The study findings are critical in the development of preventative strategies for diabetic osteoporosis.
A study through the North American Menopause Society has found that a history of first-degree family members with diabetes is linked to increased bone mineral density (BMD), as well as to insulin resistance.
Understanding the early pathophysiology of altered BMD could be critical in the development of preventative strategies for diabetic osteoporosis, because patients with type 2 diabetes are often at an increased risk of fracture. Yet, while strong evidence has revealed normal to high BMD in most patients with type 2 diabetes, no data supports whether BMD is altered in patients with first-degree family history of diabetes.
This study included approximately 900 normoglycemic postmenopausal women with or without a first-degree family history of diabetes. BMD was measured using dual-energy x-ray absorptiometry. It was found that the BMD of the lumbar spine and femoral neck was significantly higher in participants with a first-degree family history of diabetes than in those without a history, even in women with normal blood glucose levels. These same participants additionally showed increased insulin resistance and hyperinsulinemia.
The findings, published in the journalMenopause, showed an association between a family history of diabetes and an increased bone density in postmenopausal women. Researchers believe that this finding may be related to higher insulin levels in women with a hereditary predisposition to diabetes, because insulin has a bone-building effect.
The researchers caution women of this cohort that they are at a higher risk of developing diabetes, which is associated with skeletal fragility and increased fracture risk.
Reference
Family History of Diabetes Linked to Increased Bone Mineral Density [press release]. Cleveland, Ohio. Published August 21, 2019.https://www.menopause.org/docs/default-source/press-release/bone-mineral-density-and-diabetes-family-history-8-21-19.pdf. Accessed August 26, 2019.