| Project/Area Number |
16K00868
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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 |
Eating habits
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| Research Institution | University of Shizuoka (2018-2019)
Kyorin University (2016-2017) |
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Principal Investigator |
HOSAKA TOSHIO 静岡県立大学, 食品栄養科学部, 教授 (60403698)
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| Co-Investigator(Kenkyū-buntansha) |
石田 均 杏林大学, 医学部, 教授 (80212893)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 乳酸 / 糖尿病 / インスリン抵抗性 / GPT / 肝機能障害 / GOT / ビリルビン / 脂肪肝 / アディポカイン / 代謝学 |
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| Outline of Final Research Achievements |
Fasting serum lactate levels, hematological and inflammatory serum markers and anthropometric parameters, obtained employing bioelectric impedance analysis, were measured in 103 patients with T2DM. As a result, stepwise regression analysis showed ALT to be independently positively associated with total bilirubin, while being negatively associated with serum lactate levels. Furthermore, serum lactate levels were significantly higher in patients with ALT-predominant liver dysfunction. From those results, we concluded that fasting serum lactate elevation in T2DM patients to be associated with the serum levels of ALT and total bilirubin independently of blood glucose control.
At the same time, we reported the mechanism of palmitate, represented for unsaturated fatty acid, induces insulin resistance in several cell line, but not found precisely or constantly relationship to lactate receptor signaling in those cells.
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| Academic Significance and Societal Importance of the Research Achievements |
2型糖尿病患者では、インスリン抵抗性状態で血清乳酸値の上昇を認め、更なる解析で、空腹時血清乳酸値と肝関連因子との重相関を認めたことから、乳酸値が特に、インスリン抵抗性を背景とした肝臓での従来のマーカーとは異なる、早期からの脂肪肝の新たな非侵襲マーカーとなりうる可能性が示唆された。
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