise of varying intensities. Following 10 weeks of oil supplementation there was an increased capacity for fat utilisation during low and moderate intensity exercise as indicated by a lower respiratory exchange ratio (RER) (P<0.05). We suggest that this was contributed to by a parallel increase in the oxidative capacity of muscle as indicated by a significant increase in the activity of muscle citrate synthase (CS) (P<0.05) and trend towards an increase in beta-Hydroxy acyl CoA dehydrogenase (beta-HAD), (P>0.05). In addition, low and moderate intensity exercise was associated with an exercise-induced increase in plasma free fatty acids (FFA) and there was an increased facility for uptake of FFA by working muscle from circulating triglycerides, as suggested by an increase in TL activity (P<0.01). The response to oil supplementation varied between individual horses and the magnitude of response, during the low intensity exercise test, in terms of difference in RER was correlated to the increase in CS activity (r2 = 0.95, P<0.05) following oil supplementation. There was no similar significant correlation with respect to FFA, TL or beta-HAD activity (P>0.05). The hypothesis in this study was that the metabolic adaptation to oil supplementation, in terms of exercise response, was related to individual increases in the activities of CS, beta-HAD or TL. However, the relationship between these parameters was unequivocal and requires further investigation, ideally with a larger group of horses.
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PMID:Effect of dietary lipid on response to exercise: relationship to metabolic adaptation. 1240 63


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