Regulation of skeletal muscle UCP-2 and UCP-3 gene expression by exercise and denervation

1999 ◽  
Vol 276 (1) ◽  
pp. E217-E221 ◽  
Author(s):  
Ronald N. Cortright ◽  
Donghai Zheng ◽  
Jared P. Jones ◽  
James D. Fluckey ◽  
Stephen E. DiCarlo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Acute Exercise ◽  
Wheel Running ◽  
Treadmill Running ◽  
Mrna Levels ◽  
Chronic Exercise ◽  
Regulate Gene Expression ◽  
Gastrocnemius Muscles ◽  
Regulate Gene

The factors that regulate gene expression of uncoupling proteins 2 and 3 (UCP-2 and UCP-3) in skeletal muscle are poorly understood, but both genes are clearly responsive to the metabolic state of the organism. Therefore, we tested the hypothesis that denervation and acute and/or chronic exercise (factors that profoundly affect metabolism) would alter UCP-2 and UCP-3 gene expression. For the denervation studies, the sciatic nerve of rat and mouse hindlimb was sectioned in one leg while the contralateral limb served as control. Northern blot analysis revealed that denervation was associated with a 331% increase ( P < 0.001) in UCP-3 mRNA and a 200% increase ( P < 0.01) in UCP-2 mRNA levels in rat mixed gastrocnemius (MG) muscle. In contrast, denervation caused a 53% decrease ( P< 0.001) in UCP-3 and a 63% increase ( P < 0.01) in UCP-2 mRNA levels in mouse MG. After acute exercise (2-h treadmill running), rat UCP-3 mRNA levels were elevated (vs. sedentary control) 252% ( P < 0.0001) in white gastrocnemius and 63% ( P < 0.05) in red gastrocnemius muscles, whereas UCP-2 levels were unaffected. To a lesser extent, elevations in UCP-3 mRNA (22%; P < 0.01) and UCP-2 mRNA (55%; P < 0.01) levels were observed after acute exercise in the mouse MG. There were no changes in either UCP-2 or UCP-3 mRNA levels after chronic exercise (9 wk of wheel running). These results indicate that acute exercise and denervation regulate gene expression of skeletal muscle UCPs.

Exercise increases the plasma membrane content of the Na+ -K+ pump and its mRNA in rat skeletal muscles

1996 ◽  
Vol 80 (2) ◽  
pp. 699-705 ◽  
Author(s):  
T. Tsakiridis ◽  
P. P. Wong ◽  
Z. Liu ◽  
C. D. Rodgers ◽  
M. Vranic ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Skeletal Muscles ◽  
Plasma Membranes ◽  
Acute Exercise ◽  
Treadmill Running ◽  
Type I ◽  
Mrna Levels ◽  
Subunit Mrna ◽  
White Type

Muscle fibers adapt to ionic challenges of exercise by increasing the plasma membrane Na+-K+ pump activity. Chronic exercise training has been shown to increase the total amount of Na+-K+ pumps present in skeletal muscle. However, the mechanism of adaptation of the Na+-K+ pump to an acute bout of exercise has not been determined, and it is not known whether it involves alterations in the content of plasma membrane pump subunits. Here we examine the effect of 1 h of treadmill running (20 m/min, 10% grade) on the subcellular distribution and expression of Na+-K+ pump subunits in rat skeletal muscles. Red type I and IIa (red-I/IIa) and white type IIa and IIb (white-IIa/IIb) hindlimb muscles from resting and exercised female Sprague-Dawley rats were removed for subcellular fractionation. By homogenization and gradient centrifugation, crude membranes and purified plasma membranes were isolated and subjected to gel electrophoresis and immunoblotting by using pump subunit-specific antibodies. Furthermore, mRNA was isolated from specific red type I (red-I) and white type IIb (white-IIb) muscles and subjected to Northern blotting by using subunit-specific probes. In both red-I/IIa and white-IIa/IIb muscles, exercise significantly raised the plasma membrane content of the alpha1-subunit of the pump by 64 +/- 24 and 55 +/- 22%, respectively (P < 0.05), and elevated the alpha2-polypeptide by 43 +/- 22 and 94 +/- 39%, respectively (P < 0.05). No significant effect of exercise could be detected on the amount of these subunits in an internal membrane fraction or in total membranes. In addition, exercise significantly increased the alpha1-subunit mRNA in red-I muscle (by 50 +/- 7%; P < 0.05) and the beta2-subunit mRNA in white-IIb muscles (by 64 +/- 19%; P < 0.01), but the alpha2- and beta1-mRNA levels were unaffected in this time period. We conclude that increased presence of alpha1- and alpha2-polypeptides at the plasma membrane and subsequent elevation of the alpha1- and beta2-subunit mRNAs may be mechanisms by which acute exercise regulates the Na+-K+ pump of skeletal muscle.

scholarly journals Role of GDF15 in active lifestyle induced metabolic adaptations and acute exercise response in mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Carla Igual Gil ◽  
Mario Ost ◽  
Juliane Kasch ◽  
Sara Schumann ◽  
Sarah Heider ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Acute Exercise ◽  
Treadmill Running ◽  
Exercise Stress ◽  
Metabolic Phenotype ◽  
Obese Mice ◽  
Active Lifestyle ◽  
Post Exercise ◽  
Stress Markers

AbstractPhysical activity is an important contributor to muscle adaptation and metabolic health. Growth differentiation factor 15 (GDF15) is established as cellular and nutritional stress-induced cytokine but its physiological role in response to active lifestyle or acute exercise is unknown. Here, we investigated the metabolic phenotype and circulating GDF15 levels in lean and obese male C57Bl/6J mice with long-term voluntary wheel running (VWR) intervention. Additionally, treadmill running capacity and exercise-induced muscle gene expression was examined in GDF15-ablated mice. Active lifestyle mimic via VWR improved treadmill running performance and, in obese mice, also metabolic phenotype. The post-exercise induction of skeletal muscle transcriptional stress markers was reduced by VWR. Skeletal muscle GDF15 gene expression was very low and only transiently increased post-exercise in sedentary but not in active mice. Plasma GDF15 levels were only marginally affected by chronic or acute exercise. In obese mice, VWR reduced GDF15 gene expression in different tissues but did not reverse elevated plasma GDF15. Genetic ablation of GDF15 had no effect on exercise performance but augmented the post exercise expression of transcriptional exercise stress markers (Atf3, Atf6, and Xbp1s) in skeletal muscle. We conclude that skeletal muscle does not contribute to circulating GDF15 in mice, but muscle GDF15 might play a protective role in the exercise stress response.

Dietary lipids regulate β-oxidation enzyme gene expression in the developing rat kidney

1998 ◽  
Vol 275 (5) ◽  
pp. F777-F784 ◽  
Author(s):  
F. Ouali ◽  
F. Djouadi ◽  
C. Merlet-Bénichou ◽  
J. Bastin
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Renal Cortex ◽  
Dietary Lipids ◽  
Mrna Levels ◽  
High Fat ◽  
Regulate Gene Expression ◽  
Enzyme Gene ◽  
Oxidation Enzyme ◽  
Regulate Gene

This study examines the ability of dietary lipids to regulate gene expression of mitochondrial and peroxisomal fatty acid β-oxidation enzymes in the kidney cortex and medulla of 3-wk-old rats and evaluates the role of glucagon or of the α-isoform of peroxisome proliferator-activated receptor (PPARα) in mediating β-oxidation enzyme gene regulation in the immature kidney. The long-chain (LCAD) and medium-chain acyl-CoA dehydrogenases (MCAD) and acyl-CoA oxidase (ACO) mRNA levels were found coordinately upregulated in renal cortex, but not in medulla, of pups weaned on a high-fat diet from day 16 to 21. Further results establish that switching pups from a low- to a high-fat diet for only 1 day was sufficient to induce large increases in cortical LCAD, MCAD, and ACO mRNA levels, and gavage experiments show that this upregulation of β-oxidation gene expression is initiated within 6 h following lipid ingestion. Treatment of pups with clofibrate, a PPARα agonist, demonstrated that PPARα can mediate regulation of cortical β-oxidation enzyme gene expression, whereas glucagon was found ineffective. Thus dietary lipids physiologically regulate gene expression of mitochondrial and peroxisomal β-oxidation enzymes in the renal cortex of suckling pups, and this might involve PPARα-mediated mechanisms.

Effects of acute and chronic exercise on skeletal muscle glucose transport in aged rats

1995 ◽  
Vol 78 (5) ◽  
pp. 1750-1756 ◽  
Author(s):  
J. F. Youngren ◽  
R. J. Barnard
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Dehydrogenase Activity ◽  
Glucose Transport ◽  
Acute Exercise ◽  
Treadmill Running ◽  
Aged Rats ◽  
Chronic Exercise ◽  
Glut 4 ◽  
Muscle Glucose Transport

The purpose of this study was to investigate the effects of acute and chronic exercise on skeletal muscle glucose transport in aged rats by using an isolated sarcolemmal membrane preparation. In 24-mo-old female Fischer 344 rats, a maximum dose of insulin increased glucose transport from 43 +/- 6 to 82 +/- 6 pmol.mg protein-1.15 s-1. A 45-min bout of exhaustive treadmill running increased glucose transport to the same maximum level (88 +/- 5 pmol.mg protein-1.15 s-1). Eight weeks of progressive exercise training resulted in a 65% increase in succinic dehydrogenase activity in hindlimb muscles and a 55% increase in total cellular GLUT-4 content. Despite these biochemical adaptations, there was no change in either basal or maximum insulin-stimulated glucose transport between control (43 +/- 6 and 82 +/- 6 pmol.mg protein-1.15 s-1, respectively) and trained (42 +/- 2 and 82 +/- 8 pmol.mg protein-1.15 s-1, respectively) animals. When hindlimb muscle succinate dehydrogenase activity and GLUT-4 content were compared for both the combined sedentary and trained groups, a significant correlation (r = 0.68) was obtained. This study demonstrates that the skeletal muscle glucose transport system of 24-mo-old rats is fully stimulated by acute exercise and that, although GLUT-4 levels are increased in aged animals after exercise training, this does not result in an enhancement of maximal insulin-stimulated glucose transport. Thus increases in GLUT-4 are not sufficient to improve muscle insulin responsiveness with training.

Human cytomegalovirus US3 and UL36-38 immediate-early proteins regulate gene expression.

1992 ◽  
Vol 66 (1) ◽  
pp. 95-105 ◽  
Author(s):  
A M Colberg-Poley ◽  
L D Santomenna ◽  
P P Harlow ◽  
P A Benfield ◽  
D J Tenney
Keyword(s):  
Gene Expression ◽  
Human Cytomegalovirus ◽  
Immediate Early ◽  
Regulate Gene Expression ◽  
Early Proteins ◽  
Immediate Early Proteins ◽  
Regulate Gene

scholarly journals Arabidopsis heat shock transcription factor HSFA7b positively mediates salt stress tolerance by binding to an E-box-like motif to regulate gene expression

2019 ◽  
Vol 70 (19) ◽  
pp. 5355-5374 ◽  
Author(s):  
Dandan Zang ◽  
Jingxin Wang ◽  
Xin Zhang ◽  
Zhujun Liu ◽  
Yucheng Wang
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Heat Shock ◽  
Salt Tolerance ◽  
Stress Responses ◽  
Ion Homeostasis ◽  
Cellulose Synthase ◽  
Regulate Gene Expression ◽  
E Box ◽  
Regulate Gene

Abstract Plant heat shock transcription factors (HSFs) are involved in heat and other abiotic stress responses. However, their functions in salt tolerance are little known. In this study, we characterized the function of a HSF from Arabidopsis, AtHSFA7b, in salt tolerance. AtHSFA7b is a nuclear protein with transactivation activity. ChIP-seq combined with an RNA-seq assay indicated that AtHSFA7b preferentially binds to a novel cis-acting element, termed the E-box-like motif, to regulate gene expression; it also binds to the heat shock element motif. Under salt conditions, AtHSFA7b regulates its target genes to mediate serial physiological changes, including maintaining cellular ion homeostasis, reducing water loss rate, decreasing reactive oxygen species accumulation, and adjusting osmotic potential, which ultimately leads to improved salt tolerance. Additionally, most cellulose synthase-like (CSL) and cellulose synthase (CESA) family genes were inhibited by AtHSFA7b; some of them were randomly selected for salt tolerance characterization, and they were mainly found to negatively modulate salt tolerance. By contrast, some transcription factors (TFs) were induced by AtHSFA7b; among them, we randomly identified six TFs that positively regulate salt tolerance. Thus, AtHSFA7b serves as a transactivator that positively mediates salinity tolerance mainly through binding to the E-box-like motif to regulate gene expression.

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