| 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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