Endurance training increases FFA oxidation and reduces triacylglycerol utilization in contracting rat soleus

Dyck, David J.; Miskovic, Dragana; Code, L. M.; Luiken, Joost J. F. P.; Bonen, Arend

doi:10.1152/ajpendo.2000.278.5.e778

Cited by 57 publications

(63 citation statements)

References 43 publications

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“…Recent studies in our laboratory (12,23,24) and others (28,29) have demonstrated that fatty acid transporter expression is regulated by the metabolic demand of skeletal muscle (23), obesity (28,29), and diabetes (29). These latter studies (28,29) suggest that there may be hormonal regulation of fatty acid transporter expression, resulting in altered rates of plasmalemmal fatty acid transport.…”

Section: Discussionmentioning

confidence: 96%

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Chronic Leptin Administration Decreases Fatty Acid Uptake and Fatty Acid Transporters in Rat Skeletal Muscle

Steinberg¹,

Dyck²,

Calles-Escandon³

et al. 2002

Journal of Biological Chemistry

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Chronic leptin administration reduces triacylglycerol content in skeletal muscle. We hypothesized that chronic leptin treatment, within physiologic limits, would reduce the fatty acid uptake capacity of red and white skeletal muscle due to a reduction in transport protein expression (fatty acid translocase (FAT/CD36) and plasma membrane-associated fatty acid-binding protein (FABPpm)) at the plasma membrane. Female Sprague-Dawley rats were infused for 2 weeks with leptin (0.5 mg/kg/day) using subcutaneously implanted miniosmotic pumps. Control and pair-fed animals received saline-filled implants. Leptin levels were significantly elevated (ϳ4-fold; p < 0.001) in treated animals, whereas pair-fed treated animals had reduced serum leptin levels (approximately ؊2-fold; p < 0.01) relative to controls. Palmitate transport rates into giant sarcolemmal vesicles were reduced following leptin treatment in both red (؊45%) and white (؊84%) skeletal muscle compared with control and pair-fed animals (p < 0.05). Leptin treatment reduced FAT mRNA (red, ؊70%, p < 0.001; white, ؊48%, p < 0.01) and FAT/CD36 protein expression (red, ؊32%; p < 0.05) in whole muscle homogenates, whereas FABPpm mRNA and protein expression were unaltered. However, in leptin-treated animals plasma membrane fractions of both FAT/CD36 and FABPpm protein expression were significantly reduced in red (؊28 and ؊34%, respectively) and white (؊44 and ؊56%, respectively) muscles (p < 0.05). Across all experimental treatments and muscles, palmitate uptake by giant sarcolemmal vesicles was highly correlated with the plasma membrane FAT/CD36 protein (r ‫؍‬ 0.88, p < 0.01) and plasma membrane FABPpm protein (r ‫؍‬ 0.94, p < 0.01). These studies provide the first evidence that proteinmediated long chain fatty acid transport is subject to long term regulation by leptin.

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Section: Discussionmentioning

confidence: 96%

“…To detect FAT/ CD36 and FABPpm, we used antibodies and procedures that have been described previously (12,15,17,23). Messenger RNA for FAT and FABPpm were measured in red and white vastus muscle using procedures previously described (24).…”

Section: Methodsmentioning

confidence: 99%

Chronic Leptin Administration Decreases Fatty Acid Uptake and Fatty Acid Transporters in Rat Skeletal Muscle

Steinberg¹,

Dyck²,

Calles-Escandon³

et al. 2002

Journal of Biological Chemistry

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“…Chronic effects of exercise training (8-12 wk) on skeletal muscles CS activity have been extensively examined in rats (1,6,20) and humans (4,14). In the present study, we have found that soleus muscle from the trained rats 48 h after the last training session had a 25% higher level of CS activity compared with the sedentary rats (T 48 vs. C: 412 Ϯ 10.9 vs. 330 Ϯ 6.6 nmol ⅐ mg protein Ϫ1 ⅐ min Ϫ1 , P Ͻ 0.01).…”

Section: Discussionmentioning

confidence: 99%

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

Siu

Donley

Bryner

2003

Journal of Applied Physiology

117

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. Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles. J Appl Physiol 94: 555-560, 2003; 10.1152/ japplphysiol.00821.2002.-The present study was designed to examine the acute and chronic effects of endurance treadmill training on citrate synthase (CS) gene expression and enzymatic activity in rat skeletal and cardiac muscles. Adult rats were endurance trained for 8 wk on a treadmill. They were killed 1 h (T1, n ϭ 8) or 48 h (T48, n ϭ 8) after their last bout of exercise training. Eight rats were sedentary controls (C) during the training period. CS mRNA levels and enzymatic activities of the soleus and ventricle muscles were determined. Training resulted in higher CS mRNA levels in both the soleus muscles (21% increase in T1; 18% increase in T48, P Ͻ 0.05) and ventricle muscles (23% increase in T1; 17% increase in T48, P Ͻ 0.05) when compared with the C group. The CS enzyme activities were 42 (P Ͻ 0.01) and 25% (P Ͻ 0.01) greater in the soleus muscles of T1 and T48 groups, respectively, when compared with that of the C group. Soleus CS enzyme activity was significantly greater in the T1 vs. T48 groups (P Ͻ 0.05). However, no appreciable alterations in CS enzyme activities were observed in the ventricle muscles in both training groups. These findings suggest differential responses of skeletal and cardiac muscles in CS enzymatic activity but similar responses in CS gene expression at 1 and 48 h after the last session of endurance training. Moreover, our data support the existence of an acute effect of exercise on the training-induced elevation in CS activity in rat soleus but not ventricle muscles. physical activity; oxidative enzyme; gene transcriptional expression; soleus muscle; heart muscle CITRATE SYNTHASE (CS) is one of the key regulatory enzymes in the energy-generating metabolic pathway that catalyzes the condensation of oxaloacetate and acetyl coenzyme A to form citrate in the tricarboxylic acid cycle. It has been extensively used as a metabolic marker in assessing oxidative and respiratory capacity (22). More than 30 years ago, Holloszy and his colleagues (8) reported that endurance exercise training increases the oxidative enzyme activities in skeletal muscle. After that, numerous studies were conducted to examine the effect of exercise training on muscle oxidative capacity and metabolic characteristics (7,15,20,22,29). It is generally recognized that the skeletal muscle oxidative capacity and the activities of mitochondrial enzymes are elevated by endurance exercise training.

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“…In addition, palmitate incorporation into phospholipids, triacylglycerol, and diacylglycerol was determined by measuring [ 14 C]palmitate accumulation in these depots in selected rat hindlimb muscles (soleus and red and white gastrocnemius) as we have previously reported (10)(11)(12)(13). This permitted us to calculate the incorporation rates of palmitate in the whole rat hindlimb musculature from the known muscle fiber composition of these muscles and the known proportions of their muscle fiber mass in the rat hindlimb (3), as we (20) have done previously when determining glucose transport for the whole hindlimb muscle from selected individual muscles.…”

Section: Methodsmentioning

confidence: 99%

Insulin induces the translocation of the fatty acid transporter FAT/CD36 to the plasma membrane

Luiken

Dyck

Han³

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

189

173

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-It is well known that muscle contraction and insulin can independently translocate GLUT-4 from an intracellular depot to the plasma membrane. Recently, we have shown that the fatty acid transporter FAT/CD36 is translocated from an intracellular depot to the plasma membrane by muscle contraction (Ͻ30 min) (Bonen et al. J Biol Chem 275: 14501-14508, 2000). In the present study, we examined whether insulin also induced the translocation of FAT/CD36 in rat skeletal muscle. In studies in perfused rat hindlimb muscles, we observed that insulin increased fatty acid uptake by ϩ51%. Insulin increased the rate of palmitate incorporation into triacylglycerols, diacylglycerols, and phospholipids (P Ͻ 0.05) while reducing muscle palmitate oxidation (P Ͻ 0.05). Perfusing rat hindlimb muscles with insulin increased plasma membrane FAT/CD36 by ϩ48% (P Ͻ 0.05), whereas concomitantly the intracellular FAT/CD36 depot was reduced by 68% (P Ͻ 0.05). These insulin-induced effects on FAT/CD36 translocation were inhibited by the phosphatidylinositol 3-kinase inhibitor LY-294002. Thus these studies have shown for the first time that insulin can induce the translocation of FAT/CD36 from an intracellular depot to the plasma membrane.This reveals a previously unknown level of regulation of fatty acid transport by insulin and may well have important consequences in furthering our understanding of the relation between fatty acid metabolism and insulin resistance.

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Endurance training increases FFA oxidation and reduces triacylglycerol utilization in contracting rat soleus

Abstract: We examined the effects of 8 wk of intense endurance training on free fatty acid (FFA) transporters and metabolism in resting and contracting soleus muscle using pulse-chase procedures. Endurance training increased maximal citrate synthase activity in red muscles (+54 to +91%; P Show more

Cited by 57 publications

References 43 publications

Chronic Leptin Administration Decreases Fatty Acid Uptake and Fatty Acid Transporters in Rat Skeletal Muscle

Chronic Leptin Administration Decreases Fatty Acid Uptake and Fatty Acid Transporters in Rat Skeletal Muscle

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

Insulin induces the translocation of the fatty acid transporter FAT/CD36 to the plasma membrane

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