Abstract:
AIM To investigate the underlying mechanism of blood glucose regulating myocardial 18F-FDG uptake in fasting rats.
METHODS The body weight, blood glucose and blood ketone levels of male SD rats were measured at different fasting duration and re-feeding groups. M-mode echocardiography was used to measure the cardiac pumping function of rats after fasting. Rats in different fasting groups underwent 18F-FDG PET/CT scanning to observe and quantitatively analyze the myocardial 18F-FDG uptake. The expression and activity of mTOR and AMPK were detected in cardiomyocytes cultured with different glucose concentrations.
RESULTS The body weight of rats decreased significantly with the prolonged fasting and returned to approximately pre-fasting level after re-feeding for 24 hours. The blood glucose decreased significantly in the 24h-fasting group and reached a lower and stable level in 48h-fasting and 72h-fasting groups. On the contrary, the blood ketone increased significantly in the 24h-fasting group and reached a higher and stable level in 48h-fasting and 72h-fasting groups. Twenty-four hours after re-feeding, blood glucose and blood ketone were completely reversed. There was no significant difference in cardiac performance between fasting groups and their synchronous control groups. PET/CT imaging showed that myocardial 18F-FDG uptake (SUV ratio) was significantly reduced after 24h-fasting and completely recovered after 24h-refeeding. When the glucose concentration was reduced in cultured cardiomyocytes, the activity of mTOR decreased, but the activity of AMPK increased significantly.
CONCLUSION Fasting leads to hypoglycemia which directly inhibits mTOR in the myocardium. On the other hand, activated AMPK by hypoglycemia indirectly inhibits mTOR and the reduction of mTOR activity may decrease the myocardial 18F-FDG uptake in fasting rats.
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