Effects of muscle activity and fiber composition on glucose transport and GLUT-4

Megeney, L. A.; Neufer, P. Darrell; Dohm, G. Lynis; Tan, M. H.; Blewett, Cameron; Elder, Geoffrey C. B.; Bonen, Arend

doi:10.1152/ajpendo.1993.264.4.e583

Cited by 88 publications

(103 citation statements)

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“…In addition, the effect of prolonged SB has been demonstrated on muscle GLUT proteins, which are integral for insulin-and exercise-stimulated uptake of plasma glucose. A study of spinal cord injury by Megeney et al found reductions in GLUT content and glucose uptake within 3 days of muscle denervation [28]. Our finding of effect modification by MVPA on the relationship between SB and the components of triacylglycerol, HDL-cholesterol and fasting glucose implies that SB and MVPA may exert their effects through similar pathways for some biomarkers but different pathways for others.…”

Section: Discussionmentioning

confidence: 50%

Dose–response relationships between sedentary behaviour and the metabolic syndrome and its components

et al. 2014

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Aims/hypothesis The aim of this study was to examine the relationship among sedentary behaviour (SB) and the metabolic syndrome and its components by age, moderate-tovigorous physical activity (MVPA) and sex. Methods A cross-sectional analysis was performed on 2003-2006 National Health and Nutrition Examination Survey data from 5,076 adults aged ≥18 years (mean±SD =43.8±19.5). SB was measured using ActiGraph accelerometers worn for 1 week and defined as <100 counts/min. Metabolic syndrome was defined using the Adult Treatment Panel III criteria. Natural cubic spline logistic regression models were used to estimate the odds of meeting criteria for the metabolic syndrome and its components by total daily SB time and breaks in SB. Statistical interactions between SB and age, sex and MVPA were explored. Results The prevalence of the metabolic syndrome was 19% and the average daily SB time was 8.1±2.8 h, with 90±25 breaks/day. The relationship between daily SB time and the metabolic syndrome was linear and characterised by an OR of 1.09 (95% CI 1.01, 1.18) for each hour of SB. Total SB was associated with the following components: high triacylglycerol, low HDL-cholesterol and high fasting glucose. All three associations were modified by MVPA level. No relationship between breaks in SB and the metabolic syndrome was found. Conclusions/interpretation There appears to be no SB threshold at which the risk of the metabolic syndrome is elevated. Therefore, an effort should be made to maintain low levels of total time spent in SB and so lessen the risk of the metabolic syndrome.

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Section: Discussionmentioning

confidence: 50%

Dose–response relationships between sedentary behaviour and the metabolic syndrome and its components

et al. 2014

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“…Similarly, in CD36 null mice, a greater reduction in fatty acid uptake occurred in oxidative muscles than in glycolytic muscles (45). When we examined the effects of reduced muscle activity (denervation) on the changes in glucose transport and transporters (46,47) and lactate transport (48) and monocarboxylate transporters (49), the greatest effects were also observed in the more oxidative types of muscles. Thus, it appears that oxidative types of skeletal muscle are more susceptible to alterations in their substrate transport capacities and transporter expression than glycolytic muscles.…”

Section: Discussionmentioning

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 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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“…This effect is temporally coincident with the process of innervation of the muscle fiber (3). Therefore, denervated muscle shows a decrease in GLUT4 and an increase in GLUT1 expression (3)(4)(5)(6)(7). A program of electrical stimulation of the denervated muscle prevents GLUT4 gene repression (3), which suggests that basal contractile activity dependent on innervation regulates the expression of GLUT4 in skeletal muscle.…”

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confidence: 99%

“…A program of electrical stimulation of the denervated muscle prevents GLUT4 gene repression (3), which suggests that basal contractile activity dependent on innervation regulates the expression of GLUT4 in skeletal muscle. Furthermore, GLUT4 is more sensitive than GLUT1 to the lack of muscle contraction (5,8), and the extent of induction of GLUT1 depends mainly on the fiber type (6,7,9).…”

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confidence: 99%

A Novel Role of Neuregulin in Skeletal Muscle

Suárez¹,

Bach²,

Cadefau

et al. 2001

Journal of Biological Chemistry

100

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Neuregulins regulate the expression of acetylcholine receptor genes and induce development of the neuromuscular junction in muscle. In studying whether neuregulins regulate glucose uptake in muscle, we analyzed the effect of a recombinant neuregulin, r heregulin-␤1-(177-244) (HRG), on L6E9 muscle cells, which express the neuregulin receptors ErbB2 and ErbB3. L6E9 responded acutely to HRG by a time-and concentrationdependent stimulation of 2-deoxyglucose uptake. HRGinduced stimulation of glucose transport was additive to the effect of insulin. The acute stimulation of the glucose transport induced by HRG was a consequence of the translocation of GLUT4, GLUT1, and GLUT3 glucose carriers to the cell surface. The effect of HRG on glucose transport was dependent on phosphatidylinositol 3-kinase activity. HRG also stimulated glucose transport in the incubated soleus muscle and was additive to the effect of insulin. Chronic exposure of L6E9 cells to HRG potentiated myogenic differentiation, and under these conditions, glucose transport was also stimulated. The activation of glucose transport after chronic HRG exposure was due to enhanced cell content of GLUT1 and GLUT3 and to increased abundance of these carriers at the plasma membrane. However, under these conditions, GLUT4 expression was markedly down-regulated. Muscle denervation is associated with GLUT1 induction and GLUT4 repression. In this connection, muscle denervation caused a marked increase in the content of ErbB2 and ErbB3 receptors, which occurred in the absence of alterations in neuregulin mRNA levels. This fact suggests that neuregulins regulate glucose transporter expression in denervated muscle. We conclude that neuregulins regulate glucose uptake in L6E9 muscle cells by mechanisms involving the recruitment of glucose transporters to the cell surface and modulation of their expression. Neuregulins may also participate in the adaptations in glucose transport that take place in the muscle fiber after denervation.

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Effects of muscle activity and fiber composition on glucose transport and GLUT-4

Cited by 88 publications

References 0 publications

Dose–response relationships between sedentary behaviour and the metabolic syndrome and its components

Dose–response relationships between sedentary behaviour and the metabolic syndrome and its components

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

A Novel Role of Neuregulin in Skeletal Muscle

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