研究課題/領域番号 |
22KF0422
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補助金の研究課題番号 |
21F21406 (2021-2022)
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研究種目 |
特別研究員奨励費
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配分区分 | 基金 (2023) 補助金 (2021-2022) |
応募区分 | 外国 |
審査区分 |
小区分48020:生理学関連
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研究機関 | 大学共同利用機関法人自然科学研究機構(機構直轄研究施設) |
研究代表者 |
根本 知己 大学共同利用機関法人自然科学研究機構(機構直轄研究施設), 生命創成探究センター, 教授 (50291084)
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研究分担者 |
LEE MING-LIANG 大学共同利用機関法人自然科学研究機構(機構直轄研究施設), 生命創成探究センター, 外国人特別研究員
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研究期間 (年度) |
2023-03-08 – 2024-03-31
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研究課題ステータス |
完了 (2023年度)
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配分額 *注記 |
2,200千円 (直接経費: 2,200千円)
2023年度: 500千円 (直接経費: 500千円)
2022年度: 1,100千円 (直接経費: 1,100千円)
2021年度: 600千円 (直接経費: 600千円)
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キーワード | Body temperature / glucose metabolism / QIH / torpor / hypothermia / glucose sensing / body temperature / Q-neuron / hypometabolism |
研究開始時の研究の概要 |
We first study the glucose homeostasis of Q-neuron-induced hypothermia and hypometabolism (QIH) mice such as glucose expenditure and gluconeogenesis in QIH animals. Because QIH decreases heat production and body temperature, relationship between body temperature of glucose metabolism was also studied. We also investigate brain glucose sensing in QIH animals by using in vivo calcium imaging. Finally, glucose-sensing neurons in QIH mice will be artificially activated to understand the role of these neurons in regulation of glucose metabolism.
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研究実績の概要 |
Using the QIH model, we found that QIH mice are glucose hypometabolic with insulin resistance. These QIH mice were pyruvate intolerant, but lower liver PEPCK expression suggested lower gluconeogenesis after fasting. The 2DG uptake assay indicated extremely reduced glucose utilization and insulin sensitivity in peripheral tissues. The net effect of lower glucose production and utilization resulted in higher fasting blood glucose and pyruvate intolerance in QIH mice. Increasing the body temperature of QIH mice by raising the ambient temperature improved glucose metabolism, whereas raising the ambient temperature did not significantly affect glucose metabolism in the control animal. Taken together, body temperature rather than ambient temperature is a strong factor to regulate glucose metabolism. In addition, food intake and locomotor activity, which are severely affected by QIH-mediated hypothermia, were also restored by increasing body temperature. We conclude that the QIH-mediated glucose hypometabolism and torpid behavior are regulated by hypothermia rather than Qrfp neurons, and body temperature rather than ambient temperature is a strong factor to regulate physiological responses. A manuscript regarding the above results has been submitted to peer-reviewed academic journals.
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