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野村和弘

徳島大学

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2024年9月20日更新

職名: 講師
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電子メール: nomura.kazuhiro@tokushima-u.ac.jp
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学位: 博士(医学) (神戸大学)
職歴・経歴: 2023/4: 徳島大学講師, 大学院医歯薬学研究部

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2024年9月20日更新

専門分野・研究分野: 研究者総覧に該当データはありませんでした。
担当経験のある授業科目: ライフステージ栄養学総合演習 (学部)
応用栄養学実習 (学部)
応用栄養学演習 (学部)
栄養と薬 (学部)
疾患栄養管理学Ⅱ (学部)
臨床栄養管理学実習(病院) (学部)
食事管理学 (学部)
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2024年9月20日更新

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論文

Kazuhiro Nomura, Shinichi Kinoshita, Nao Mizusaki, Yoko Senga, Tsutomu Sasaki, Tadahiro Kitamura, Hiroshi Sakaue, Aki Emi, Tetsuya Hosooka, Masahiro Matsuo, Hitoshi Okamura, Taku Amo, M Alexander Wolf, Naomi Kamimura, Shigeo Ohta, Tomoo Itoh, Yoshitake Hayashi, Hiroshi Kiyonari, Anna Krook, R Juleen Zierath, Masato Kasuga and Wataru Ogawa :
Adaptive gene expression of alternative splicing variants of PGC-1α regulates whole-body energy metabolism.,
Molecular Metabolism, Vol.86, 101968, 2024.

(要約): The transcriptional coactivator PGC-1α has been implicated in the regulation of multiple metabolic processes. However, the previously reported metabolic phenotypes of mice deficient in PGC-1α have been inconsistent. PGC-1α exists as multiple isoforms, including variants transcribed from an alternative first exon. We show here that alternative PGC-1α variants are the main entity that increases PGC-1α during exercise. These variants, unlike the canonical isoform of PGC-1α, are robustly upregulated in human skeletal muscle after exercise. Furthermore, the extent of this upregulation correlates with oxygen consumption. Mice lacking these variants manifest impaired energy expenditure during exercise, leading to the development of obesity and hyperinsulinemia. The alternative variants are also upregulated in brown adipose tissue in response to cold exposure, and mice lacking these variants are intolerant of a cold environment. Our findings thus indicate that an increase in PGC-1α expression, attributable mostly to upregulation of alternative variants, is pivotal for adaptive enhancement of energy expenditure and heat production and thereby essential for the regulation of whole-body energy metabolism.
(キーワード): エネルギー代謝 (energy metabolism) / Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / Alternative Splicing / Skeletal Muscle / 肥満症 (obesity) / Exercise / ノックアウトマウス (knockout mice)
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.molmet.2024.101968
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38885788; ● Summary page in Scopus @ Elsevier: 2-s2.0-85196522822

(DOI: 10.1016/j.molmet.2024.101968, PubMed: 38885788, Elsevier: Scopus) Kazuhiro Nomura, Satoshi Inagaki, Naokazu Muramae, Hiroaki Takahashi, Kozue Abe, Kenji Kato, Yoshiaki Kido and Tomokazu Matsuda :
Association of short-term changes in HbA1c with body composition and the importance of muscle maintenance in patients with Type 2 diabetes.,
Journal of Diabetes and its Complications, Vol.38, No.6, 108746, 2024.

(要約): HbA1c levels were significantly decreased at 6 months (P < 0.01), but there was no significant change in BMI. A linear multiple regression analysis showed that ΔHbA1c was negatively correlated with changes in muscle mass (β = -0.18; P = 0.047) and bone mineral content (β = -0.28; P < 0.001), but there was no significant association between ΔHbA1c levels and a change in body fat percentage.
(キーワード): Diabetes Mellitus, Type 2 / Glycated Hemoglobin / Body Composition / Muscle, Skeletal / Bone Density / Body Mass Index
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jdiacomp.2024.108746
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38749296; ● Search Scopus @ Elsevier (PMID): 38749296; ● Search Scopus @ Elsevier (DOI): 10.1016/j.jdiacomp.2024.108746

(DOI: 10.1016/j.jdiacomp.2024.108746, PubMed: 38749296) Hiromi Matsuo, Ryota Matsui, Koshi Kumagai, Satoshi Ida, Yoko Saino, Aya Fujihara, Kumi Takagi, Yukiko Itami, Misuzu Ishii, Naoki Moriya, Yuna Izumi-Mishima, Kazuhiro Nomura, M Yasuo Tsutsumi, Souya Nunobe, Rie Tsutsumi and Hiroshi Sakaue :
Impact of Olfactory Change on Postoperative Body Weight Loss in Patients with Gastric Cancer after Gastrectomy.,
Nutrients, Vol.16, No.6, 851, 2024.

(要約): = 0.048). In conclusion, olfactory changes emerged as an independent risk factor for postoperative weight loss at one month in patients with gastric cancer following gastrectomy.
(キーワード): Humans / Stomach Neoplasms / Postoperative Complications / Olfaction Disorders / Gastrectomy / Weight Loss / Retrospective Studies
(徳島大学機関リポジトリ): ● Metadata: 119382
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/nu16060851
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38542761; ● Search Scopus @ Elsevier (PMID): 38542761; ● Search Scopus @ Elsevier (DOI): 10.3390/nu16060851

(徳島大学機関リポジトリ: 119382, DOI: 10.3390/nu16060851, PubMed: 38542761) Yu Hirata, Kazuhiro Nomura, Daisuke Kato, Yoshihisa Tachibana, Takahiro Niikura, Kana Uchiyama, Tetsuya Hosooka, Tomoaki Fukui, Keisuke Oe, Ryosuke Kuroda, Yuji Hara, Takahiro Adachi, Koji Shibasaki, Hiroaki Wake and Wataru Ogawa :
A Piezo1/KLF15/IL-6 axis mediates immobilization-induced muscle atrophy.,
The Journal of Clinical Investigation, Vol.132, No.10, 1-13, 2022.

(要約): Although immobility is a common cause of muscle atrophy, the mechanism underlying this causality is unclear. We here show that Krüppel-like factor 15 (KLF15) and IL-6 are upregulated in skeletal muscle of limb-immobilized mice and that mice with KLF15 deficiency in skeletal muscle or with systemic IL-6 deficiency are protected from immobility-induced muscle atrophy. A newly developed Ca2+ bioimaging revealed that the cytosolic Ca2+ concentration ([Ca2+]i) of skeletal muscle is reduced to below the basal level by immobilization, which is associated with the downregulation of Piezo1. Acute disruption of Piezo1 in skeletal muscle induced Klf15 and Il6 expression as well as muscle atrophy, which was prevented by antibodies against IL-6. A role for the Piezo1/KLF15/IL-6 axis in immobility-induced muscle atrophy was validated in human samples. Our results thus uncover a paradigm for Ca2+ signaling in that a decrease in [Ca2+]i from the basal level triggers a defined biological event.
(キーワード): Animals / Calcium / Calcium Signaling / Humans / Interleukin-6 / Ion Channels / Kruppel-Like Transcription Factors / Mice / Muscle, Skeletal / Muscular Atrophy
(出版サイトへのリンク): ● Publication site (DOI): 10.1172/JCI154611
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35290243; ● Search Scopus @ Elsevier (PMID): 35290243; ● Search Scopus @ Elsevier (DOI): 10.1172/JCI154611

(DOI: 10.1172/JCI154611, PubMed: 35290243) Naoki Kuramoto, Kazuhiro Nomura, Daisuke Kohno, Tadahiro Kitamura, Gerard Karsenty, Tetsuya Hosooka and Wataru Ogawa :
Role of PDK1 in skeletal muscle hypertrophy induced by mechanical load.,
Scientific Reports, Vol.11, No.1, 3447, 2021.

(要約): Phosphatidylinositol 3-kinase (PI3K) plays an important role in protein metabolism and cell growth. We here show that mice (M-PDK1KO mice) with skeletal muscle-specific deficiency of 3'-phosphoinositide-dependent kinase 1 (PDK1), a key component of PI3K signaling pathway, manifest a reduced skeletal muscle mass under the static condition as well as impairment of mechanical load-induced muscle hypertrophy. Whereas mechanical load-induced changes in gene expression were not affected, the phosphorylation of ribosomal protein S6 kinase (S6K) and S6 induced by mechanical load was attenuated in skeletal muscle of M-PDK1KO mice, suggesting that PDK1 regulates muscle hypertrophy not through changes in gene expression but through stimulation of kinase cascades such as the S6K-S6 axis, which plays a key role in protein synthesis. Administration of the β₂-adrenergic receptor (AR) agonist clenbuterol activated the S6K-S6 axis in skeletal muscle and induced muscle hypertrophy in mice. These effects of clenbuterol were attenuated in M-PDK1KO mice, and mechanical load-induced activation of the S6K-S6 axis and muscle hypertrophy were inhibited in mice with skeletal muscle-specific deficiency of β₂-AR. Our results suggest that PDK1 regulates skeletal muscle mass under the static condition and that it contributes to mechanical load-induced muscle hypertrophy, at least in part by mediating signaling from β₂-AR.
(キーワード): 3-Phosphoinositide-Dependent Protein Kinases / Adrenergic beta-Agonists / Animals / Cell Line / Clenbuterol / Hypertrophy / Insulin / Mechanical Phenomena / Mice / Mice, Knockout / Muscle, Skeletal / Phosphorylation / Proto-Oncogene Proteins c-akt / Receptors, Adrenergic, beta-2 / Ribosomal Protein S6 Kinases / Signal Transduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1038/s41598-021-83098-z
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33568757; ● Search Scopus @ Elsevier (PMID): 33568757; ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-021-83098-z

(DOI: 10.1038/s41598-021-83098-z, PubMed: 33568757) Nao Mizusaki, Kazuhiro Nomura, Tetsuya Hosooka, Masashi Shiomi, Kazuo Ogawa, Tetsuto Tsunoda, Yoshikazu Tamori and Wataru Ogawa :
The Novel Lipid-Lowering Drug D-47 Ameliorates Hepatic Steatosis and Promotes Brown/Beige-Like Change of White Adipose Tissue in db/db Mice.,
The Kobe Journal of Medical Sciences, Vol.65, No.1, E36-E43, 2019.

(要約): D-47 is a newly developed solid dispersion of the arginine salt of (S)-(+)-4-[1-(4-tert-butylphenyl)-2-oxo-pyrrolidin-4-yl]methoxybenzoic acid (S-2E), which inhibits sterol and fatty acid synthesis. D-47 was recently shown to lower the serum level and hepatic content of both triglyceride and cholesterol in a rabbit model of familial hypercholesterolemia. We here investigated the effects of D-47 on dyslipidemia and hepatic steatosis in comparison with those of bezafibrate in the db/db mouse model of obesity. Treatment of db/db mice with D-47 or bezafibrate for 14 days lowered the serum triglyceride concentration without affecting that of cholesterol. D-47, but not bezafibrate, almost completely eliminated lipid droplets in hepatocytes and markedly lowered the triglyceride content of the liver in these mice. The two agents induced similar changes in the hepatic expression of genes including those related to β-oxidation or fatty acid synthesis. D-47 however significantly reduced the mass of white adipose tissue and up-regulated the expression of genes related to energy expenditure, mitochondrial function, fatty acid oxidation or lipolysis in this tissue, indicating that D-47 induced the brown/beige adipocyte-like change in white adipose tissue, whereas bezafibrate had no such effects. Treatment of 3T3-L1 adipocytes with D-47 provoked the expression of genes related to mitochondrial function, fatty acid oxidation or lipolysis. Our data have thus shown that D-47 ameliorated hypertriglyceridemia and hepatic steatosis in an animal model of obesity, and they suggest that this latter effect might be mediated through the change of adipose tissue characteristics.
(キーワード): 3T3-L1 Cells / Adipose Tissue, White / Animals / Blood Glucose / Disease Models, Animal / Fatty Liver / Hydroxybenzoate Ethers / Hypolipidemic Agents / Insulin / Lipids / Male / Mice / Obesity / Pyrrolidinones
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31341155; ● Search Scopus @ Elsevier (PMID): 31341155

(PubMed: 31341155) Yu Hirata, Kazuhiro Nomura, Yoko Senga, Yuko Okada, Kenta Kobayashi, Shiki Okamoto, Yasuhiko Minokoshi, Michihiro Imamura, Shin'ichi Takeda, Tetsuya Hosooka and Wataru Ogawa :
Hyperglycemia induces skeletal muscle atrophy via a WWP1/KLF15 axis.,
JCI Insight, Vol.4, No.4, e124952, 2019.

(要約): Diabetes mellitus is associated with various disorders of the locomotor system including the decline in mass and function of skeletal muscle. The mechanism underlying this association has remained ambiguous, however. We now show that the abundance of the transcription factor KLF15 as well as the expression of genes related to muscle atrophy are increased in skeletal muscle of diabetic model mice, and that mice with muscle-specific KLF15 deficiency are protected from the diabetes-induced decline of skeletal muscle mass. Hyperglycemia was found to upregulate the KLF15 protein in skeletal muscle of diabetic animals, which is achieved via downregulation of the E3 ubiquitin ligase WWP1 and consequent suppression of the ubiquitin-dependent degradation of KLF15. Our results revealed that hyperglycemia, a central disorder in diabetes, promotes muscle atrophy via a WWP1/KLF15 pathway. This pathway may serve as a therapeutic target for decline in skeletal muscle mass accompanied by diabetes mellitus.
(キーワード): Animals / Benzhydryl Compounds / COS Cells / Chlorocebus aethiops / Diabetes Mellitus, Experimental / Down-Regulation / Female / Gene Expression Profiling / Glucosides / HEK293 Cells / Humans / Hyperglycemia / Kruppel-Like Transcription Factors / Male / Mice / Mice, Knockout / Muscle, Skeletal / Muscular Atrophy / Proteolysis / Signal Transduction / Sodium-Glucose Transporter 2 Inhibitors / Streptozocin / Ubiquitin-Protein Ligases / Up-Regulation
(出版サイトへのリンク): ● Publication site (DOI): 10.1172/jci.insight.124952
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30830866; ● Search Scopus @ Elsevier (PMID): 30830866; ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.124952

(DOI: 10.1172/jci.insight.124952, PubMed: 30830866) Kenji Sugawara, Kazuhiro Nomura, Yuko Okada, Aki Sugano, Masaaki Matsumoto, Toru Takarada, Atsuko Takeuchi, Hiroyuki Awano, Yushi Hirota, Hisahide Nishio, Yutaka Takaoka and Wataru Ogawa :
In silico and in vitro analyses of the pathological relevance of the R258H mutation of hepatocyte nuclear factor 4α identified in maturity-onset diabetes of the young type 1.,
Journal of Diabetes Investigation, Vol.10, No.3, 680-684, 2018.

(要約): Mutations of the hepatocyte nuclear factor 4α (HNF4α) gene give rise to maturity-onset diabetes of the young type 1. Although many such mutations have been identified in affected individuals, part of these mutations has been characterized with regard to their pathological relevance. We here identified a missense mutation (c.773G>A, p.R258H) of HNF4A in a mother and daughter with early-onset diabetes and impaired insulin secretion. In silico simulation and in vitro luciferase reporter analyses showed that the mutation impairs the stability of self-dimerization and the transactivation activity of HNF4α. Although arginine-258 does not appear to participate directly in dimerization, its mutation alters the electrostatic surface potential of the dimer interface. Our results thus suggest that this mutation impairs the function of HNF4α and thereby contributes to the pathogenesis of maturity-onset diabetes of the young type 1.
(キーワード): Computer Simulation / Diabetes Mellitus, Type 2 / Female / Hepatocyte Nuclear Factor 4 / Humans / In Vitro Techniques / Infant, Newborn / Mutation, Missense / Prognosis
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/jdi.12960
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30325586; ● Search Scopus @ Elsevier (PMID): 30325586; ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.12960

(DOI: 10.1111/jdi.12960, PubMed: 30325586) Kaku Matsugi, Tetsuya Hosooka, Kazuhiro Nomura and Wataru Ogawa :
Thrombospondin 1 Suppresses Insulin Signaling in C2C12 Myotubes.,
The Kobe Journal of Medical Sciences, Vol.62, No.1, E13-8, 2016.

(要約): Thrombospondin 1 (TSP-1) is abundantly expressed in visceral adipose tissue and this expression is up-regulated in obese humans and rodents. Recent studies showed that genetic deletion of TSP-1 protects mice from diet-induced insulin resistance. However, the molecular mechanism is largely unknown. In this study, we examined the effect of recombinant TSP-1 on insulin signaling in cultured cells from insulin sensitive tissues to investigate whether TSP-1 could act as an adipokine. Here we show that treatment with recombinant TSP-1 suppressed insulin signaling in cultured muscle cells, which was accompanied by the activation of stress signaling such as JNK, p38, and IKK. These results suggest that TSP-1 acts as an adipokine which is involved in the pathogenesis of obesity-induced insulin resistance. Thus, TSP-1 could be a potential target for the treatment of insulin resistance and metabolic disease related to insulin resistance.
(キーワード): Adipokines / Animals / Cell Line / Hep G2 Cells / Humans / Insulin / Insulin Resistance / MAP Kinase Signaling System / Male / Mice / Mice, Inbred C57BL / Muscle Fibers, Skeletal / Recombinant Proteins / Signal Transduction / Thrombospondin 1
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27492207; ● Search Scopus @ Elsevier (PMID): 27492207

(PubMed: 27492207) Yukiko Kawasaki-Ogita, Yoshiyuki Hamamoto, Sachiko Honjo, Hiroki Ikeda, Yoshiharu Wada, Kazuhiro Nomura, Yorihiro Iwasaki, Ryuji Nohara and Hiroyuki Koshiyama :
The limited usefulness of the treadmill test or a risk-guided approach in screening for asymptomatic coronary heart disease in Japanese patients with type 2 diabetes.,
Internal medicine (Tokyo, Japan), Vol.51, No.24, 3337-3342, 2012.

(要約): Neither the TTT as a first-line test nor the ADA guidelines are sufficiently adequate screening methods to detect asymptomatic CHD in Japanese subjects with type 2 diabetes. Conducting routine screening for asymptomatic CHD in Japanese patients with type 2 diabetes may therefore not be very useful.
(キーワード): Asian People / Asymptomatic Diseases / Coronary Disease / Diabetes Mellitus, Type 2 / Diabetic Angiopathies / Exercise Test / Female / Humans / Male / Middle Aged / Myocardial Perfusion Imaging / Prospective Studies / Reproducibility of Results / Risk Assessment
(出版サイトへのリンク): ● Publication site (DOI): 10.2169/internalmedicine.51.7878
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23257517; ● Search Scopus @ Elsevier (PMID): 23257517; ● Search Scopus @ Elsevier (DOI): 10.2169/internalmedicine.51.7878

(DOI: 10.2169/internalmedicine.51.7878, PubMed: 23257517) Kazuhiro Nomura, Hiroki Ikeda, Kanako Mori, Yoshiyuki Hamamoto, Sachiko Honjo, Yukiko Kawasaki, Yoshiharu Wada and Hiroyuki Koshiyama :
Less variation of R-R interval of electrocardiogram in nonobese type 2 diabetes with nocturnal intermittent hypoxia.,
Endocrine journal, Vol.60, No.2, 225-230, 2012.

(要約): Obesity is a major risk factor for sleep-disordered breathing (SDB). However, many Japanese subjects with diabetes are less obese despite compared with Caucasian. We evaluated the relationship between SDB and clinical characteristics other than obesity, especially in relation to cardiac autonomic neuropathy (CAN) in Japanese subjects with diabetes. The study included a total of 261 consecutive Japanese subjects with type 2 diabetes, including nonobese subjects defined as BMI <25 kg/m² for Japanese. SDB was screened by 4% oxygen desaturation index (ODI) level of 5 or more events per hour, which was measured by nocturnal pulse oximetry. CAN was examined with the variation of R-R intervals (CVRR). The SDB were found in 24.5% of total subjects and 16.3% of nonobese subjects with type 2 diabetes, respectively. The nonobese type 2 diabetes subjects with SDB had significantly lower coefficient of CVRR than those without SDB. Multiple regression analysis revealed that BMI and heart rate were significant independent factors for SDB in total subjects with type 2 diabetes, but CVRR was the only significant independent factor for SDB in nonobese subjects with type 2 diabetes. These findings suggest that the presence of SDB should be kept in mind in type 2 diabetic patients with abnormality in CVRR variation in electrocardiogram even though they are not obese.
(キーワード): Aged / Arrhythmias, Cardiac / Autonomic Nervous System Diseases / Blood Gas Monitoring, Transcutaneous / Body Mass Index / Diabetes Mellitus, Type 2 / Diabetic Neuropathies / Electrocardiography / Female / Heart / Heart Rate / Humans / Japan / Male / Middle Aged / Overweight / Prevalence / Risk Factors / Sleep Apnea Syndromes
(出版サイトへのリンク): ● Publication site (DOI): 10.1507/endocrj.ej11-0327
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23018979; ● Search Scopus @ Elsevier (PMID): 23018979; ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.ej11-0327

(DOI: 10.1507/endocrj.ej11-0327, PubMed: 23018979) Yoshiyuki Hamamoto, Sachiko Honjo, Yukiko Kawasaki, Hiroki Ikeda, Kanako Mori, Kanta Fujimoto, Hisato Tatsuoka, Yorihiro Iwasaki, Kazuhiro Nomura, Yoshiharu Wada and Hiroki Koshiyama :
Relationship between telmisartan dose and glycaemic control in Japanese patients with type 2 diabetes mellitus and hypertension: a retrospective study.,
Clinical drug investigation, Vol.32, No.9, 577-582, 2012.

(要約): Our results suggest that telmisartan influences glycaemic control in a dose-dependent manner; doses 40 mg/day may be needed to improve glycaemic control. Our data also suggest that patients with higher baseline HbA(1c) may experience greater improvements in glycaemic control with telmisartan.
(キーワード): Angiotensin II Type 1 Receptor Blockers / Benzimidazoles / Benzoates / Blood Glucose / Diabetes Mellitus, Type 2 / Dose-Response Relationship, Drug / Female / Humans / Hypertension / Japan / Male / Middle Aged / Retrospective Studies / Telmisartan
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/BF03261912
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22812514; ● Search Scopus @ Elsevier (PMID): 22812514; ● Search Scopus @ Elsevier (DOI): 10.1007/BF03261912

(DOI: 10.1007/BF03261912, PubMed: 22812514) Tomohisa Aoyama, Hiroki Ikeda, Yoshiyuki Hamamoto, Sachiko Honjo, Kazuhiro Nomura, Yoshiharu Wada, Jun Fujikawa, Yasuaki Hayashino, Shunichi Fukuhara and Hiroyuki Koshiyama :
Clinical heterogeneity of adult Japanese diabetes depending on titers of glutamic acid decarboxylase autoantibodies.,
Journal of diabetes investigation, Vol.3, No.3, 266-270, 2012.

(要約): These results show that the clinical phenotype of adult Japanese diabetes correlates with GADAb levels, and that patients with GADAb (≥2.5 U/mL) show different characteristics from those without GADAb, although further longitudinal studies are required. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00190.x, 2011).
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.2040-1124.2011.00190.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24843575; ● Search Scopus @ Elsevier (PMID): 24843575; ● Search Scopus @ Elsevier (DOI): 10.1111/j.2040-1124.2011.00190.x

(DOI: 10.1111/j.2040-1124.2011.00190.x, PubMed: 24843575) Shuying Li, Wataru Ogawa, Aki Emi, Kumiko Hayashi, Yoko Senga, Kazuhiro Nomura, Kenta Hara, Demin Yu and Masato Kasuga :
Role of S6K1 in regulation of SREBP1c expression in the liver.,
Biochemical and biophysical research communications, Vol.412, No.2, 197-202, 2011.

(要約): The transcription factor sterol regulatory element-binding protein 1c (SREBP1c) plays an important role in the control of fatty acid metabolism in the liver. Evidence suggests that mammalian target of rapamycin (mTOR) complex 1 (mTORC1) contributes to the regulation of SREBP1c expression, but signaling downstream of mTORC1 remains unclear. We have now shown that medium rich in branched-chain amino acids stimulates expression of the SREBP1c gene in cultured hepatocytes in a manner sensitive both to rapamycin, a pharmacological inhibitor of mTORC1, and to a short hairpin RNA (shRNA) specific for S6 kinase 1 (S6K1), a downstream effector of mTORC1. The phosphorylation of S6K1 was increased in the liver of obese db/db mice. Furthermore, depletion of hepatic S6K1 in db/db mice with the use of an adenovirus vector encoding S6K1 shRNA resulted in down-regulation of SREBP1c gene expression in the liver as well as a reduced hepatic triglyceride content and serum triglyceride concentration. These results thus suggest that S6K1 regulates SREBP1c expression both in cultured hepatocytes and in mouse liver, and that increased hepatic activity of S6K1 contributes at least in part to the pathogenesis of obesity-induced hepatic steatosis and hypertriglyceridemia.
(キーワード): Animals / Cell Line / Chromones / Fatty Liver / Gene Expression Regulation / Hepatocytes / Hypertriglyceridemia / Liver / Mechanistic Target of Rapamycin Complex 1 / Mice / Mice, Inbred Strains / Morpholines / Multiprotein Complexes / Obesity / Proteins / RNA, Small Interfering / Ribosomal Protein S6 Kinases, 90-kDa / Sirolimus / Sterol Regulatory Element Binding Protein 1 / TOR Serine-Threonine Kinases
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.bbrc.2011.07.038
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21806970; ● Search Scopus @ Elsevier (PMID): 21806970; ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2011.07.038

(DOI: 10.1016/j.bbrc.2011.07.038, PubMed: 21806970) Kazuhiro Nomura, Yoshiyuki Hamamoto, Shiho Takahara, Osamu Kikuchi, Sachiko Honjo, Hiroki Ikeda, Yoshiharu Wada, Koichro Nabe, Ryosuke Okumra and Hiroyuki Koshiyama :
Relationship between carotid intima-media thickness and silent cerebral infarction in Japanese subjects with type 2 diabetes.,
Diabetes care, Vol.33, No.1, 168-170, 2009.

(要約): CCA-IMT, but not pulse wave velocity, was independently associated with SCI in Japanese subjects with type 2 diabetes.
(キーワード): Aged / Asian People / Cerebral Infarction / Diabetes Mellitus, Type 2 / Female / Humans / Magnetic Resonance Imaging / Male / Middle Aged / Risk Factors / Tunica Intima / Tunica Media / Ultrasonography
(出版サイトへのリンク): ● Publication site (DOI): 10.2337/dc09-0453
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19808915; ● Search Scopus @ Elsevier (PMID): 19808915; ● Search Scopus @ Elsevier (DOI): 10.2337/dc09-0453

(DOI: 10.2337/dc09-0453, PubMed: 19808915) Tetsuya Kimura, Hiroki Ikeda, Jun Fujikawa, Kazuhiro Nomura, Tomohisa Aoyama, Yoshiharu Wada, Koichiro Nabe, Yoshiyuki Hamamoto, Sachiko Honjo and Hiroyuki Koshiyama :
Usefulness of serum cystatin C in Japanese patients with type 2 diabetes mellitus and nephropathy.,
Diabetes research and clinical practice, Vol.83, No.2, e58-61, 2008.

(要約): We examined usefulness of serum cystatin C to detect chronic kidney disease (CKD) stage >or=3, which was defined by Modification of Diet in Renal Disease formula. Serum cystatin C could detect CKD stage >or=3 with high efficacy in 289 Japanese patients with type 2 diabetes and nephropathy.
(キーワード): Adult / Aged / Aged, 80 and over / Cross-Sectional Studies / Cystatin C / Diabetes Mellitus, Type 2 / Diabetic Nephropathies / Disease Progression / Female / Glomerular Filtration Rate / Humans / Kidney Failure, Chronic / Male / Middle Aged / Predictive Value of Tests / ROC Curve / Sensitivity and Specificity
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.diabres.2008.11.032
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19118914; ● Search Scopus @ Elsevier (PMID): 19118914; ● Search Scopus @ Elsevier (DOI): 10.1016/j.diabres.2008.11.032

(DOI: 10.1016/j.diabres.2008.11.032, PubMed: 19118914) Yasuyuki Arai, Koichiro Nabe, Hiroki Ikeda, Sachiko Honjo, Yoshiharu Wada, Yoshiyuki Hamamoto, Kazuhiro Nomura, Tomokazu Aoki, Toshiaki Sano and Hiroyuki Koshiyama :
A case of lymphocytic panhypophysitis (LPH) during pregnancy.,
Endocrine, Vol.32, No.1, 117-121, 2007.

(要約): A 37-year-old pregnant woman developed continuous headache in the 10th week of pregnancy, followed by bilateral visual field defect and general malaise in the 24th week. The brain magnetic resonance imaging showed a pituitary mass. In laboratory examination, plasma concentration of free thyroxine, thyroid stimulating hormone (TSH), cortisol, and adrenocorticotropic hormone (ACTH) was low. General malaise vanished shortly after the replacement therapy of glucocorticoid and thyroid hormone, but partial central diabetes insipidus (CDI) appeared, which could be treated with desmopressin acetate (DDAVP). The visual field defect having enlarged, transsphenoidal surgery was performed in the 31st week of pregnancy. Adenohypophysis could be resected, and it showed infiltration of mature lymphocytes. After the surgery, the visual defect had improved, but hormone replacement was still necessary. She delivered a baby in the 38th week without any trouble. Provocative tests after delivery revealed a low response in TSH, prolactin (PRL), and follicle stimulating hormone (FSH). Hormone replacement and DDAVP administration was necessary in the same doses after delivery. The diagnosis was lymphocytic panhypophysitis (LPH). In the case of pregnant woman, LPH should be included in the differential diagnosis of pituitary mass for the fetomaternal safety.
(キーワード): Adult / Female / Headache / Humans / Lymphocytosis / Pituitary Diseases / Pregnancy / Pregnancy Complications / Pregnancy Trimester, First / Pregnancy Trimester, Second / Vision Disorders
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s12020-007-9001-6
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17992609; ● Search Scopus @ Elsevier (PMID): 17992609; ● Search Scopus @ Elsevier (DOI): 10.1007/s12020-007-9001-6

(DOI: 10.1007/s12020-007-9001-6, PubMed: 17992609) Kazuhiro Nomura, Hoshimi Kanemura, Takaya Satoh and Tohru Kataoka :
Identification of a novel domain of Ras and Rap1 that directs their differential subcellular localizations.,
The Journal of biological chemistry, Vol.279, No.21, 22664-22673, 2004.

(要約): The small GTPase Ha-Ras and Rap1A exhibit high mutual sequence homology and share various target proteins. However, they exert distinct biological functions and exhibit differential subcellular localizations; Rap1A is predominantly localized in the perinuclear region including the Golgi apparatus and endosomes, whereas Ha-Ras is predominantly localized in the plasma membrane. Here, we have identified a small region in Rap1A that is crucial for its perinuclear localization. Analysis of a series of Ha-Ras-Rap1A chimeras shows that Ha-Ras carrying a replacement of amino acids 46-101 with that of Rap1 exhibits the perinuclear localization. Subsequent mutational studies indicate that Rap1A-type substitutions within five amino acids at positions 85-89 of Ha-Ras, such as NNTKS85-89TAQST, NN85-86TA, and TKS87-89QST, are sufficient to induce the perinuclear localization of Ha-Ras. In contrast, substitutions of residues surrounding this region, such as FAI82-84YSI and FEDI90-93FNDL, have no effect on the plasma membrane localization of Ha-Ras. A chimeric construct consisting of amino acids 1-134 of Rap1A and 134-189 of Ha-Ras, which harbors both the palmitoylation and farnesylation sites of Ha-Ras, exhibits the perinuclear localization like Rap1A. Introduction of a Ha-Ras-type substitution into amino acids 85-89 (TAQST85-89NNTKS) of this chimeric construct causes alteration of its predominant subcellular localization site from the perinuclear region to the plasma membrane. These results indicate that a previously uncharacterized domain spanning amino acids 85-89 of Rap1A plays a pivotal role in its perinuclear localization. Moreover, this domain acts dominantly over COOH-terminal lipid modification of Ha-Ras, which has been considered to be essential and sufficient for the plasma membrane localization.
(キーワード): Amino Acid Sequence / Amino Acids / Animals / COS Cells / Cell Membrane / Cell Nucleus / DNA Mutational Analysis / DNA, Complementary / Gene Deletion / Golgi Apparatus / Guanosine Triphosphate / Humans / Lipids / Microscopy, Confocal / Molecular Sequence Data / Mutation / Palmitic Acid / Plasmids / Protein Prenylation / Protein Structure, Tertiary / Recombinant Proteins / Sequence Homology, Amino Acid / Subcellular Fractions / Time Factors / Transfection / rap1 GTP-Binding Proteins / ras Proteins
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.M314169200
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15031297; ● Search Scopus @ Elsevier (PMID): 15031297; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M314169200

(DOI: 10.1074/jbc.M314169200, PubMed: 15031297) Hirotaka Imai, Tomoko Koumura, Ryo Nakajima, Kazuhiro Nomura and Yasuhito Nakagawa :
Protection from inactivation of the adenine nucleotide translocator during hypoglycaemia-induced apoptosis by mitochondrial phospholipid hydroperoxide glutathione peroxidase.,
The Biochemical journal, Vol.371, No.Pt 3, 799-809, 2003.

(要約): We demonstrated that mitochondrial phospholipid hydroperoxide glutathione peroxidase (PHGPx) first suppressed the dissociation of cytochrome c (cyt c) from cardiolipin (CL) in mitochondrial inner membranes and then apoptosis caused by the hypoglycaemia by the prevention of peroxidation of CL [Nomura, Imai, Koumura, Arai and Nakagawa (1999) J. Biol. Chem. 274, 29294-29302; Nomura, Imai, Koumura, Kobayashi and Nakagawa (2000) Biochem. J. 351, 183-193]. The present study shows the involvement of peroxidation of CL in the inactivation of adenine nucleotide translocator (ANT) and the opening of permeability transition pores by using the system of ANT-reconstituted liposome and isolated mitochondria. ANT activity appeared in dioleoyl phosphatidylcholine proteoliposome containing 10% (mol/mol) CL or phosphatidylglycerol (PG), but not other classes of phospholipids. ANT activity was competitively inhibited by the addition of cardiolipin hydroperoxide (CLOOH) in reconstituted liposomes containing CL. However, phosphatidylcholine hydroperoxide failed to inactivate the activity of ANT. The activity of ANT in reconstituted liposomes, including CLOOH, recovered when CLOOH in reconstituted liposome was reduced to hydroxycardiolipin by incubation with PHGPx. The activity of ANT was determined in rat basophil leukaemia RBL2H3 cells after their exposure to 2-deoxyglucose. ANT activity decreased to 50% of the control level by 4 h in response to apoptosis. In parallel, cyt c and apoptosis-inducing factor (AIF) were released from mitochondria. Suppression of the accumulation of CLOOH by overexpression of PHGPx in mitochondria effectively prevented the inactivation of ANT, the opening of permeability transition pores and the release of cyt c and AIF from mitochondria in hypoglycaemia-induced apoptotic cells. These findings suggest that mitochondrial PHGPx might be involved in the modulation of the activity of ANT and the opening of pores for the release of cyt c via the modulation of levels of CLOOH in the mitochondria.
(キーワード): Animals / Apoptosis / Cardiolipins / Cell Line / Glutathione Peroxidase / Hypoglycemia / Liposomes / Mitochondria / Mitochondrial ADP, ATP Translocases / Phospholipid Hydroperoxide Glutathione Peroxidase / Rats
(出版サイトへのリンク): ● Publication site (DOI): 10.1042/BJ20021342
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12534348; ● Search Scopus @ Elsevier (PMID): 12534348; ● Search Scopus @ Elsevier (DOI): 10.1042/BJ20021342

(DOI: 10.1042/BJ20021342, PubMed: 12534348) Kazuhiro Nomura, H Imai, T Koumura, T Kobayashi and Y Nakagawa :
Mitochondrial phospholipid hydroperoxide glutathione peroxidase inhibits the release of cytochrome c from mitochondria by suppressing the peroxidation of cardiolipin in hypoglycaemia-induced apoptosis.,
The Biochemical journal, Vol.351, No.Pt 1, 183-193, 2000.

(要約): Cytochrome c (cyt. c) is a proapoptotic factor that binds preferentially to cardiolipin (CL), a mitochondrial lipid, but not to cardiolipin hydroperoxide (CL-OOH). Cyt. c that had bound to CL liposomes was liberated on peroxidation of the liposomes by a radical. The generation of CL-OOH in mitochondria occurred before the release of cyt. c in rat basophile leukaemia (RBL)2H3 cells that had been induced to undergo apoptosis by exposure to hypoglycaemia with 2-deoxyglucose (2DG). The amount of cyt. c bound to CL prepared from the mitochondria of 2DG-treated cells was lower than that of untreated cells. The release of cyt. c was completely suppressed when the production of CL-OOH in mitochondria was inhibited by the overexpression of mitochondrial phospholipid hydroperoxide glutathione peroxidase (PHGPx). The fluorescence from CL-labelling dye (10-N-nonyl Acridine Orange) decreased on the induction of apoptosis by 2DG. However, no decrease in fluorescence was observed in PHGPx-overexpressing cells. Cyt. c was released from mitochondria that had been isolated from control cells on peroxidation by t-butylhydroperoxide, but no similar liberation of cyt. c from mitochondria isolated from mitochondrial PHGPx-overexpressing cells was observed. These findings suggest that the generation of CL-OOH in mitochondria might be a primary event that triggers the release of cyt. c from mitochondria in the apoptotic process in which mitochondrial PHGPx participates as an anti-apoptotic factor by preventing the formation of CL-OOH.
(キーワード): Acridine Orange / Animals / Apoptosis / Cardiolipins / Cytochrome c Group / Deoxyglucose / Fluorescence / Glutathione Peroxidase / Hypoglycemia / Intracellular Membranes / Lipid Peroxidation / Liposomes / Malates / Mitochondria / Oxidation-Reduction / Phospholipid Hydroperoxide Glutathione Peroxidase / Phospholipids / Protein Binding / Rats / Tumor Cells, Cultured / tert-Butylhydroperoxide
(出版サイトへのリンク): ● Publication site (DOI): 10.1042/0264-6021:3510183
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10998361; ● Search Scopus @ Elsevier (PMID): 10998361; ● Search Scopus @ Elsevier (DOI): 10.1042/0264-6021:3510183

(DOI: 10.1042/0264-6021:3510183, PubMed: 10998361) Kazuhiro Nomura, H Imai, T Koumura, M Arai and Y Nakagawa :
Mitochondrial phospholipid hydroperoxide glutathione peroxidase suppresses apoptosis mediated by a mitochondrial death pathway.,
The Journal of biological chemistry, Vol.274, No.41, 29294-29302, 1999.

(要約): Phospholipid hydroperoxide glutathione peroxidase (PHGPx) is a key enzyme in the protection of biomembranes exposed to oxidative stress. We investigated the role of mitochondrial PHGPx in apoptosis using RBL2H3 cells that overexpressed mitochondrial PHGPx (M15 cells), cells that overexpressed non-mitochondrial PHGPx (L9 cells), and control cells (S1 cells). The morphological changes and fragmentation of DNA associated with apoptosis occurred within 15 h in S1 and L9 cells upon exposure of cells to 2-deoxyglucose (2DG). The release of cytochrome c from mitochondria was observed in S1 cells after 4 h and was followed by the activation of caspase-3 within 6 h. Overexpression of mitochondrial PHGPx prevented the release of cytochrome c, the activation of caspase-3, and apoptosis, but non-mitochondrial PHGPx lacked the ability to prevent the induction of apoptosis by 2DG. An ability to protect cells from 2DG-induced apoptosis was abolished when the PHGPx activity of M15 cells was inhibited by diethylmalate, indicating that the resistance of M15 cells to apoptosis was indeed due to the overexpression of PHGPx in the mitochondria. The expression of members of the Bcl-2 family of proteins, such as Bcl-2, Bcl-xL, Bax, and Bad, was unchanged by the overexpression of PHGPx in cells. The levels of hydroperoxides, including hydrogen and lipid peroxide, in mitochondria isolated from S1 and L9 cells were significantly increased after the exposure to 2DG for 2 h, while the level of hydroperoxide in mitochondria isolated from M15 cells was lower than that in S1 and L9 cells. M15 cells were also resistant to apoptosis induced by etoposide, staurosporine, UV irradiation, cycloheximide, and actinomycin D, but not to apoptosis induced by Fas-specific antibodies, which induces apoptosis via a pathway distinct from the pathway initiated by 2DG. Our results suggest that hydroperoxide, produced in mitochondria, is a major factor in apoptosis and that mitochondrial PHGPx might play a critical role as an anti-apoptotic agent in mitochondrial death pathways.
(キーワード): Adenosine Triphosphate / Animals / Apoptosis / Caspase 3 / Caspases / Cell Survival / Cytochrome c Group / DNA Fragmentation / Deoxyglucose / Glucose / Glutathione Peroxidase / Malates / Mitochondria / Oxidative Stress / Peroxides / Phospholipid Hydroperoxide Glutathione Peroxidase / Proto-Oncogene Proteins c-bcl-2 / Rats / Signal Transduction / Superoxides / Tumor Cells, Cultured
(出版サイトへのリンク): ● Publication site (DOI): 10.1074/jbc.274.41.29294
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10506188; ● Search Scopus @ Elsevier (PMID): 10506188; ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.274.41.29294

(DOI: 10.1074/jbc.274.41.29294, PubMed: 10506188) M Arita, Kazuhiro Nomura, H Arai and K Inoue :
alpha-tocopherol transfer protein stimulates the secretion of alpha-tocopherol from a cultured liver cell line through a brefeldin A-insensitive pathway.,
Proceedings of the National Academy of Sciences of the United States of America, Vol.94, No.23, 12437-12441, 1997.

(要約): Vitamin E (alpha-tocopherol) is a fat-soluble antioxidant that is transported by plasma lipoproteins in the body. alpha-Tocopherol taken up by the liver with lipoprotein is thought to be resecreted into the plasma in very low density lipoprotein (VLDL). alpha-Tocopherol transfer protein (alphaTTP), which was recently identified as a product of the causative gene for familial isolated vitamin E deficiency, is a cytosolic liver protein and plays an important role in the efficient recycling of plasma vitamin E. To throw light on the mechanism of alphaTTP-mediated alpha-tocopherol transfer in the liver cell, we devised an assay system using the hepatoma cell line McARH7777. Using this system, we found that the secretion of alpha-tocopherol was more efficient in cells expressing alphaTTP than in matched cells lacking alphaTTP. Brefeldin A, which effectively inhibits VLDL secretion by disrupting the Golgi apparatus, had no effect on alpha-tocopherol secretion, indicating that alphaTTP-mediated alpha-tocopherol secretion is not coupled to VLDL secretion. Among other agents tested, only 25-hydroxycholesterol, a modulator of cholesterol metabolism, inhibited alpha-tocopherol secretion. This inhibition is most likely mediated by oxysterol-binding protein. These results suggest that alphaTTP present in the liver cytosol functions to stimulate secretion of cellular alpha-tocopherol into the extracellular medium and that the reaction utilizes a novel non-Golgi-mediated pathway that may be linked to cellular cholesterol metabolism and/or transport.
(キーワード): Animals / Brefeldin A / Carrier Proteins / Cyclopentanes / Gene Expression / Liver / Liver Neoplasms, Experimental / Rats / Signal Transduction / Tumor Cells, Cultured / Vitamin E
(出版サイトへのリンク): ● Publication site (DOI): 10.1073/pnas.94.23.12437
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9356467; ● Search Scopus @ Elsevier (PMID): 9356467; ● Search Scopus @ Elsevier (DOI): 10.1073/pnas.94.23.12437

(DOI: 10.1073/pnas.94.23.12437, PubMed: 9356467)

MISC

宮部由利, 奈部浩一郎, 〓田ひろみ, 中尾哲史, 野村和弘, 青山倫久, 木村哲也, 池田弘毅, 本庶祥子, 越山裕行 :
後腹膜腫瘍を合併し，診断に苦慮したクッシング病の1例,
日本内分泌学会雑誌, Vol.84, 76-79, 2008年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1572543025585395840

(CiNii: 1572543025585395840) 福田旭伸, 本庶祥子, 青山倫久, 木村哲也, 野村和弘, 奈部浩一郎, 池田弘毅, 和田良春, 越山裕行 :
成人期に診断された Prader-Willi syndrome の一例,
日本内分泌学会雑誌, Vol.84, 105-106, 2008年.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1571698600655152768

(CiNii: 1571698600655152768) 佐久間洋二朗, 奈部浩一郎, 本庶祥子, 池田弘毅, 青山倫久, 木村哲也, 野村和弘, 浜本芳之, 和田良春, 越山裕行 :
Case Record症例報告多発性内分泌腺腫症I型(MEN1)に糖尿病を合併した症例-MEN1も糖尿病を合併しやすい内分泌疾患の1つである,
糖尿病診療マスター, Vol.6, No.3, 309-313, 2008年.

(出版サイトへのリンク): ● Publication site (DOI): 10.11477/mf.1415100818
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390565159930841472; ● Search Scopus @ Elsevier (DOI): 10.11477/mf.1415100818

(DOI: 10.11477/mf.1415100818, CiNii: 1390565159930841472) Tetsuya Hosooka, Kazuhiro Nomura and Wataru Ogawa :
Vascular endothelial growth factor-B as a therapeutic target to prevent ectopic fat deposition.,
Journal of diabetes investigation, Vol.4, No.6, 525-527, 2013.

(出版サイトへのリンク): ● Publication site (DOI): 10.1111/jdi.12099
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24843704; ● Search Scopus @ Elsevier (PMID): 24843704; ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.12099

(DOI: 10.1111/jdi.12099, PubMed: 24843704) Wataru Ogawa and Kazuhiro Nomura :
Does adiponectin mimic exercise?,
Journal of diabetes investigation, Vol.1, No.6, 239-241, 2010.

(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.2040-1124.2010.00057.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24843438; ● Search Scopus @ Elsevier (PMID): 24843438; ● Search Scopus @ Elsevier (DOI): 10.1111/j.2040-1124.2010.00057.x

(DOI: 10.1111/j.2040-1124.2010.00057.x, PubMed: 24843438)

総説・解説

野村和弘, 小川渉 :
骨格筋の分子生物学,
日本臨床 = Japanese journal of clinical medicine, Vol.80, No.4, 681-686, 2022年4月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1523106606091371136

(CiNii: 1523106606091371136) 野村和弘, 平田悠, 小川渉 :
糖尿病とサルコペニア,
医学のあゆみ, Vol.276, No.5, 405-409, 2021年1月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1523669556008449664

(CiNii: 1523669556008449664) K Nabe, S Honjo, H Ikeda, Y Wada, Kazuhiro Nomura, Y Hamamoto, T Koh, Y Tatsuoka and H Koshiyama :
Diabetes insipidus and cognitive function.,
Medical hypotheses, Vol.69, No.4, 764-766, Apr. 2007.

(要約): It has been well known that several neuropeptides may affect human behavior, and that some endocrinopathies are associated with impaired higher function of the brain. There have been increasing evidences that vasopressin has both peripheral and central effects, the latter of which is involved in memory. In experimental animals, male mice with a null mutation in the V1a receptor (V1aR) exhibit a profound impairment in social recognition and changes in anxiety-like behavior. An AVP fragment analog has been reported to facilitate memory retention and recall in mice through protein kinase C-independent pathways. In human, a few recent reports have suggested that a familial central diabetes insipidus, caused by a heterozygous mutation in the gene for vasopressin prohormone, have minor disturbances in central nervous system. Taken together, it is hypothesized that the subject with central diabetes insipidus may frequently present with an impaired cognitive ability. It is justified to examine the cognitive function, when we make a diagnosis of central diabetes insipidus and to perform a clinical study to investigate whether central diabetes insipidus may be associated with impairment of higher brain functions.
(キーワード): Animals / Brain / Cognition / Diabetes Mellitus / Disease Models, Animal / Humans / Male / Mice / Neuropeptides / Vasopressins
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.mehy.2007.01.081
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17467188; ● Search Scopus @ Elsevier (PMID): 17467188; ● Search Scopus @ Elsevier (DOI): 10.1016/j.mehy.2007.01.081

(DOI: 10.1016/j.mehy.2007.01.081, PubMed: 17467188) M Noda, Kazuhiro Nomura, Y Asou, H Nemoto, M Ishijima, M Takamoto, M Usui and K Kashimada :
[Bone metabolism and angiogenesis].,
Clinical calcium, Vol.11, No.4, 404-410, Apr. 2001.

(要約): Bone metabolism is regulated not only by the nutrition supplied by vessel but also by the signals from the cells in vascular tissues. Identification of such signaling molecules has been the major issue in the field of research on the relationship between bone and vasculatures. This review touches on the recent findings on the expression and functions of such signaling molecules including VEGF, MMP and non-collagenous bone matrix proteins.
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15775533; ● Search Scopus @ Elsevier (PMID): 15775533

(PubMed: 15775533) Kazuhiro Nomura, H Imai, T Koumura and Y Nakagawa :
Involvement of mitochondrial phospholipid hydroperoxide glutathione peroxidase as an antiapoptotic factor.,
Biological signals and receptors, Vol.10, No.1-2, 81-92, 2001.

(要約): Although reactive oxygen species (ROS) such as superoxide and hydroperoxide are known to induce apoptotic cell death, little is known as to the apoptotic death signaling of mitochondrial ROS. Recent evidence has suggested that antioxidant enzymes in mitochondria may be responsible for the regulation of cytochrome c release and apoptotic cell death. This paper examines the current state of knowledge regarding the role of mitochondrial antioxidant enzymes, especially phospholipid hydroperoxide glutathione peroxidase. A model for the release of cytochrome c by lipid hydroperoxide has also been proposed.
(キーワード): Antioxidants / Apoptosis / Cardiolipins / Cytochrome c Group / Glutathione Peroxidase / Lipid Peroxides / Mitochondria / Models, Biological / Phosphatidylcholines / Phospholipid Hydroperoxide Glutathione Peroxidase / Reactive Oxygen Species
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000046877
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11223642; ● Search Scopus @ Elsevier (PMID): 11223642; ● Search Scopus @ Elsevier (DOI): 10.1159/000046877

(DOI: 10.1159/000046877, PubMed: 11223642)

講演・発表

K Uchiyama, Y Hirata, Kazuhiro Nomura, H Wijaya, M Taniguchi, S Kitaoka, T Furuyashiki and W Ogawa :
Mental stress induces muscle atrophy through brain inflammation and the C/EBPβδ pathway in skeletal muscle,
The 50th European Muscle Conference, Sep. 2023. K Hozumi, K Sugawara, Y Hirata, Kazuhiro Nomura and W Ogawa :
Effects of Imeglimin on Mitochondrial Function, AMPK Activation, and Gene Expression in Hepatocytes and Myocytes,
The 50th European Muscle Conference, Sep. 2023. T Inoue, Y Hirata, Kazuhiro Nomura and W Ogawa :
Role of myofiber Piezo1 in skeletal muscle hypertrophy induced by mechanical load,
The 50th European Muscle Conference, Sep. 2023. Y Hirata, Kazuhiro Nomura and W Ogawa :
A Piezo1/KLF15/IL-6 axis mediates immobilization-induced muscle atrophy,
The 50th European Muscle Conference, Sep. 2023. 野村和弘, 小川渉 :
運動療法に抵抗性を示す痩せにくい肥満,
第67回日本糖尿病学会年次学術集会シンポジウム, 2024年5月. 山田苑子, 久保みゆ, 和泉優奈, 野村和弘, 神村盛一郎, 柏原秀也, 齋藤裕, 北村嘉章, 島田光生, 濵田康弘, 阪上浩 :
簡便に得られるデータから作成した四肢骨格筋量を予測する回帰式の妥当性検証,
第27回日本病態栄養学会年次学術集会, 2024年1月. 橋本脩平, 鈴木佳子, 小笠有加, 筑後桃子, 橋本一郎, 岩本晃一, 美馬俊介, 大藤純, 野村和弘, 阪上浩 :
自家培養表皮(ジェイス)移植を受けた広範囲熱傷患者の栄養管理シングル・ケース・スタディ,
第27回日本病態栄養学会年次学術集会, 2024年1月. 和泉優奈, 藤本紗織, 谷口萌々花, 大村皐月, 山田苑子, 志内哲也, 岡松優子, 米代武司, 野村和弘, 堤理恵, 阪上浩 :
骨格筋-BAT間アミノ酸代謝連関に対する制御機構の解明,
第44回日本肥満学会学術集会, 2023年11月. 大村皐月, 和泉優奈, 野村和弘, 山田苑子, 志内哲也, 岡松優子, 米代武司, 堤理恵, 阪上浩 :
臓器間アミノ酸代謝連関の調節因子としての骨格筋由来IL-6発現メカニズムの解明,
第56回栄養・食糧学会中国四国支部大会, 2023年10月. 村上遥音, 和泉優奈, 鈴木由紀, 山田苑子, 野村和弘, 堤理恵, 阪上浩 :
廃用性筋萎縮の骨格筋代謝動態に対するMCT配合ケトン食の影響,
第56回栄養・食糧学会中国四国支部大会, 2023年10月. 筑後桃子, 堤理恵, 山田静恵, 小笠有加, 橋本脩平, 藤本紗織, 鈴木佳子, 野村和弘, 阪上浩 :
当院における早期栄養介入の現状と今後の課題,
第15回日本臨床栄養代謝学会中国四国支部学術集会, 2023年9月. 和泉優奈, 藤本紗織, 谷口萌々花, 大村皐月, 志内哲也, 岡松優子, 米代武司, 黒田雅士, 野村和弘, 堤理恵, 阪上浩 :
骨格筋による新たな体温維持機構の発見とその制御分子の同定,
第9回日本筋学会学術集会, 2023年8月. 平田悠, 野村和弘, 小川渉 :
不動化における筋量制御のメカニズム,
第96回日本内分泌学会学術総会, 2023年6月. 内山奏, 平田悠, 野村和弘, Wijaya Hendy, 谷口将之, 北岡志保, 古屋敷智之, 小川渉 :
脳内炎症は骨格筋のC/EBP経路を介してストレス性筋萎縮を促進する,
第66回日本糖尿病学会年次学術総会, 2023年5月. 内山奏, 平田悠, 野村和弘, Wijaya Hendy, 谷口将之, 北岡志保, 古屋敷智之, 小川渉 :
脳内炎症は骨格筋のC/EBP経路を介してストレス性筋萎縮を促進する,
第58回日本臨床分子医学会学術総会, 2023年4月. 野村和弘, 小川渉 :
運動による骨格筋リモデリングの活性化と加齢による破綻メカニズム,
第65回日本糖尿病学会年次学術集会シンポジウム, 2022年5月. 野村和弘, Krook Anna, Zierath Juleen, 小川渉 :
肥満と老化による骨格筋機能の低下メカニズム,
40回日本肥満学会シンポジウム, 2019年11月. 野村和弘, 細岡哲也, 佐々木努, 北村忠弘, 阪上浩, 春日雅人, 小川渉 :
肥満における骨格筋アドレナリン抵抗性の関与とPGC-1α新規アイソフォームの役割,
日本内分泌学会雑誌, Vol.92, No.1, 247, 2016年4月. 野村和弘, 水崎奈央, 細岡哲也, 佐々木努, 北村忠弘, 阪上浩, 春日雅人, 小川渉 :
骨格筋のアドレナリン抵抗性はPGC-1α新規アイソフォームの誘導不全により肥満を惹起する,
日本臨床分子医学会学術総会, 2014年4月. 野村和弘, 水崎奈央, 細岡哲也, 佐々木努, 北村忠弘, 阪上浩, 春日雅人, 小川渉 :
骨格筋のアドレナリン抵抗性はPGC1α新規アイソフォームの誘導不全により肥満を惹起する,
糖尿病, Vol.57, No.Suppl.1, S-423, 2014年.

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Jグローバル最終確認日: 2024/9/14 01:06
氏名（漢字）: 野村和弘
氏名（フリガナ）: ノムラカズヒロ
氏名（英字）: NOMURA Kazuhiro
所属機関: 徳島大学大学院講師

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researchmap最終確認日: 2024/9/15 01:25
氏名（漢字）: 野村和弘
氏名（フリガナ）: ノムラカズヒロ
氏名（英字）: NOMURA Kazuhiro
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所属: 徳島大学大学院
部署: 医歯薬学研究部　代謝栄養学分野
職名: 講師
学位: 医学博士
学位授与機関: 神戸大学
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研究者番号: 70450236

所属（現在）: 2024/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 講師

所属（過去の研究課題 情報に基づく）*注記: 2023/4/1 – 2024/4/1 : 徳島大学, 大学院医歯薬学研究部(医学域), 講師
2020/4/1 – 2022/4/1 : 神戸大学, 医学研究科, 特定助教
2020/4/1 – 2022/4/1 : 神戸大学, 医学部附属病院, 特定助教
2018/4/1 – 2019/4/1 : 神戸大学, 医学研究科, 医学研究員
2018/4/1 : 神戸大学, 医学部附属病院, その他
2016/4/1 – 2017/4/1 : 神戸大学, 医学部附属病院, 医員
2013/4/1 – 2015/4/1 : 神戸大学, 医学部附属病院, その他
2012/4/1 – 2014/4/1 : 神戸大学, 医学部附属病院, 医員

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生物系 / 医歯薬学 / 内科系臨床医学 / 代謝学
小区分54040:代謝および内分泌学関連
小区分59040:栄養学および健康科学関連

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生物系 / 医歯薬学 / 内科系臨床医学 / 代謝学
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中区分54:生体情報内科学およびその関連分野
小区分59040:栄養学および健康科学関連

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エネルギー・糖質代謝異常 / PGC-1α / 肥満 / エネルギー代謝 / 骨格筋 / PGC1α / 運動 / アドレナリン抵抗性 / ＰＧＣ-1α / アドレナリンシグナル / エネルギー消費 / アドレナリン / 糖尿病 / サルコペニア / 加齢 / 骨格筋リモデリング / メカノセンシング / 筋萎縮 / 筋肥大

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肥満 / 異所性脂肪蓄積 / インスリン抵抗性 / エネルギー代謝 / 糖尿病 / 遺伝子発現 / 脂肪肝 / 遺伝子転写 / 転写因子 / 脂質異常症 / S6K1 / 骨格筋 / 糖代謝 / 運動 / エネルギー消費 / 不動化 / 骨格筋量 / サルコペニア / 炎症 / 筋萎縮 / 筋量制御 / KLF15 / 代謝 / sarcopenia / タイチン / バイオマーカー

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