Objective: This study was conducted to investigate energy metabolism based on
changes in organic acids in diabetes and to establish a correlation between metabolites or
bone microarchitecture and the glucose index in type 2 diabetic mice.
Methods: Seven-week-old male C57BL/6 mice were randomly divided into a non-diabetic
group and a diabetic group. The diabetic group was fed a high-fat diet (HFD) that induced
insulin resistance for 5 weeks. Afterwards, diabetes was induced by a single streptozotocin
injection. Both the groups were fed a normal diet and HFD diet for 9 weeks.
Results: The fasting blood glucose level glycosylated hemoglobin (HbA1c) significantly increased
in diabetic mice. Bone-alkaline phosphatase activity 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 the 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 that uncontrolled HbA1c can affect bone loss, production
of ketone bodies and utilization of glucose metabolites for energy production in type 2