Faculty Profiles - HIGASHIDA Kazuhiko

Papers - HIGASHIDA Kazuhiko

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Interaction Between Sarcopenic Obesity and Nonlocomotive Physical Activity on the Risk of Depressive Symptoms in Community-Dwelling Older Adult Japanese Women Reviewed

Yu Osugi, Aiko Imai, Toshiyuki Kurihara, Keiko Kishigami, Kazuhiko Higashida, Kiyoshi Sanada

Journal of Aging and Physical Activity 17 1 - 17 2023.1

Inhibition of the mitochondrial respiratory chain reduces catecholamine‑stimulated lipolysis via increasing lactate production in 3T3‑L1 adipocytes Reviewed

Nodoka Takeuchi, Kazuhiko Higashida, Naoya Nakai

2023

Intermittent fasting reduces mouse body fat while maintaining muscle mass by regulating protein synthesis and autophagy Reviewed

Rikako Yoshii, Kazuhiko Higashida, Naoya Nakai

Nutrition 2023

Low-carbohydrate, high-fat diet, and running exercise influence bone parameters in old mice. International journal

Yuki Aikawa, Takenori Yamashita, Naoya Nakai, Kazuhiko Higashida

Journal of applied physiology (Bethesda, Md. : 1985) 132 ( 5 ) 1204 - 1212 2022.5

Language：English Publishing type：Research paper (scientific journal)

We examined the effects and interactions of a low-carbohydrate, high-fat (LCHF) diet and voluntary running exercise on bone in older mice. Male 19-mo-old mice were divided into four groups by diet (control vs. LCHF) and exercise (sedentary vs. voluntary running). The control diet was 55% carbohydrate, 23% protein, and 22% fat, and the LCHF diet was 10% carbohydrate, 33% protein, and 57% fat as percentages of calories. The experiment ended when the mice reached 24 mo old. Statistical analysis was conducted using two-way analysis of variance with diet and exercise. The LCHF diet decreased bone mineral content (BMC), bone mineral density, bone volume fraction, and trabecular number. There was no significant interaction between diet and exercise on many bone parameters. However, there were significant diet and exercise interactions on lumbar BMC and tibial trabecular total tissue volume and average cortical thickness. The LCHF diet attenuated the benefit of running exercise on lumbar BMC and caused running to have a negative effect on tibial trabecular total tissue volume. Our study suggests that the LCHF diet impairs bone mass and some trabecular microstructure and reduces the benefit of exercise on lumbar BMC in old mice.NEW & NOTEWORTHY An LCHF diet is used in treatment and prevention of diseases or improving exercise performance. However, some studies have shown that an LCHF diet diminishes bone in young rodents. Our study demonstrates that an LCHF diet impairs bone mass and some trabecular microstructure in old mice, which are similar to the previous studies using young rodents. Moreover, our study shows that an LCHF diet reduces the benefit of exercise on lumbar BMC in old mice.

DOI： 10.1152/japplphysiol.00789.2021

PubMed

BDK knockout skeletal muscle satellite cells exhibit enhanced protein translation initiation signal in response to BCAA in vitro Reviewed

Nakai N, Iida N, Kitai S, Shimomura Y, Kitaura Y, Higashida K

Biosci Biotechnol Biochem Zbac021 2022.2

c-Myc overexpression increases ribosome biogenesis and protein synthesis independent of mTORC1 activation in mouse skeletal muscle Reviewed

Mori T, Ato S, Knudsen JR, Henriquez-Olguin C, Li Z, Wakabayashi K, Suginohara T, Higashida K, Tamura Y, Nakazato K, Jensen TE, Ogasawara R.

Am J Physiol Endocrinol Metab 321 ( 4 ) 551 - 559 2021.10

Glucose enhances catecholamine-stimulated lipolysis via increased glycerol-3-phosphate synthesis in 3T3-L1 adipocytes and rat adipose tissue Reviewed

Takeuchi N, Higashida K, Li X, Nakai N.

Mol Biol Rep 48 ( 6 ) 6269 - 6276 2021.9

Basal and resistance exercise-induced increase in protein synthesis is impaired in skeletal muscle of iron-deficient rats

Kazuhiko Higashida, Sachika Inou, Nodoka Takeuchi, Satoru Ato, Riki Ogasawara, Naoya Nakai

Nutrition 111389 - 111389 2021.6

Ketogenic diet feeding improves aerobic metabolism property in extensor digitorum longus muscle of sedentary male rats Reviewed

Ogura Y, Kakehashi C, Yoshihara T, Kurosaka M, Kakigi R, Higashida K, Fujiwara SE, Akema T, Funabashi T.

Plos one 2020.10

Iron deficiency attenuates protein synthesis stimulated by branched-chain amino acids and insulin in myotubes. International journal

Kazuhiko Higashida, Sachika Inoue, Naoya Nakai

Biochemical and biophysical research communications 531 ( 2 ) 112 - 117 2020.10

Language：English Publishing type：Research paper (scientific journal)

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

PubMed

Autophagy under glucose starvation enhances protein translation initiation in response to re-addition of glucose in C2C12 myotubes. International journal

Naoya Nakai, Saki Kitai, Noriko Iida, Sachika Inoue, Kazuhiko Higashida

FEBS open bio 10 ( 10 ) 2149 - 2156 2020.10

Language：English Publishing type：Research paper (scientific journal)

Proteolysis is known to play a crucial role in maintaining skeletal muscle mass and function. Autophagy is a conserved intracellular process for the bulk degradation of proteins in lysosomes. Although nutrient starvation is known to induce autophagy, the effect of nutrient repletion following starvation on the mTOR pathway-mediated protein translation remains unclear. In the present study, we examined the effect of glucose starvation on the initiation of protein translation in response to glucose re-addition in C2C12 myotubes. Glucose starvation decreased the phosphorylation of p70 S6 kinase (p70S6K), a bonafide marker for protein translation initiation. Following re-addition of glucose, phosphorylation of p70S6K markedly increased only in glucose-starved cells. Inhibiting autophagy using pharmacological inhibitors diminished the effect of glucose re-addition on the phosphorylation of p70S6K, whereas inhibition of the ubiquitin-proteasome system did not exert any effect. In conclusion, autophagy under glucose starvation partially accounts for the activation of translation initiation by re-addition of glucose.

DOI： 10.1002/2211-5463.12970

PubMed

Iron deficiency attenuates catecholamine-stimulated lipolysis via downregulation of lipolysis-related proteins and glucose utilization in 3T3-L1 adipocytes Reviewed International journal

Higashida K, Takeuchi N, Inoue N, Hashimoto T, Nakai N

Molecular Medicine Reports 2020.3

Application of Molecular Hydrogen as a Novel Antioxidant in Sports Science Reviewed

Kawamura T, Higashida K, Muraoka I

Oxidative Medicine and Cellular Longevity 2020.1

Induction of Autophagy and Changes in Cellular Metabolism in Glucose Starved C2C12 Myotubes Reviewed

Naoya Nakai, Saki Kitai, Noriko Iida, Sachika Inoue, Ken Nakata, Taro Murakami, Kazuhiko Higashida

J Nutr Sci Vitaminol (Tokyo) . 66 ( 1 ) 41 - 47 2020.1

Ketogenic diet feeding improves aerobic metabolism property in extensor digitorum longus muscle of sedentary male rats. International journal

Yuji Ogura, Chiaki Kakehashi, Toshinori Yoshihara, Mitsutoshi Kurosaka, Ryo Kakigi, Kazuhiko Higashida, Sei-Etsu Fujiwara, Tatsuo Akema, Toshiya Funabashi

PloS one 15 ( 10 ) e0241382 2020

Language：English Publishing type：Research paper (scientific journal)

Recent studies of the ketogenic diet, an extremely high-fat diet with extremely low carbohydrates, suggest that it changes the energy metabolism properties of skeletal muscle. However, ketogenic diet effects on muscle metabolic characteristics are diverse and sometimes countervailing. Furthermore, ketogenic diet effects on skeletal muscle performance are unknown. After male Wistar rats (8 weeks of age) were assigned randomly to a control group (CON) and a ketogenic diet group (KD), they were fed for 4 weeks respectively with a control diet (10% fat, 10% protein, 80% carbohydrate) and a ketogenic diet (90% fat, 10% protein, 0% carbohydrate). After the 4-week feeding period, the extensor digitorum longus (EDL) muscle was evaluated ex vivo for twitch force, tetanic force, and fatigue. We also analyzed the myosin heavy chain composition, protein expression of metabolic enzymes and regulatory factors, and citrate synthase activity. No significant difference was found between CON and KD in twitch or tetanic forces or muscle fatigue. However, the KD citrate synthase activity and the protein expression of Sema3A, citrate synthase, succinate dehydrogenase, cytochrome c oxidase subunit 4, and 3-hydroxyacyl-CoA dehydrogenase were significantly higher than those of CON. Moreover, a myosin heavy chain shift occurred from type IIb to IIx in KD. These results demonstrated that the 4-week ketogenic diet improves skeletal muscle aerobic capacity without obstructing muscle contractile function in sedentary male rats and suggest involvement of Sema3A in the myosin heavy chain shift of EDL muscle.

DOI： 10.1371/journal.pone.0241382

PubMed

A Lactate-based compound containing caffeine in addition to voluntary running exercise decreases subcutaneous fat mass and improves glucose metabolism in obese rats Reviewed

Hashimoto T, Yokokawa T, Narusawa R, Okada Y, Kawaguchi R, Higashida K

Journal of Functional Foods 56 84 - 91 2019.3

Low-carbohydrate high-protein diet diminishes the insulin response to glucose load via suppression of SGLT-1 in mice. International journal

Kazuhiko Higashida, Shin Terada, Xi Li, Sachika Inoue, Noriko Iida, Saki Kitai, Naoya Nakai

Bioscience, biotechnology, and biochemistry 83 ( 2 ) 365 - 371 2019.2

Language：English Publishing type：Research paper (scientific journal)

The purpose of this study was to examine the effects of a low-carbohydrate high-protein (LCHP) diet on the expression of glucose transporters and their relationships to glucose metabolism. Male C57BL/6 mice were fed a normal control or LCHP diet for 2 weeks. An oral glucose tolerance test and insulin tolerance test (ITT) were performed, and the expression of glucose transporters was determined in the gastrocnemius muscle, jejunum and pancreas. The increase in plasma insulin concentrations after glucose administration was reduced in the LCHP group. However, LCHP diet had no effects on peripheral insulin sensitivity or glucose transporters expression in the gastrocnemius and pancreas. Soluble glucose transporter (SGLT)-1 protein content in jejunum was lower in the LCHP group. Taken together, these results suggest that the blunted insulin response after glucose administration in LCHP diet-fed mice might be due to decreased SGLT-1 expression, but not to an increase in peripheral insulin sensitivity. Abbreviations: LCHP: low-carbohydrate high-protein; ITT: insulin tolerance test; GLUT: glucose transporter; SGLT: soluble glucose transporter; OGTT: oral glucose tolerance test; AUC: area under the curve.

DOI： 10.1080/09168451.2018.1533803

PubMed

Time Course of Decrease in Skeletal Muscle Mitochondrial Biogenesis after Discontinuation of High-Fat Diet.

Li X, Higashida K, Kawamura T, Higuchi M

J Nutr Sci Vitaminol (Tokyo) 2018.6

Effects of exhaustive exercises, with different intensities, on oxidative stress markers in rat plasma and skeletal muscle Reviewed

Kawamura T, Fujii R, Li X, Higashida K, Muraoka I

Science and Sports 33 ( 3 ) 169 - 175 2018.6

Language：English Publishing type：Research paper (scientific journal) Publisher：Elsevier Masson SAS

Objectives: The purpose of this study was to examine the effects of exhaustive exercises, with different intensities, on oxidative stress markers in rat plasma and skeletal muscle. Methods: Male Sprague-Dawley rats (n = 24) were randomly divided into the following four groups: control (CON), low-intensity exercise (LE), high-intensity interval exercise (HE) and incremental exercise (IE). The animals in the latter three groups performed exercises in which they ran until exhaustion as follows: Animals in the LE group ran at 20 m/min (6° graded)
the HE group ran at 40 m/min for 30 s (0° graded) with a rest interval of 60 s between each run
and the IE group ran at 15 m/min (6° graded), initially, with the running speed gradually increased by 5 m/min, every 10 min. Immediately following the exercise, a blood sample was drawn, and followed by the gastrocnemius muscle and liver were quickly removed. These samples were analysed for lactate concentration, oxidative stress markers, and glycogen contents. Results: Plasma oxidative stress markers in the LE and HE groups demonstrated no change, while plasma protein carbonyl (PC) levels and total antioxidant capacity (TAC) in the IE group were significantly increased compared with the CON group (P &lt
0.05). In contrast, all the oxidative stress markers, in the skeletal muscle of the three exercise groups, demonstrated no change compared with the CON group. Conclusion: Incremental exhaustive exercise elevates the plasma PC levels and TAC, but does not change skeletal muscle oxidative stress markers in rats.

DOI： 10.1016/j.scispo.2017.08.008

Scopus

Leucine supplementation after mechanical stimulation activates protein synthesis via L-type amino acid transporter 1 in vitro Reviewed International journal

Nakai N, Kawano F, Murakami T, Nakata K, Higashida K.

J Cell Biochem 119 ( 2 ) 2094 - 2101 2018.2

PPARβ Is Essential for Maintaining Normal Levels of PGC-1α and Mitochondria and for the Increase in Muscle Mitochondria Induced by Exercise. Reviewed International journal

Jin-Ho Koh, Chad R Hancock, Shin Terada, Kazuhiko Higashida, John O Holloszy, Dong-Ho Han

Cell metabolism 25 ( 5 ) 1176 - 1185 2017.5

Language：English Publishing type：Research paper (scientific journal) Publisher：CELL PRESS

The objective of this study was to evaluate the specific mechanism(s) by which PPARβ regulates mitochondrial content in skeletal muscle. We discovered that PPARβ increases PGC-1α by protecting it from degradation by binding to PGC-1α and limiting ubiquitination. PPARβ also induces an increase in nuclear respiratory factor 1 (NRF-1) expression, resulting in increases in mitochondrial respiratory chain proteins and MEF2A, for which NRF-1 is a transcription factor. There was also an increase in AMP kinase phosphorylation mediated by an NRF-1-induced increase in CAM kinase kinase-β (CaMKKβ). Knockdown of PPARβ resulted in large decreases in the levels of PGC-1α and mitochondrial proteins and a marked attenuation of the exercise-induced increase in mitochondrial biogenesis. In conclusion, PPARβ induces an increase in PGC-1α protein, and PPARβ is a transcription factor for NRF-1. Thus, PPARβ plays essential roles in the maintenance and adaptive increase in mitochondrial enzymes in skeletal muscle by exercise.

DOI： 10.1016/j.cmet.2017.04.029

Web of Science

PubMed

Effects of rapid or slow body weight reduction on intramuscular protein degradation pathways during equivalent weight loss on rats Reviewed

Nonaka Y., Urashima S., Inai M., Nishimura S., Higashida K., Terada S.

Physiological Research 66 ( 5 ) 823 - 831 2017.1

A Mechanism Underlying Preventive Effect of High-Intensity Training on Colon Cancer

Matsuo K, Sato K, Suemoto K, Miyamoto-Mikami E, Fuku N, Higashida K, Tsuji K, Xu Y, Liu X, Iemitsu M, Hamaoka T, Tabata I

Med Sci Sports Exerc 2017

Alternate-Day High-Fat Diet Induces an Increase in Mitochondrial Enzyme Activities and Protein Content in Rat Skeletal Muscle. International journal

Xi Li, Kazuhiko Higashida, Takuji Kawamura, Mitsuru Higuchi

Nutrients 8 ( 4 ) 203 - 203 2016.4

Language：English Publishing type：Research paper (scientific journal)

Long-term high-fat diet increases muscle mitochondrial enzyme activity and endurance performance. However, excessive calorie intake causes intra-abdominal fat accumulation and metabolic syndrome. The purpose of this study was to investigate the effect of an alternating day high-fat diet on muscle mitochondrial enzyme activities, protein content, and intra-abdominal fat mass in rats. Male Wistar rats were given a standard chow diet (CON), high-fat diet (HFD), or alternate-day high-fat diet (ALT) for 4 weeks. Rats in the ALT group were fed a high-fat diet and standard chow every other day for 4 weeks. After the dietary intervention, mitochondrial enzyme activities and protein content in skeletal muscle were measured. Although body weight did not differ among groups, the epididymal fat mass in the HFD group was higher than those of the CON and ALT groups. Citrate synthase and beta-hydroxyacyl CoA dehydrogenase activities in the plantaris muscle of rats in HFD and ALT were significantly higher than that in CON rats, whereas there was no difference between HFD and ALT groups. No significant difference was observed in muscle glycogen concentration or glucose transporter-4 protein content among the three groups. These results suggest that an alternate-day high-fat diet induces increases in mitochondrial enzyme activities and protein content in rat skeletal muscle without intra-abdominal fat accumulation.

DOI： 10.3390/nu8040203

PubMed

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

野中雄大, 東田一彦, 木村典代, 寺田新

体力科学 65 ( 1 ) 169 - 176 2016.2

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：(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

【未来の扉をひらく運動の研究】運動による抗糖尿病効果とエピジェネティクス

寺田新, 野中雄大, 東田一彦

体育の科学 66 ( 1 ) 36 - 43 2016.1

Dehydroepiandrosterone activates AMP kinase and regulates GLUT4 and PGC-1α expression in C2C12 myotubes. Reviewed

Yokokawa T, Sato K, Iwanaka N, Honda H, Higashida K, Iemitsu M, Hayashi T, Hashimoto T

Biochemical and biophysical research communications 463 ( 1-2 ) 42 - 47 2015.7

Publishing type：Research paper (scientific journal)

Exercise and caloric restriction (CR) have been reported to have anti-ageing, anti-obesity, and health-promoting effects. Both interventions increase the level of dehydroepiandrosterone (DHEA) in muscle and blood, suggesting that DHEA might partially mediate these effects. In addition, it is thought that either 5'-adenosine monophosphate-activated protein kinase (AMPK) or peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) mediates the beneficial effects of exercise and CR. However, the effects of DHEA on AMPK activity and PGC-1α expression remain unclear. Therefore, we explored whether DHEA in myotubes acts as an activator of AMPK and increases PGC-1α. DHEA exposure increased glucose uptake but not the phosphorylation levels of Akt and PKCζ/λ in C2C12 myotubes. In contrast, the phosphorylation levels of AMPK were elevated by DHEA exposure. Finally, we found that DHEA induced the expression of the genes PGC-1α and GLUT4. Our current results might reveal a previously unrecognized physiological role of DHEA; the activation of AMPK and the induction of PGC-1α by DHEA might mediate its anti-obesity and health-promoting effects in living organisms.

DOI： 10.1016/j.bbrc.2015.05.013

Scopus

PubMed

Mixed lactate and caffeine compound increases satellite cell activity and anabolic signals for muscle hypertrophy. Reviewed International journal

Yoshimi Oishi, Hayato Tsukamoto, Takumi Yokokawa, Keisuke Hirotsu, Mariko Shimazu, Kenji Uchida, Hironori Tomi, Kazuhiko Higashida, Nobumasa Iwanaka, Takeshi Hashimoto

Journal of applied physiology (Bethesda, Md. : 1985) 118 ( 6 ) 742 - 9 2015.3

Language：English Publishing type：Research paper (scientific journal)

We examined whether a mixed lactate and caffeine compound (LC) could effectively elicit proliferation and differentiation of satellite cells or activate anabolic signals in skeletal muscles. We cultured C2C12 cells with either lactate or LC for 6 h. We found that lactate significantly increased myogenin and follistatin protein levels and phosphorylation of P70S6K while decreasing the levels of myostatin relative to the control. LC significantly increased protein levels of Pax7, MyoD, and Ki67 in addition to myogenin, relative to control. LC also significantly increased follistatin expression relative to control and stimulated phosphorylation of mTOR and P70S6K. In an in vivo study, male F344/DuCrlCrlj rats were assigned to control (Sed, n = 10), exercise (Ex, n = 12), and LC supplementation (LCEx, n = 13) groups. LC was orally administered daily. The LCEx and Ex groups were exercised on a treadmill, running for 30 min at low intensity every other day for 4 wk. The LCEx group experienced a significant increase in the mass of the gastrocnemius (GA) and tibialis anterior (TA) relative to both the Sed and Ex groups. Furthermore, the LCEx group showed a significant increase in the total DNA content of TA compared with the Sed group. The LCEx group experienced a significant increase in myogenin and follistatin expression of GA relative to the Ex group. These results suggest that administration of LC can effectively increase muscle mass concomitant with elevated numbers of myonuclei, even with low-intensity exercise training, via activated satellite cells and anabolic signals.

DOI： 10.1152/japplphysiol.00054.2014

PubMed

PGC-1α mediates a rapid, exercise-induced downregulation of glycogenolysis in rat skeletal muscle. International journal

Sang Hyun Kim, Jin Ho Koh, Kazuhiko Higashida, Su Ryun Jung, John O Holloszy, Dong-Ho Han

The Journal of physiology 593 ( 3 ) 635 - 43 2015.2

Language：English Publishing type：Research paper (scientific journal)

KEY POINTS: Long-term endurance exercise training results in a reduction in the rates of muscle glycogen depletion and lactic acid accumulation during submaximal exercise; this adaptation is mediated by an increase in muscle mitochondria. There is evidence suggesting that short-term training induces adaptations that downregulate glycogenolysis before there is an increase in functional mitochondria. We discovered that a single long bout of exercise induces decreases in expression of glycogenolytic and glycolytic enzymes in rat skeletal muscle; this adaptation results in slower rates of glycogenolysis and lactic acid accumulation in muscle during contractile activity. Two additional days of training amplified the adaptive response, which appears to be mediated by PGC-1α; this adaptation is biologically significant, because glycogen depletion and lactic acid accumulation are major causes of muscle fatigue. ABSTRACT: Endurance exercise training can increase the ability to perform prolonged strenuous exercise. The major adaptation responsible for this increase in endurance is an increase in muscle mitochondria. This adaptation occurs too slowly to provide a survival advantage when there is a sudden change in environment that necessitates prolonged exercise. In the present study, we discovered another, more rapid adaptation, a downregulation of expression of the glycogenolytic and glycolytic enzymes in muscle that mediates a slowing of muscle glycogen depletion and lactic acid accumulation. This adaptation, which appears to be mediated by PGC-1α, occurs in response to a single exercise bout and is further enhanced by two additional daily exercise bouts. It is biologically significant, because glycogen depletion and lactic acid accumulation are two of the major causes of muscle fatigue and exhaustion.

DOI： 10.1113/jphysiol.2014.283820

PubMed

異なる脂質含量の食餌がラットの骨格筋ミトコンドリア酵素活性および持久性運動パフォーマンスに及ぼす影響

東田一彦, 園生智広, 藤本恵理, 樋口満

スポーツ科学研究 12 137 - 144 2015

Corticosterone accelerates atherosclerosis in the apolipoprotein E-deficient mouse. International journal

Mitsuharu Okutsu, Vitor A Lira, Kazuhiko Higashida, Jonathan Peake, Mitsuru Higuchi, Katsuhiko Suzuki

Atherosclerosis 232 ( 2 ) 414 - 9 2014.2

Language：English Publishing type：Research paper (scientific journal)

Chronic stress is an important risk factor for atherosclerosis, which is a chief process in the development of cardiovascular disease. Increased circulating levels of corticosterone have been documented in several animal models of chronic stress. However, it remains to be established whether corticosterone is sufficient to exacerbate atherosclerosis. To test this hypothesis, apolipoprotein E (ApoE)-deficient mice were fed a high-fat diet for 13 weeks with exposure to either corticosterone or vehicle in the drinking water (CORT and Con). Corticosterone treatment significantly increased atherosclerotic plaque area at the aortic root. Such exacerbation of atherosclerosis was accompanied by significantly lower levels of circulating white blood cells and serum interleukin-1β (IL-1β), and significantly elevated serum concentrations of total cholesterol, low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL) and small dense low-density lipoprotein (sd-LDL) in CORT mice when compared to Con mice. These findings demonstrate that corticosterone is sufficient to exacerbate atherosclerosis in vivo despite its anti-inflammatory properties and that this marked pro-atherogenic phenotype is primarily associated with increased dyslipidaemia.

DOI： 10.1016/j.atherosclerosis.2013.11.076

PubMed

【運動刺激の正体を探る】運動刺激に伴う骨格筋代謝機能の適応

寺田新, 東田一彦

体育の科学 63 ( 8 ) 608 - 615 2013.8

β-Adrenergic Stimulation Does Not Activate p38 MAPKinase or Induce PGC-1α in Skeletal Muscle

Kim SH, Asaka M, Higashida K, Takahashi Y, Holloszy JO, Han DH

Am J Physiol Endocrinol Metab 304 ( 8 ) 844 - 852 2013

間欠的絶食による摂取エネルギー制限がラット骨格筋のPGC-1αおよびGLUT-4 蛋白発現量に及ぼす影響

東田　一彦、樋口　満、寺田　新

スポーツ科学研究 10 1 - 11 2013

Effects of alternate-day fasting on high-fat diet-induced insulin resistance in rat skeletal muscle

Higashida K, Fujimoto E, Higuchi M, Terada S

Life Sci 93 ( 5 ) 208 - 213 2013

Effects of Resveratrol and SIRT1 on PGC-1α Activity and Mitochondrial Biogenesis: A Reevaluation

Higashida　K, Kim　SH, Jung SR, Asaka M, Holloszy JO, Han DH

PLOS Biology 11 ( 7 ) e1001603 2013

Regulation of Skeletal muscle GLUT-4 expression by exercise and nutritional stimuli

Higashida K, Tabata I, Higuchi M, Terada S

J Phys Fitness Sports Med 2 ( 3 ) 355 - 360 2013

Ursolic acid stimulates mTORC1 signaling after resistance exercise in rat skeletal muscle

Ogasawara R, Sato K, Higashida K, Nakazato K, Fujita S

Am J Physiol Endocrinol Metab 305 ( 6 ) 760 - 765 2013

Modest hypoxia significantly reduces triglyceride content and lipid droplet size in 3T3-L1 adipocytes

Hashimoto T, Yokokawa T, Endo Y, Iwanaka N, Higashida K, Taguchi S

Biochem Biophys Res Commun 440 ( 1 ) 43 - 49 2013

The AMPK beta2 subunit is required for energy homeostasis during metabolic stress

Dasgupta B, Ju JS, Sasaki Y, Liu X, Jung SR, Higashida K, Lindquist D, Milbrandt J

Mol Cell Biol 32 ( 14 ) 2837 - 2848 2012

Ginsenoside Re rapidly reverses insulin resistance in muscles of high-fat diet fed rats

Han DH, Kim SH, Higashida K, Jung SR, Polonsky KS, Klein S, Holloszy JO

Metabolism 61 ( 11 ) 1615 - 1621 2011

Does calorie restriction induce mitochondrial biogenesis? A reevaluation

Hancock CR, Han DH, Higashida K, Kim SH, Holloszy JO

FASEB J 25 ( 2 ) 785 - 791 2011

Deficiency of the mitochondrial electron transport chain in muscle does not cause insulin resistance

Han DH, Hancock CR, Jung SR, Higashida K, Kim SH, Holloszy JO

PLoS One 6 ( 5 ) e19739 2011

Normal Adaptations to Exercise Despite Protection Against Oxidative Stress

Higashida K, Kim SH, Higuchi M, Holloszy JO, Han DH

Am J Physiol Endocrinol Metab 301 ( 5 ) 779 - 784 2011

Prolonged exercise training induces long-term enhancement of HSP70 expression in rat plantaris muscle

Ogata T, Oishi Y, Higashida K, Higuchi M, Muraoka I

Am J Physiol Regul Integr Comp Physiol 296 ( 5 ) 1557 - 1563 2009

Dissociation between PGC-1alpha and GLUT-4 expression in skeletal muscle of rats fed a high-fat diet

Higashida K, Higuchi M, Terada S

J Nutr Sci Vitaminol (Tokyo) 55 ( 6 ) 486 - 491 2009

Potential role of lipin-1 in exercise-induced mitochondrial biogenesis

Higashida K, Higuchi M, Terada S

Biochem Biophys Res Commun 374 ( 3 ) 587 - 591 2008

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Papers - HIGASHIDA Kazuhiko