JaLCDOI | 10.18926/AMO/54413 |
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FullText URL | 70_3_151.pdf |
Author | Wada, Jun| Nakatsuka, Atsuko| |
Abstract | The mitochondria are involved in active and dynamic processes, such as mitochondrial biogenesis, fission, fusion and mitophagy to maintain mitochondrial and cellular functions. In obesity and type 2 diabetes, impaired oxidation, reduced mitochondrial contents, lowered rates of oxidative phosphorylation and excessive reactive oxygen species (ROS) production have been reported. Mitochondrial biogenesis is regulated by various transcription factors such as peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), peroxisome proliferator-activated receptors (PPARs), estrogen-related receptors (ERRs), and nuclear respiratory factors (NRFs). Mitochondrial fusion is promoted by mitofusin 1 (MFN1), mitofusin 2 (MFN2) and optic atrophy 1 (OPA1), while fission is governed by the recruitment of dynamin-related protein 1 (DRP1) by adaptor proteins such as mitochondrial fission factor (MFF), mitochondrial dynamics proteins of 49 and 51 kDa (MiD49 and MiD51), and fission 1 (FIS1). Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and PARKIN promote DRP1-dependent mitochondrial fission, and the outer mitochondrial adaptor MiD51 is required in DRP1 recruitment and PARKIN-dependent mitophagy. This review describes the molecular mechanism of mitochondrial dynamics, its abnormality in diabetes and obesity, and pharmaceuticals targeting mitochondrial biogenesis, fission, fusion and mitophagy. |
Keywords | fusion fission oxidative stress mitochondria diabetes |
Amo Type | Review |
Publication Title | Acta Medica Okayama |
Published Date | 2016-06 |
Volume | volume70 |
Issue | issue3 |
Publisher | Okayama University Medical School |
Start Page | 151 |
End Page | 158 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2016 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 27339203 |
Web of Science KeyUT | 000379406100001 |
Author | Watanabe, Mayu| Nakatsuka, Atsuko| Murakami, Kazutoshi| Inoue, Kentaro| Terami, Takahiro| Higuchi, Chigusa| Katayama, Akihiro| Teshigawara, Sanae| Eguchi, Jun| Ogawa, Daisuke| Watanabe, Eijiro| Wada, Jun| Makino, Hirofumi| |
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Published Date | 2014-05-25 |
Publication Title | PLOS ONE |
Volume | volume9 |
Issue | issue3 |
Content Type | Journal Article |
Author | Ogawa, Daisuke| Eguchi, Jun| Wada, Jun| Terami, Naoto| Hatanaka, Takashi| Tachibana, Hiromi| Nakatsuka, Atsuko| Sato Horiguchi, Chikage| Nishii, Naoko| Makino, Hirofumi| |
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Published Date | 2014-01-22 |
Publication Title | PLOS ONE |
Volume | volume9 |
Issue | issue1 |
Content Type | Journal Article |
Author | Nakatsuka, Atsuko| Matsuyama, Makoto| Yamaguchi, Satoshi| Katayama, Akihiro| Eguchi, Jun| Murakami, Kazutoshi| Teshigawara, Sanae| Ogawa, Daisuke| Wada, Nozomu| Yasunaka, Tetsuya| Ikeda, Fusao| Takaki, Akinobu| Watanabe, Eijiro| Wada, Jun| |
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Published Date | 2016-02-17 |
Publication Title | Scientific Reports |
Volume | volume6 |
Content Type | Journal Article |
Author | Katayama, Akihiro| Nakatsuka, Atsuko| Eguchi, Jun| Murakami, Kazutoshi| Teshigawara, Sanae| Kanzaki, Motoko| Nunoue, Tomokazu| Hida, Kazuyuki| Wada, Nozomu| Yasunaka, Tetsuya| Ikeda, Fusao| Takaki, Akinobu| Yamamoto, Kazuhide| Kiyonari, Hiroshi| Makino, Hirofumi| Wada, Jun| |
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Published Date | 2015 |
Publication Title | Scientific reports |
Volume | volume5 |
Content Type | Journal Article |
Author | Wada, Jun| |
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Published Date | 2016-01 |
Publication Title | Okayama University Medical Research Updates |
Volume | volume18 |
Content Type | Others |
Author | Terami, Takahiro| Wada, Jun| Inoue, Kentaro| Nakatsuka, Atsuko| Ogawa, Daisuke| Teshigawara, Sanae| Murakami, Kazutoshi| Katayama, Akihiro| Eguchi, Jun| Makino, Hirofumi| |
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Published Date | 2013-10-22 |
Publication Title | International Journal of Nephrology and Renovascular Disease |
Volume | volume6 |
Content Type | Journal Article |
Author | Inoue, Kentaro| Wada, Jun| Eguchi, Jun| Nakatsuka, Atsuko| Teshigawara, Sanae| Murakami, Kazutoshi| Ogawa, Daisuke| Terami, Takahiro| Katayama, Akihiro| Tone, Atsuhito| Iseda, Izumi| Hida, Kazuyuki| Yamada, Masao| Ogawa, Tomohisa| Makino, Hirofumi| |
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Published Date | 2013-10-15 |
Publication Title | PLoS ONE |
Volume | volume8 |
Issue | issue10 |
Content Type | Journal Article |
Author | Nakayama, Kazunori| Nakao, Kazushi| Takatori, Yuji| Inoue, Junko| Kojo, Shoichirou| Akagi, Shigeru| Fukushima, Masaki| Wada, Jun| Makino, Hirofumi| |
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Published Date | 2013-12-18 |
Publication Title | International Journal of Nephrology and Renovascular Disease |
Volume | volume7 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/52789 |
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FullText URL | 68_4_235.pdf |
Author | Ono, Tetsuichiro| Shikata, Kenichi| Obika, Mikako| Miyatake, Nobuyuki| Kodera, Ryo| Hirota, Daisyo| Wada, Jun| Kataoka, Hitomi| Ogawa, Daisuke| Makino, Hirofumi| |
Abstract | The aim of this study was to clarify the factors associated with the remission and/or regression of microalbuminuria in Japanese patients with type 2 diabetes mellitus. We retrospectively analyzed the data of 130 patients with type 2 diabetes mellitus with microalbuminuria for 2-6 years (3.39±1.31 years). Remission was defined as improving from microalbuminuria to normoalbuminuria using the albumin/creatinine ratio (ACR), and regression of microalbuminuria was defined as a decrease in ACR of 50% or more from baseline. Progression of microalbuminuria was defined as progressing from microalbuminuria to overt proteinuria during the follow-up period. Among 130 patients with type 2 diabetes mellitus with microalbuminuria, 57 and 13 patients were defined as having remission and regression, respectively, while 26 patients progressed to overt proteinuria. Sex (female), higher HDL cholesterol and lower HbA1c were determinant factors associated with remission/regression of microalbuminuria by logistic regression analysis. Lower systolic blood pressure (SBP) was also correlated with remission/regression, but not at a significant level. These results suggest that proper control of blood glucose, BP and lipid profiles may be associated with remission and/or regression of type 2 diabetes mellitus with microalbuminuria in clinical practice. |
Keywords | microalbuminuria type 2 diabetes mellitus remission regression |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2014-08 |
Volume | volume68 |
Issue | issue4 |
Publisher | Okayama University Medical School |
Start Page | 235 |
End Page | 241 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2014 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 25145409 |
Web of Science KeyUT | 000340687500005 |
Related Url | http://ousar.lib.okayama-u.ac.jp/metadata/52828 |
Author | Sugiyama, Koichi| Sada, Ken-ei| Kurosawa, Michiko| Wada, Jun| Makino, Hirofumi| |
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Published Date | 2013-02 |
Publication Title | Clinical and Experimental Nephrology |
Volume | volume17 |
Issue | issue1 |
Content Type | Journal Article |
Author | Kurose, Yuko| Wada, Jun| Kanzaki, Motoko| Teshigawara, Sanae| Nakatsuka, Atsuko| Murakami, Kazutoshi| Inoue, Kentaro| Terami, Takahiro| Katayama, Akihiro| Watanabe, Mayu| Higuchi, Chigusa| Eguchi, Jun| Miyatake, Nobuyuki| Makino, Hirofumi| |
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Published Date | 2013-01-22 |
Publication Title | BMC Nephrology |
Volume | volume14 |
Content Type | Journal Article |
Author | Inoue, Junko| Wada, Jun| Teshigawara, Sanae| Hida, Kazuyuki| Nakatsuka, Atsuko| Takatori, Yuji| Kojo, Shoichirou| Akagi, Shigeru| Nakao, Kazushi| Miyatake, Nobuyuki| McDonald, John F.| Makino, Hirofumi| |
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Published Date | 2012-12-03 |
Publication Title | BMC Nephrology |
Volume | volume13 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/50405 |
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FullText URL | 67_3_129.pdf |
Author | Nakatsuka, Atsuko| Wada, Jun| Makino, Hirofumi| |
Abstract | In recent years, many researchers have emphasized the importance of metabolic syndrome based on its increasing prevalence and its adverse prognosis due to associated chronic vascular complications. Upstream of a cluster of metabolic and vascular disorders is the accumulation of visceral adipose tissue, which plays a central role in the pathophysiology. In the accumulation of adipose tissues, cell cycle regulation is tightly linked to cellular processes such as proliferation, hypertrophy and apoptosis. In addition, various cell cycle abnormalities have also been observed in other tissues, such as kidneys and the cardiovascular system, and they are critically involved in the progression of disease. Here, we discuss cell cycle abnormalities in metabolic syndrome in various tissues. Furthermore, we describe the role of nuclear receptors in cell growth and survival, and glucose and lipid metabolism in the whole body. Therapeutic strategies for modulating various cell cycles in metabolic disorders by targeting nuclear receptors may overcome obesity and its chronic vascular complications in the future. |
Keywords | nuclear receptor cell cycle metabolic syndrome diabetic nephropathy |
Amo Type | Review |
Publication Title | Acta Medica Okayama |
Published Date | 2013-06 |
Volume | volume67 |
Issue | issue3 |
Publisher | Okayama University Medical School |
Start Page | 129 |
End Page | 134 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2013 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 23804135 |
Web of Science KeyUT | 000320747900001 |
Author | Nakatsuka, Atsuko| Wada, Jun| Iseda, Izumi| Teshigawara, Sanae| Higashio, Kanji| Murakami, Kazutoshi| Kanzaki, Motoko| Inoue, Kentaro| Terami, Takahiro| Katayama, Akihiro| Hida, Kazuyuki| Eguchi, Jun| Horiguchi, Chikage Sato| Ogawa, Daisuke| Matsuki, Yasushi| Hiramatsu, Ryuji| Yagita, Hideo| Kakuta, Shigeru| Iwakura, Yoichiro| Makino, Hirofumi| |
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Published Date | 2012-11 |
Publication Title | Diabetes |
Volume | volume61 |
Issue | issue11 |
Content Type | Journal Article |
Author | Teshigawara, Sanae| Wada, Jun| Hida, Kazuyuki| Nakatsuka, Atsuko| Eguchi, Jun| Murakami, Kazutoshi| Kanzaki, Motoko| Inoue, Kentaro| Terami, Takahiro| Katayama, Akihiro| Iseda, Izumi| Matsushita, Yuichi| Miyatake, Nobuyuki| McDonald, John F.| Hotta, Kikuko| Makino, Hirofumi| |
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Published Date | 2012-07 |
Publication Title | Journal of Clinical Endocrinology & Metabolism |
Volume | volume97 |
Issue | issue7 |
Content Type | Journal Article |
Author | Nakatsuka, Atsuko| Wada, Jun| Makino, Hirofumi| |
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Published Date | 2012-08-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume124 |
Issue | issue2 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/46850 |
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FullText URL | 65_4_247.pdf |
Author | Watanabe, Naomi| Shikata, Kenichi| Shikata, Yasushi| Sarai, Kei| Omori, Kazuyoshi| Kodera, Ryo| Sato, Chikage| Wada, Jun| Makino, Hirofumi| |
Abstract | Inflammatory processes are involved in the pathogenesis of diabetic nephropathy. The aim of this study was to clarify the role of mitogen-activated protein kinase (MAPK) pathways for induction of intercellular adhesion molecule-1 (ICAM-1) expression in glomerular endothelial cells under diabetic conditions. We examined the expression of ICAM-1 in the kidneys of experimental diabetic rats. Human glomerular endothelial cells (GE cells) were exposed to normal glucose concentration, high glucose concentration (HG), or high mannitol concentration (HM), and then the expression of the ICAM-1 protein and the phosphorylation of the 3 subfamilies of mitogen-activated protein kinase (MAPK) were determined using Western blot analysis. Next, to evaluate the involvement of MAPKs in HG- or HM-induced ICAM-1 expression, we preincubated GE cells with the inhibitors for ERK, p38 or JNK 1h prior to the application of glucose or mannitol. Expression of ICAM-1 was increased in the glomeruli of diabetic rats. Both HG and HM induced ICAM-1 expression and phosphorylation of ERK1/2, p38 and JNK in GE cells. Expression of ICAM-1 was significantly attenuated by inhibitors of ERK, p38 and JNK. We conclude that activation of ERK1/2, p38 and JNK cascades may be involved in ICAM-1 expression in glomerular endothelial cells under diabetic conditions. |
Keywords | diabetic nephropathy ICAM-1 ERK p38 MAPK JNK |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-08 |
Volume | volume65 |
Issue | issue4 |
Publisher | Okayama University Medical School |
Start Page | 247 |
End Page | 257 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21860531 |
Web of Science KeyUT | 000294236700005 |
JaLCDOI | 10.18926/AMO/45272 |
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FullText URL | 65_2_129.pdf |
Author | Toyota, Noriko| Ogawa, Daisuke| Ishii, Keita| Hirata, Kyoji| Wada, Jun| Shikata, Kenichi| Makino, Hirofumi| |
Abstract | A 62-year-old woman with a history of poorly controlled type 2 diabetes mellitus was admitted to our hospital with a 3-week history of mild fever, vomiting, and anorexia. Abdominal computed tomography (CT) showed bilateral hydronephrosis and gas accumulation in the urinary bladder wall and left ureter. Laboratory tests showed leukocytosis and elevated C-reactive protein level. Urine culture showed heavy growth of Escherichia coli. The final diagnosis was emphysematous cystitis. The patient was treated with systemic antibiotics and drainage using a urethral catheter. The clinical and radiographic findings resolved rapidly, and she was discharged from the hospital on day 28. Emphysematous cystitis is a relatively rare urinary tract infection associated with gas formation, and has the potential for a serious outcome if untreated. Early detection by imaging studies such as CT is important in providing prompt treatment and favorable clinical outcome. |
Keywords | computed tomography diabetes mellitus emphysematous cystitis |
Amo Type | Case Report |
Publication Title | Acta Medica Okayama |
Published Date | 2011-04 |
Volume | volume65 |
Issue | issue2 |
Publisher | Okayama University Medical School |
Start Page | 129 |
End Page | 133 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21519371 |
Web of Science KeyUT | 000289818800009 |
JaLCDOI | 10.18926/AMO/45266 |
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FullText URL | 65_2_81.pdf |
Author | Sasaki, Motofumi| Shikata, Kenichi| Okada, Shinichi| Miyamoto, Satoshi| Nishishita, Shingo| Usui Kataoka, Hitomi| Sato, Chikage| Wada, Jun| Ogawa, Daisuke| Makino, Hirofumi| |
Abstract | Glomerular hyperfiltration is a common pathway leading to glomerulosclerosis in various kinds of kidney diseases. The 5/6 renal ablation is an established experimental animal model for glomerular hyperfiltration. On the other hand, low-grade inflammation is also a common mechanism for the progression of kidney diseases including diabetic nephropathy and atherosclerosis. Here we analyzed the gene expression profile in the remnant kidney tissues of 5/6 nephrectomized mice using a DNA microarray system and compared it with that of sham-operated control mice. The 5/6 nephrectomized mice showed glomerular hypertrophy and an increase in the extracellular matrix in the glomeruli. DNA microarray analysis indicated the up-regulated expression of various kinds of genes related to the inflammatory process in remnant kidneys. We confirmed the up-regulated expression of platelet factor-4, and monocyte chemoattractant protein-1, 2, and 5 in remnant kidneys by RT-PCR. The current results suggest that the inflammatory process is involved in the progression of glomerulosclerosis and is a common pathway of the pathogenesis of kidney disease. |
Keywords | kidney inflammation chemokine |
Amo Type | Original Article |
Publication Title | Acta Medica Okayama |
Published Date | 2011-04 |
Volume | volume65 |
Issue | issue2 |
Publisher | Okayama University Medical School |
Start Page | 81 |
End Page | 89 |
ISSN | 0386-300X |
NCID | AA00508441 |
Content Type | Journal Article |
language | English |
Copyright Holders | CopyrightⒸ 2011 by Okayama University Medical School |
File Version | publisher |
Refereed | True |
PubMed ID | 21519365 |
Web of Science KeyUT | 000289818800003 |