Objective: This study was conducted to investigate energy metabolism based on changes in organic acids during diabetes and to establish a correlation between metabolites or bone microarchitecture and the glucose index in diabetic mice.
Method: Male seven week old C57BL/6 mice were randomly divided into non-diabetic group and diabetes group. The diabetic group was fed high fat diet (HFD) induced insulin resistance for 5 weeks. Afterwards, diabetes was induced by a single streptozotocin injection. Both of groups were fed normal diet and HFD diet for 9 weeks, respectively.
Results: The fasting blood glucose level, glycosylated hemoglobin (HbA1c) were significantly increased in diabetic mice. Bone-alkaline phosphatase activity was decreased in the diabetic group. Diabetes increased the levels of ketone bodies, including 3-hydroxybutyric, acetoacetic and butyric acid, whereas it decreased Krebs cycle components, including succinic acid and malic acid, as well as levels of glycolytic products, including lactic acid. Diabetes also induced a shortage of trabecular bone mineral density (BMD) by regulation of trabecular morphometric parameters in the femur and tibia. Correlation analysis indicated that BMD, Krebs cycle components and lactic acid levels were negatively correlated with HbA1c, whereas ketone bodies were positively correlated with HbA1c.
Conclusion: This research suggested uncontrolled HbA1c can affect bone loss, production of ketone bodies and utilization of glucose metabolites for energy production in diabetes.