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Reduced alkaline phosphatase activity in diabetic rat bone: a re-evaluation
I Koyama1, M Yakushijin, T Nakajima
1Department of Medical Technology, Junior College, Saitama Medical School, Saitama Medical School, Japan. koyamaw@saitama-med.ac.jp
Summary
Diabetes elevates intestinal alkaline phosphatase (AP) activity, while bone AP activity decreases due to glycation and breakdown. This study investigates in vivo AP glycation in diabetic rats.
Area of Science:
- Biochemistry
- Endocrinology
- Bone Biology
Background:
- Human bone alkaline phosphatase (AP) is susceptible to glycation and reactive oxygen species (ROS) damage.
- Diabetes mellitus is associated with altered protein structure and function.
Purpose of the Study:
- To investigate in vivo glycation of bone AP in diabetic rat models.
- To examine the impact of hyperlipidemia on bone AP activity.
- To elucidate the mechanisms behind altered AP activity in diabetes.
Main Methods:
- Induction of experimental diabetes using streptozotocin and use of spontaneously diabetic rats.
- Induction of hyperlipidemia via high-fat or high-fructose diets.
- Measurement of serum and bone AP activity.
- Affinity chromatography using aminophenylboronic acid to detect glycated proteins.
- Molecular size analysis of bone AP.
Main Results:
- Serum AP activity increased significantly in early diabetes, originating from the intestinal isozyme.
- Hyperlipidemia, induced by diet, also elevated intestinal AP activity.
- Bone AP activity decreased in diabetic rats.
- Bone AP from diabetic rats showed glycation and reduced molecular size, suggesting breakdown.
Conclusions:
- Elevated serum AP in diabetes is linked to hyperlipidemia and increased intestinal AP.
- Reduced bone AP activity in diabetes may result from glycation-induced inactivation and subsequent breakdown by ROS.
- These findings highlight the detrimental effects of diabetes on bone health via AP modification.