記述言語：英語   掲載種別：研究論文（学術雑誌）   参加形態：共同（副担当）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1152/ajpendo.00164.2021

PubMed

掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.nut.2021.111389

記述言語：英語   掲載種別：研究論文（学術雑誌）   参加形態：共同（副担当）  

DOI： 10.1371/journal.pone.0241382. eCollection 2020.

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.bbrc.2020.07.041

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1002/2211-5463.12970

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Biochemical and Biophysical Research Communications  

© 2020 Elsevier Inc. Iron deficiency anemia indicates poor nutrition and is a public health problem. Iron deficiency is also associated with muscle weakness. However, the intracellular mechanisms by which iron deficiency induces muscle weakness are obscure. The purpose of the present study was to evaluate the effect of iron deficiency on protein synthesis in basal and branched-amino acids (BCAA)- and insulin-stimulated state in muscle cells. Differentiated C2C12 myotubes were incubated with an iron chelator, deferoxamine mesylate, and then stimulated with BCAA or insulin to activate protein synthesis. This iron deprivation resulted in a significant reduction in the abundance of iron-containing proteins, such as the mitochondrial complex 1 subunit protein, compared to control cells, but not of protein that does not contain iron, such as citrate synthase. Proteins involved in glucose utilization, such as glucose transpoter-1, hexokinase and AMP-activated protein kinase (AMPK), were upregulated under iron deficiency. Additionally, rates of BCAA- and insulin-stimulated protein synthesis, measured by puromycin incorporation, were lower in iron-deficient myotubes than in control cells. We suggest that low iron availability attenuates BCAA- and insulin-stimulated protein synthesis, possibly via activation of AMPK in myotubes. The present findings advance the understanding of the importance of iron to skeletal muscle protein synthesis and, thus, may contribute to the prevention of sarcopenia and frailty.

DOI： 10.1016/j.bbrc.2020.07.041

Scopus

その他リンク： https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85089189302&origin=inward

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3892/mmr.2020.10929

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）   参加形態：共同（副担当）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1155/2020/2328768

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1371/journal.pone.0241382

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3177/jnsv.66.41

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1080/09168451.2018.1533803

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3177/jnsv.64.233.

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Science and Sports  

DOI： 10.1016/j.scispo.2017.08.008

Scopus

その他リンク： https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85047430962&origin=inward

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.scispo.2017.08.008

Scopus

記述言語：英語   掲載種別：研究論文（学術雑誌）   参加形態：共同（副担当）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1002/jcb.26371

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3177/jnsv.64.233

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1249/MSS.0000000000001312

Web of Science

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.cmet.2017.04.029

Web of Science

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Physiological Research  

Scopus

その他リンク： https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85037038027&origin=inward

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1249/MSS.0000000000001312

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.cmet.2017.04.029

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3390/nu8040203

PubMed

記述言語：日本語   掲載種別：研究論文（学術雑誌）   出版者・発行元：(一社)日本体力医学会  

酪酸摂取がラット骨格筋における糖輸送体GLUT-4タンパク質の発現量に及ぼす影響について検討した。Sprague-Dawley系雄ラットを使用し、予備飼育期間と同じ粉末飼料を摂取させる対照群(C群)、もしくは酪酸を配合した粉末飼料を摂取させる群(SB群)に分けた。飼育期間中の総摂取量、飼料効率は両群間で有意差は認めなかった。クエン酸合成酵素タンパク質発現量は、滑車上筋およびヒラメ筋いずれの筋においても2群間に有意差は認めなかった。ヒラメ筋のアミノレブリン酸合成酵素タンパク質発現量は、C群と比較してSB群で有意に高値を示した。GLUT-4タンパク質発現量は、滑車上筋ではC群と比較してSB群で有意に低値、ヒラメ筋ではC群と比較してSB群で有意に低値を示した。SB群の滑車上筋およびヒラメ筋におけるMCT1タンパク質発現量は、C群に比べて有意に高値を示した。インスリン投与前、即ち空腹時の血糖値には両群間に有意差は認めなかった。食餌条件と時間における交互作用は認めなかったが、食餌条件による主効果を認め、C群と比較してSB群の血糖値は有意に高値を示した。

DOI： 10.7600/jspfsm.65.169

記述言語：日本語   出版者・発行元：(株)杏林書院  

記述言語：日本語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3390/nu8040203

掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.bbrc.2015.05.013

Scopus

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1152/japplphysiol.00054.2014

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1113/jphysiol.2014.283820

PubMed

記述言語：日本語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.atherosclerosis.2013.11.076

PubMed

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：日本語   出版者・発行元：(株)杏林書院  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：日本語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：日本語   出版者・発行元：社団法人日本体育学会  

DOI： 10.20693/jspehss.64.182_3

CiNii Books

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：英語   掲載種別：研究論文（学術雑誌）  

記述言語：日本語   出版者・発行元：早稲田大学スポーツ科学学術院  

CiNii Books

その他リンク： http://search.jamas.or.jp/link/ui/2015118621

記述言語：日本語   出版者・発行元：文光堂  

CiNii Books

その他リンク： http://search.jamas.or.jp/link/ui/2012322488

記述言語：英語   出版者・発行元：AMER PHYSIOLOGICAL SOC  

Higashida K, Kim SH, Higuchi M, Holloszy JO, Han DH. Normal adaptations to exercise despite protection against oxidative stress. Am J Physiol Endocrinol Metab 301: E779-E784, 2011. First published July 12, 2011; doi: 10.1152/ajpendo.00655.2010.-It has been reported that supplementation with the antioxidant vitamins C and E prevents the adaptive increases in mitochondrial biogenesis and GLUT4 expression induced by endurance exercise. We reevaluated the effects of these antioxidants on the adaptive responses of rat skeletal muscle to swimming in a short-term study consisting of 9 days of vitamins C and E with exercise during the last 3 days and a longer-term study consisting of 8 wk of antioxidant vitamins with exercise during the last 3 wk. The rats in the antioxidant groups were given 750 mg . kg body wt(-1) . day(-1) vitamin C and 150 mg . kg body wt(-1) . day(-1) vitamin E. In rats euthanized immediately after exercise, plasma TBARs were elevated in the control rats but not in the antioxidant-supplemented rats, providing evidence for an antioxidant effect. In rats euthanized 18 h after exercise there were large increases in insulin responsiveness of glucose transport in epitrochlearis muscles mediated by an approximately twofold increase in GLUT4 expression in both the short-and long-term treatment groups. The protein levels of a number of mitochondrial marker enzymes were also increased about twofold. Superoxide dismutases (SOD) 1 and 2 were increased about twofold in triceps muscle after 3 days of exercise, but only SOD2 was increased after 3 wk of exercise. There were no differences in the magnitudes of any of these adaptive responses between the control and antioxidant groups. These results show that very large doses of antioxidant vitamins do not prevent the exercise-induced adaptive responses of muscle mitochondria, GLUT4, and insulin action to exercise and have no effect on the level of these proteins in sedentary rats.

DOI： 10.1152/ajpendo.00655.2010

Web of Science

記述言語：英語   出版者・発行元：AMER PHYSIOLOGICAL SOC  

It has been reported that supplementation with the antioxidant vitamins C and E prevents the adaptive increases in mitochondrial biogenesis and GLUT4 expression induced by endurance exercise. We reevaluated the effects of these antioxidants on the adaptive responses of rat skeletal muscle to swimming in a short-term study consisting of 9 days of vitamins C and E with exercise during the last 3 days and a longer-term study consisting of 8 wk of antioxidant vitamins with exercise during the last 3 wk. The rats in the antioxidant groups were given 750 mg·kg body wt(-1)·day(-1) vitamin C and 150 mg·kg body wt(-1)·day(-1) vitamin E. In rats euthanized immediately after exercise, plasma TBARs were elevated in the control rats but not in the antioxidant-supplemented rats, providing evidence for an antioxidant effect. In rats euthanized 18 h after exercise there were large increases in insulin responsiveness of glucose transport in epitrochlearis muscles mediated by an approximately twofold increase in GLUT4 expression in both the short- and long-term treatment groups. The protein levels of a number of mitochondrial marker enzymes were also increased about twofold. Superoxide dismutases (SOD) 1 and 2 were increased about twofold in triceps muscle after 3 days of exercise, but only SOD2 was increased after 3 wk of exercise. There were no differences in the magnitudes of any of these adaptive responses between the control and antioxidant groups. These results show that very large doses of antioxidant vitamins do not prevent the exercise-induced adaptive responses of muscle mitochondria, GLUT4, and insulin action to exercise and have no effect on the level of these proteins in sedentary rats.

DOI： 10.1152/ajpendo.00655.2010

Web of Science

PubMed

記述言語：英語   出版者・発行元：PUBLIC LIBRARY SCIENCE  

BACKGROUND: It has been proposed that muscle insulin resistance in type 2 diabetes is due to a selective decrease in the components of the mitochondrial electron transport chain and results from accumulation of toxic products of incomplete fat oxidation. The purpose of the present study was to test this hypothesis. METHODOLOGY/PRINCIPAL FINDINGS: Rats were made severely iron deficient, by means of an iron-deficient diet. Iron deficiency results in decreases of the iron containing mitochondrial respiratory chain proteins without affecting the enzymes of the fatty acid oxidation pathway. Insulin resistance was induced by feeding iron-deficient and control rats a high fat diet. Skeletal muscle insulin resistance was evaluated by measuring glucose transport activity in soleus muscle strips. Mitochondrial proteins were measured by Western blot. Iron deficiency resulted in a decrease in expression of iron containing proteins of the mitochondrial respiratory chain in muscle. Citrate synthase, a non-iron containing citrate cycle enzyme, and long chain acyl-CoA dehydrogenase (LCAD), used as a marker for the fatty acid oxidation pathway, were unaffected by the iron deficiency. Oleate oxidation by muscle homogenates was increased by high fat feeding and decreased by iron deficiency despite high fat feeding. The high fat diet caused severe insulin resistance of muscle glucose transport. Iron deficiency completely protected against the high fat diet-induced muscle insulin resistance. CONCLUSIONS/SIGNIFICANCE: The results of the study argue against the hypothesis that a deficiency of the electron transport chain (ETC), and imbalance between the ETC and β-oxidation pathways, causes muscle insulin resistance.

DOI： 10.1371/journal.pone.0019739

Web of Science

PubMed

記述言語：英語   出版者・発行元：PUBLIC LIBRARY SCIENCE  

Background: It has been proposed that muscle insulin resistance in type 2 diabetes is due to a selective decrease in the components of the mitochondrial electron transport chain and results from accumulation of toxic products of incomplete fat oxidation. The purpose of the present study was to test this hypothesis.
Methodology/Principal Findings: Rats were made severely iron deficient, by means of an iron-deficient diet. Iron deficiency results in decreases of the iron containing mitochondrial respiratory chain proteins without affecting the enzymes of the fatty acid oxidation pathway. Insulin resistance was induced by feeding iron-deficient and control rats a high fat diet. Skeletal muscle insulin resistance was evaluated by measuring glucose transport activity in soleus muscle strips. Mitochondrial proteins were measured by Western blot. Iron deficiency resulted in a decrease in expression of iron containing proteins of the mitochondrial respiratory chain in muscle. Citrate synthase, a non-iron containing citrate cycle enzyme, and long chain acyl-CoA dehydrogenase (LCAD), used as a marker for the fatty acid oxidation pathway, were unaffected by the iron deficiency. Oleate oxidation by muscle homogenates was increased by high fat feeding and decreased by iron deficiency despite high fat feeding. The high fat diet caused severe insulin resistance of muscle glucose transport. Iron deficiency completely protected against the high fat diet-induced muscle insulin resistance.
Conclusions/Significance: The results of the study argue against the hypothesis that a deficiency of the electron transport chain (ETC), and imbalance between the ETC and beta-oxidation pathways, causes muscle insulin resistance.

DOI： 10.1371/journal.pone.0019739

Web of Science

記述言語：英語   出版者・発行元：FEDERATION AMER SOC EXP BIOL  

It has been reported that 30% calorie restriction (CR) for 3 mo results in large increases in mitochondrial biogenesis in heart, brain, liver, and adipose tissue, with concomitant increases in respiration and ATP synthesis. We found these results surprising, and performed this study to determine whether 30% CR does induce an increase in mitochondria in heart, brain, liver, adipose tissue, and/or skeletal muscle. To this end, we measured the levels of a range of mitochondrial proteins, and mRNAs. With the exception of long-chain acyl-CoA dehydrogenase protein level, which was increased similar to 60% in adipose tissue, none of the mitochondrial proteins or mRNAs that we measured were increased in rats subjected to 30% CR for 14 wk. There was also no increase in citrate synthase activity. Because it is not possible to have an increase in mitochondria without any increase in key mitochondrial proteins, we conclude that 30% CR does not induce an increase in mitochondria in heart, brain, liver, adipose tissue, or skeletal muscle in laboratory rodents.-Hancock, C. R., Han, D.-H., Higashida, K., Kim, S. H., Holloszy, J. O. Does calorie restriction induce mitochondrial biogenesis? A reevaluation. FASEB J. 25, 785-791 (2011). www.fasebj.org

DOI： 10.1096/fj.10-170415

Web of Science

記述言語：英語  

It has been reported that 30% calorie restriction (CR) for 3 mo results in large increases in mitochondrial biogenesis in heart, brain, liver, and adipose tissue, with concomitant increases in respiration and ATP synthesis. We found these results surprising, and performed this study to determine whether 30% CR does induce an increase in mitochondria in heart, brain, liver, adipose tissue, and/or skeletal muscle. To this end, we measured the levels of a range of mitochondrial proteins, and mRNAs. With the exception of long-chain acyl-CoA dehydrogenase protein level, which was increased ∼60% in adipose tissue, none of the mitochondrial proteins or mRNAs that we measured were increased in rats subjected to 30% CR for 14 wk. There was also no increase in citrate synthase activity. Because it is not possible to have an increase in mitochondria without any increase in key mitochondrial proteins, we conclude that 30% CR does not induce an increase in mitochondria in heart, brain, liver, adipose tissue, or skeletal muscle in laboratory rodents.

DOI： 10.1096/fj.10-170415

PubMed

記述言語：英語  

It has recently been reported that a 4-wk high-fat diet gradually increases skeletal muscle peroxisome proliferator activated receptor (PPAR) gamma coactivator-1alpha (PGC-1alpha) protein content, which has been suggested to regulate GLUT-4 gene transcription. However, it has not been reported that a high-fat diet enhances GLUT-4 mRNA expression and protein content in skeletal muscle, suggesting that an increase in PGC-1alpha protein content is not sufficient to induce muscle GLUT-4 biogenesis in a high-fat fed animal. Therefore, we first evaluated the relationship between PGC-1alpha and GLUT-4 expression in skeletal muscle of rats fed a high-fat diet for 4 wk. The PGC-1alpha protein content in rat epitrochlearis muscle significantly increased by twofold after the 4-wk high-fat diet feeding. However, the high-fat diet had no effect on GLUT-4 protein content and induced a 30% decrease in GLUT-4 mRNA expression in rat skeletal muscle (p<0.05). To clarify the mechanism by which a high-fat diet downregulates GLUT-4 mRNA expression, we next examined the effect of PPARdelta activation, which is known to occur in response to a high-fat diet, on GLUT-4 mRNA expression in L6 myotubes. Incubation with 500 nM GW501516 (PPARdelta activator) for 24 h significantly decreased GLUT-4 mRNA in L6 myotubes. Taken together, these findings suggest that a high-fat diet downregulates GLUT-4 mRNA, possibly through the activation of PPARdelta, despite an increase in PGC-1alpha protein content in rat skeletal muscle, and that a posttranscriptional regulatory mechanism maintains GLUT-4 protein content in skeletal muscle of rats fed a high-fat diet.

DOI： 10.3177/jnsv.55.486

Scopus

PubMed

記述言語：英語   出版者・発行元：AMER PHYSIOLOGICAL SOC  

Ogata T, Oishi Y, Higashida K, Higuchi M, Muraoka I. Prolonged exercise training induces long-term enhancement of HSP70 expression in rat plantaris muscle. Am J Physiol Regul Integr Comp Physiol 296: R1557-R1563, 2009. First published February 25, 2009; doi:10.1152/ajpregu.90911.2008.-Skeletal muscle may develop adaptive molecular chaperone enhancements as a potential defense system through repeated daily exercise stimulation. The present study investigated whether prolonged exercise training alters the expression of molecular chaperone proteins for the long term in skeletal muscle. Mature male Wistar rats were subjected for 8 wk to either a single bout of acute intermittent treadmill running (30 m/min, 5 min x 4, 5 degrees grade) or prolonged treadmill running training (15-40 m/min, 5 min x 4, 5-7 degrees grade). Levels of five molecular chaperone proteins [ heat shock protein (HSP) 25, HSP60, glucose-regulated protein (GRP) 78, HSP70, and heat shock cognate (HSC) 70] were measured in response to acute exercise and prolonged training. HSP70 levels were increased 6 and 24 h after acute exercise, but expression returned to control level within 2 days. In contrast, prolonged training had a long-term effect on HSP70 expression. Levels of HSP70 were notably increased by 4.5-fold over control 2 days after prolonged training; the enhancement was maintained for at least 14 days after training ended. However, other molecular chaperone proteins did not show adaptive changes in response to prolonged training. In addition, HSP70 enhancement by prolonged exercise training was not accompanied by transcription of HSP70 mRNA. These findings demonstrate that prolonged training can induce long-term enhancement of HSP70 expression without change at the mRNA level in skeletal muscle.

DOI： 10.1152/ajpregu.90911.2008

Web of Science

記述言語：英語   出版者・発行元：AMER PHYSIOLOGICAL SOC  

Skeletal muscle may develop adaptive molecular chaperone enhancements as a potential defense system through repeated daily exercise stimulation. The present study investigated whether prolonged exercise training alters the expression of molecular chaperone proteins for the long term in skeletal muscle. Mature male Wistar rats were subjected for 8 wk to either a single bout of acute intermittent treadmill running (30 m/min, 5 min x 4, 5 degrees grade) or prolonged treadmill running training (15-40 m/min, 5 min x 4, 5-7 degrees grade). Levels of five molecular chaperone proteins [heat shock protein (HSP)25, HSP60, glucose-regulated protein (GRP)78, HSP70, and heat shock cognate (HSC)70] were measured in response to acute exercise and prolonged training. HSP70 levels were increased 6 and 24 h after acute exercise, but expression returned to control level within 2 days. In contrast, prolonged training had a long-term effect on HSP70 expression. Levels of HSP70 were notably increased by 4.5-fold over control 2 days after prolonged training; the enhancement was maintained for at least 14 days after training ended. However, other molecular chaperone proteins did not show adaptive changes in response to prolonged training. In addition, HSP70 enhancement by prolonged exercise training was not accompanied by transcription of HSP70 mRNA. These findings demonstrate that prolonged training can induce long-term enhancement of HSP70 expression without change at the mRNA level in skeletal muscle.

DOI： 10.1152/ajpregu.90911.2008

Web of Science

PubMed

記述言語：英語  

It has recently been reported that a 4-wk high-fat diet gradually increases skeletal muscle peroxisome proliferator activated receptor (PPAR) γ coactivator-1 α (PGC-1α) protein content, which has been suggested to regulate GLUT-4 gene transcription. However, it has not been reported that a high-fat diet enhances GLUT-4 mRNA expression and protein content in skeletal muscle, suggesting that an increase in PGC-lα protein content is not sufficient to induce muscle GLUT-4 biogenesis in a high-fat fed animal. Therefore, we first evaluated the relationship between PGC-1α and GLUT-4 expression in skeletal muscle of rats fed a high-fat diet for 4 wk. The PGC-1 protein content in rat epitrochlearis muscle significantly increased by twofold after the 4-wk high-fat diet feeding. However, the high-fat diet had no effect on GLUT-4 protein content and induced a 30% decrease in GLUT-4 mRNA expression in rat skeletal muscle (p&lt
0.05). To clarify the mechanism by which a high-fat diet downregulates GLUT-4 mRNA expression, we next examined the effect of PPARδ activation, which is known to occur in response to a high-fat diet, on GLUT-4 mRNA expression in L6 myotubes. Incubation with 500 nM GW501516 (PPARδ activator) for 24 h significantly decreased GLUT-4 mRNA in L6 myotubes. Taken together, these findings suggest that a high-fat diet downregulates GLUT-4 mRNA, possibly through the activation of PPARδ, despite an increase in PGC-1α protein content in rat skeletal muscle, and that a posttranscriptional regulatory mechanism maintains GLUT-4 protein content in skeletal muscle of rats fed a high-fat diet.

DOI： 10.3177/jnsv.55.486

Scopus

PubMed

記述言語：日本語   出版者・発行元：日本体力医学会  

CiNii Books

記述言語：日本語   出版者・発行元：日本体力医学会  

CiNii Books

記述言語：日本語   出版者・発行元：日本体力医学会  

CiNii Books

記述言語：英語   出版者・発行元：ACADEMIC PRESS INC ELSEVIER SCIENCE  

Endurance exercise induces mitochondrial biogenesis in skeletal muscle. It has been shown that lipin-1 acts as a transcriptional coactivator in liver, and stimulates gene expression of mitochondrial enzymes. We hypothesized that lipin-1 might be involved in exercise-induced mitochondrial biogenesis in skeletal muscle. The present investigation first demonstrated that lipin-1 mRNA in rat triceps muscle was increased by approximately 2-fold after an acute bout of endurance swimming exercise. Second, ectopic expression of lipin-1 in L6 myotube increased carnitine palmitoyltransferase-1 and delta-aminolevulinate synthase gene expression. Finally, lipin-1 mRNA expression in rat triceps muscle was significantly elevated at 6h after subcutaneous injections of 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) or clenbuterol, which are 5'-AMP-activated protein kinase (AMPK) and beta2-adrenergic receptor (beta2-AR) activators, respectively. These results may suggest that enhanced expression of lipin-1 is involved in exercise-induced mitochondrial enzyme adaptations, possibly through AMPK- and beta2-AR-related mechanisms.

DOI： 10.1016/j.bbrc.2008.07.079

Web of Science

PubMed

記述言語：英語   出版者・発行元：ACADEMIC PRESS INC ELSEVIER SCIENCE  

Endurance exercise induces mitochondrial biogenesis in skeletal muscle. It has been shown that lipin-1 acts as a transcriptional coactivator in liver, and Stimulates gene expression of mitochondrial enzymes. We hypothesized that lipin-1 might be involved in exercise-induced mitochondrial biogenesis in skeletal muscle. The present investigation first demonstrated that lipin-1 mRNA in rat triceps muscle was increased by approximately 2-fold after an acute bout of endurance swimming exercise. Second, ectopic expression of lipin-1 in L6 myotube increased carnitine palmitoyltransferase-1 and delta-aminolevulinate synthase gene expression. Finally, lipin-1 mRNA expression in rat triceps muscle was significantly elevated at 6 h after subcutaneous injections of 5-aminomidazole-4-carboxamide ribonucleciside (AICAR) or clenbuterol, which are 5&apos;-AMP-activated protein kinase (AMPK) and beta 2-adrenergic receptor (beta 2-AR) activators, respectively. These results may suggest that enhanced expression of lipin-1 is involved in exercise-induced mitochondrial enzyme adaptations, possibly through AMPK- and beta 2-AR-related mechanisms. (C) 2008 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2008.07.079

Web of Science

記述言語：日本語   出版者・発行元：日本運動生理学会事務局  

The purposes of this study were 1) to examine whether fatty acid composition of the diet might affect mitochondrial enzyme activities in rat skeletal muscle, and 2) to assess the effects of the high-fat diets on skeletal muscle peroxisome proliferator activated receptor γ coactivator-1α (PGC-1α) protein content, which is a key regulator of adaptive mitochondrial biogenesis. Four-week-old male Sprague-Dawley rats were fed for 30 days either a rodent chow (12% calorie from fat, CON group; n=5) or a high-fat diet (50% calorie from fat) containing lard (LARD group; n=5) or olive oil (OLIVE group; n=5). Citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (3-HAD) activities in plantaris muscles were significantly higher in both LARD and OLIVE groups than CON group (p<0.05). Furthermore, the 3-HAD activity in OLIVE group was significantly higher than that in LARD group (p<0.05). PGC-1α protein contents in epitrochlearis muscle were significantly higher in both LARD and OLIVE groups than CON group by 88 and 70%, respectively(p<0.05). No significant difference in PGC-1α protein content was observed between LARD and OLIVE groups. In conclusion, these results indicate that 1) olive oil, which consists mostly of unsaturated fatty acids, has more pronounced effects on the fatty acid oxidation enzyme activity in skeletal muscle, compared with lard enriched in saturated fatty acids, and 2) feeding high-fat diets increases transcription coactivator PGC-1α protein content in rat skeletal muscle.

CiNii Books

その他リンク： http://dl.ndl.go.jp/info:ndljp/pid/10563281