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Interaction between bone and glucose metabolism [Review]
1Internal Medicine 1, Shimane University Faculty of Medicine, Izumo 693-8501, Japan.
Endocrine Journal
|October 3, 2017
Summary
Diabetes mellitus (DM) increases fracture risk, causing bone fragility. Targeting adenosine monophosphate-activated protein kinase (AMPK) in bone cells may offer a therapeutic strategy for diabetic bone complications.
Area of Science:
- Endocrinology
- Metabolic Bone Disease
- Diabetology
Background:
- Diabetes mellitus (DM) is linked to increased osteoporotic fracture risk, classifying osteoporosis as a diabetic complication.
- Advanced glycation end products (AGEs) and homocysteine impair osteoblast and osteocyte function, contributing to DM-induced bone fragility.
- Bone, as an endocrine organ, influences glucose metabolism via osteocalcin, though human intervention studies are needed.
Purpose of the Study:
- To explore the intricate relationship between bone and glucose metabolism in the context of diabetes.
- To investigate the role of cellular mechanisms, including adenosine monophosphate-activated protein kinase (AMPK), in diabetic bone fragility.
- To identify potential therapeutic targets for managing DM-induced bone fragility.
Main Methods:
- Review of existing literature on the association between bone metabolism and diabetes.
- Analysis of the impact of advanced glycation end products (AGEs) and homocysteine on bone cells.
- Examination of the role of osteocalcin in glucose homeostasis and the function of adenosine monophosphate-activated protein kinase (AMPK) in bone cells.
Main Results:
- Diabetes mellitus leads to bone fragility through impaired osteoblast and osteocyte function, exacerbated by AGEs and homocysteine.
- Osteocalcin, secreted by osteoblasts, may regulate glucose metabolism, but its clinical efficacy requires further investigation.
- Adenosine monophosphate-activated protein kinase (AMPK) activation influences osteoblast differentiation and osteocyte survival, suggesting its therapeutic potential.
Conclusions:
- Diabetic bone fragility is a significant complication involving metabolic dysregulation and cellular dysfunction.
- Adenosine monophosphate-activated protein kinase (AMPK) presents a promising therapeutic target for mitigating diabetic bone fragility by enhancing bone formation and osteocyte protection.
- Further research into osteocalcin's role and AMPK activation is crucial for developing effective treatments for diabetic bone disease.

