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Diabetes can pose serious complications to bone health. “Clinical trials have revealed a startling elevation in fracture risk in diabetic patients,” says Liyun Wang, PhD, Associate Professor of Mechanical Engineering at the University of Delaware in Newark, Delaware. “Bone fractures can be life threatening — nearly 1 in 6 hip fracture patients dies within a year of injury.”
Because physical exercise is proven to improve bone properties and reduce fracture risk in non-diabetic people, Dr. Wang and colleagues tested its efficacy in type 1 diabetes. Their findings were published online ahead of print July 13 in Bone.
The researchers hypothesized that diabetic bone’s response to anabolic mechanical loading would be attenuated, partially due to impaired mechanosensing of osteocytes under hyperglycemia. For their study, heterozygous male and female diabetic mice and their age- and gender-matched wild-type controls were subjected to unilateral axial ulnar loading with a peak strain of 3500 με at 2 Hz and 3 minutes per day for 5 days.
Overall, the study demonstrated that exercise-induced bone formation was maintained in mildly diabetic mice at a similar level as non-diabetic controls, while the positive effects of exercise were nearly abolished in severely diabetic mice. At the cellular level, the researchers found that hyperglycemia reduced the sensitivity of osteocytes to mechanical stimulation and suppressed osteocytes’ secretion of proteins and signaling molecules that help build stronger bone.
“Our work demonstrates that diabetic bone can respond to exercise when the hyperglycemia is not severe, which suggests that mechanical interventions may be useful to improve bone health and reduce fracture risk in mildly affected diabetic patients,” said Dr. Wang. These results, along with previous findings showing adverse effects of hyperglycemia on osteoblasts and mesenchymal stem cells, suggest that failure to maintain normal glucose levels may impair bone’s responses to mechanical loading in diabetics.
To translate the findings of the study to patient care, Ms. Wang’s team has begun to collaborate with M. James Lenhard, MD, Director of the Center for Diabetes and Metabolic Diseases at Christiana Care Health System in Wilmington, Delaware.
“The plan for collaboration between the University of Delaware and Christiana Care is to evaluate these research findings in humans and expand the research to include other complications of diabetes, such as cardiovascular disease.
Suggested Reading
Parajuli A, Liu C, Wen L, et al. Bone’s responses to mechanical loading are impaired in type 1 diabetes. Bone. 2015 July 13 [Epub ahead of print].
Diabetes can pose serious complications to bone health. “Clinical trials have revealed a startling elevation in fracture risk in diabetic patients,” says Liyun Wang, PhD, Associate Professor of Mechanical Engineering at the University of Delaware in Newark, Delaware. “Bone fractures can be life threatening — nearly 1 in 6 hip fracture patients dies within a year of injury.”
Because physical exercise is proven to improve bone properties and reduce fracture risk in non-diabetic people, Dr. Wang and colleagues tested its efficacy in type 1 diabetes. Their findings were published online ahead of print July 13 in Bone.
The researchers hypothesized that diabetic bone’s response to anabolic mechanical loading would be attenuated, partially due to impaired mechanosensing of osteocytes under hyperglycemia. For their study, heterozygous male and female diabetic mice and their age- and gender-matched wild-type controls were subjected to unilateral axial ulnar loading with a peak strain of 3500 με at 2 Hz and 3 minutes per day for 5 days.
Overall, the study demonstrated that exercise-induced bone formation was maintained in mildly diabetic mice at a similar level as non-diabetic controls, while the positive effects of exercise were nearly abolished in severely diabetic mice. At the cellular level, the researchers found that hyperglycemia reduced the sensitivity of osteocytes to mechanical stimulation and suppressed osteocytes’ secretion of proteins and signaling molecules that help build stronger bone.
“Our work demonstrates that diabetic bone can respond to exercise when the hyperglycemia is not severe, which suggests that mechanical interventions may be useful to improve bone health and reduce fracture risk in mildly affected diabetic patients,” said Dr. Wang. These results, along with previous findings showing adverse effects of hyperglycemia on osteoblasts and mesenchymal stem cells, suggest that failure to maintain normal glucose levels may impair bone’s responses to mechanical loading in diabetics.
To translate the findings of the study to patient care, Ms. Wang’s team has begun to collaborate with M. James Lenhard, MD, Director of the Center for Diabetes and Metabolic Diseases at Christiana Care Health System in Wilmington, Delaware.
“The plan for collaboration between the University of Delaware and Christiana Care is to evaluate these research findings in humans and expand the research to include other complications of diabetes, such as cardiovascular disease.
Diabetes can pose serious complications to bone health. “Clinical trials have revealed a startling elevation in fracture risk in diabetic patients,” says Liyun Wang, PhD, Associate Professor of Mechanical Engineering at the University of Delaware in Newark, Delaware. “Bone fractures can be life threatening — nearly 1 in 6 hip fracture patients dies within a year of injury.”
Because physical exercise is proven to improve bone properties and reduce fracture risk in non-diabetic people, Dr. Wang and colleagues tested its efficacy in type 1 diabetes. Their findings were published online ahead of print July 13 in Bone.
The researchers hypothesized that diabetic bone’s response to anabolic mechanical loading would be attenuated, partially due to impaired mechanosensing of osteocytes under hyperglycemia. For their study, heterozygous male and female diabetic mice and their age- and gender-matched wild-type controls were subjected to unilateral axial ulnar loading with a peak strain of 3500 με at 2 Hz and 3 minutes per day for 5 days.
Overall, the study demonstrated that exercise-induced bone formation was maintained in mildly diabetic mice at a similar level as non-diabetic controls, while the positive effects of exercise were nearly abolished in severely diabetic mice. At the cellular level, the researchers found that hyperglycemia reduced the sensitivity of osteocytes to mechanical stimulation and suppressed osteocytes’ secretion of proteins and signaling molecules that help build stronger bone.
“Our work demonstrates that diabetic bone can respond to exercise when the hyperglycemia is not severe, which suggests that mechanical interventions may be useful to improve bone health and reduce fracture risk in mildly affected diabetic patients,” said Dr. Wang. These results, along with previous findings showing adverse effects of hyperglycemia on osteoblasts and mesenchymal stem cells, suggest that failure to maintain normal glucose levels may impair bone’s responses to mechanical loading in diabetics.
To translate the findings of the study to patient care, Ms. Wang’s team has begun to collaborate with M. James Lenhard, MD, Director of the Center for Diabetes and Metabolic Diseases at Christiana Care Health System in Wilmington, Delaware.
“The plan for collaboration between the University of Delaware and Christiana Care is to evaluate these research findings in humans and expand the research to include other complications of diabetes, such as cardiovascular disease.
Suggested Reading
Parajuli A, Liu C, Wen L, et al. Bone’s responses to mechanical loading are impaired in type 1 diabetes. Bone. 2015 July 13 [Epub ahead of print].
Suggested Reading
Parajuli A, Liu C, Wen L, et al. Bone’s responses to mechanical loading are impaired in type 1 diabetes. Bone. 2015 July 13 [Epub ahead of print].