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- Maeyama, T., et al.
(author)
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Production of a fluorescence probe in ion-beam radiolysis of aqueous coumarin-3-carboxylic acid solution-2: Effects of nuclear fragmentation and its simulation with PHITS
- 2011
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In: Radiation Physics and Chemistry. - : Elsevier BV. - 1879-0895 .- 0969-806X. ; 80:12, s. 1352-1357
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Journal article (peer-reviewed)abstract
- The G(OH) values in aqueous coumarin-3-carboxylic-acid (3-CCA) solutions irradiated with (12)C(6+) beams having the energies of 135, 290 and 400 MeV/u were measured by a fluorescent method around the Bragg peak, with 0.6 mm intervals, and quartz cells of 1 cm optical lengths, at the Heavy Ion Medical Accelerator in Chiba, National Institute of Radiological Sciences (NIRS). For each ion, the G(OH) has been calculated as a function of dose average LET and position. The calculated results have been compared to measurements, and the results, reproducibility and reliability of the calculations are discussed in the paper.
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- Morita, M, et al.
(author)
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Hepatic posttranscriptional network comprised of CCR4-NOT deadenylase and FGF21 maintains systemic metabolic homeostasis
- 2019
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In: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 116:16, s. 7973-7981
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Journal article (peer-reviewed)abstract
- Whole-body metabolic homeostasis is tightly controlled by hormone-like factors with systemic or paracrine effects that are derived from nonendocrine organs, including adipose tissue (adipokines) and liver (hepatokines). Fibroblast growth factor 21 (FGF21) is a hormone-like protein, which is emerging as a major regulator of whole-body metabolism and has therapeutic potential for treating metabolic syndrome. However, the mechanisms that control FGF21 levels are not fully understood. Herein, we demonstrate that FGF21 production in the liver is regulated via a posttranscriptional network consisting of the CCR4–NOT deadenylase complex and RNA-binding protein tristetraprolin (TTP). In response to nutrient uptake, CCR4–NOT cooperates with TTP to degrade AU-rich mRNAs that encode pivotal metabolic regulators, including FGF21. Disruption of CCR4–NOT activity in the liver, by deletion of the catalytic subunit CNOT6L, increases serum FGF21 levels, which ameliorates diet-induced metabolic disorders and enhances energy expenditure without disrupting bone homeostasis. Taken together, our study describes a hepatic CCR4–NOT/FGF21 axis as a hitherto unrecognized systemic regulator of metabolism and suggests that hepatic CCR4–NOT may serve as a target for devising therapeutic strategies in metabolic syndrome and related morbidities.
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