Glutamine metabolism network linked to obesity, diabetes mellitus and tumorigenesis
| Project/Area Number |
26430105
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Tumor biology
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| Research Institution | Chiba University |
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Principal Investigator |
SUZUKI Sawako 千葉大学, 医学部附属病院, 助教 (60400892)
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| Co-Investigator(Kenkyū-buntansha) |
田中 知明 千葉大学, 大学院医学研究院, 教授 (50447299)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | グルタミン代謝 / エネルギー代謝 / 抗酸化作用 / 生活習慣病 / 肝癌 / メタボリック症候群 / NASH / 肥満 / 糖尿病 |
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| Outline of Final Research Achievements |
Recently, several meta analyses revealed obesity and diabetes are oncogenic risk factors and associated with a rise of incidence, prevalence, and the mortality of the cancer. In this context, I focused on the glutamine metabolism which is the main energy source for cancer development. And we reported that GLS2, which is the central in the conversion of glutamine to glutamate, is localized in the mitochondria and promotes the TCA cycle via α-ketoglutarate. On the other hand, at the same time, GLS2 increases production of glutathione to antagonize the reactive oxygen species levels. In this study, I examined the roles of GLS2 in life-style related diseases and cancer development in vivo using Gls2 knockout mice. We found that high fat diet Gls2 knockout mice showed decreased survival and presented so-called metabolic syndrome such as obesity, diabetes and dyslipidemia. Furthermore, we revealed that Gls2 knockout mice developed early-onset hepatocellular carcinoma.
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Report
(4 results)
Research Products
(22 results)
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[Journal Article] The RB-IL-6 axis controls self-renewal and endocrine therapy resistance by fine-tuning mitochondrial activity.2017
Author(s)
Kitajima S, Yoshida A, Kohno S, Li F, Suzuki S, Nagatani N, Nishimoto Y, Nishimoto Y, Sasaki N, Muranaka H, Wan Y, Nishiuchi T, Suzuki Y, Tominaga K, Gotoh N, Suzuki M, Ewen M, Baebie D, Hirose O, Tanaka T
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Journal Title
Related Report
Peer Reviewed
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[Journal Article] MicroRNA-140 mediates RB tumor suppressor function to control stem cell-like activity through interleukin-6.2017
Author(s)
Yoshida A, Kitajima S, Li F, Chaoyang C, Yujiro T, Susumu K, Wan Y, Naoyuki H, Hayato M, Nishimoto Y, Nagatani N, Nishiuchi T, Thai T C, Suzuki S, Nakao S, Tanaka T, Hirose O, Barbie D A and Takahashi C.
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Journal Title
Oncotarget
Volume: 印刷中
Issue: 8
Pages: 13872-85
DOI
NAID
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Cushing Syndrome Due to ACTH-Secreting Pheochromocytoma, Aggravated by Glucocorticoid-Driven Positive-Feedback Loop.2015
Author(s)
Sakuma I, Higuchi S, Fujimoto M, Takiguchi T, Nakayama A, Tamura A, Kohno T, Komai E, Shiga A, Nagano H, Hashimoto N, Suzuki S, Mayama T, Koide H, Ono K, Sasano H, Tatsuno I, Yokote K, Tanaka T.
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Journal Title
J Clin Endocrinol Metab.
Volume: 101(3)
Issue: 3
Pages: 841-846
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] GERMLINE DELETION OF ARMC5 IN FAMILIAL PRIMARY MACRONODULAR ADRENAL HYPERPLASIA.2015
Author(s)
Suzuki S, Tatsuno I, Oohara E, Nakayama A, Komai E, Shiga A, Kono T, Takiguchi T, Higuchi S, Sakuma I, Nagano H, Hashimoto N, Mayama T, Koide H, Sasano H, Nakatani Y, Imamoto T, Ichikawa T, Yokote K, Tanaka T.
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Journal Title
Endocr Pract.
Volume: 21
Issue: 10
Pages: 1152-60
DOI
Related Report
Peer Reviewed / Open Access
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[Book] 細胞2017
Author(s)
中山哲俊、鈴木佐和子、田中知明
Publisher
（株）ニューサイエンス社
Related Report
