PTH Treatment of Type 1 Diabetes-induced Osteoporosis
Promising Results in a Mice Study
Type 1 diabetes can cause a particular type of osteoporosis; it can impair osteoblast activity and death, thus leading to poor bone health. One of the typical osteoporosis treatments—anti-resorptive treatments—won’t work in this patient population. An article was published in the April 2012 edition of the Journal of Cellular Physiology addressing a possible treatment option for type 1 diabetes-induced osteoporosis.
The article is “Amelioration of type 1 diabetes-induced osteoporosis by parathyroid hormone is associated with improved osteoblast survival,” and it covers a study done by researchers from Michigan State University. They investigated the use of intermittent parathyroid hormone (PTH) treatment as a way to stimulate bone remodeling in patients with type 1 diabetes-induced osteoporosis. In health subjects, that treatment does, in fact, stimulate bone remodeling, and it increases bone density: will it work in this patient population?
The researchers looked at how well 8 µg/kg and 40 µg/kg intermittent PTH worked in counteracting diabetic bone loss in mice. They compared non-diabetic mice and diabetic mice, and they saw that PTH treatment lowered fat pad mass and blood glucose levels in the non-diabetic mice—but not in type 1 diabetic mice.
The 40 µg/kg dose of PTH significantly increased tibial trabecular bone density in non-diabetic and diabetic mice. The lower dose (8 µg/kg) increased trabecular bone density in the diabetic mice; the increase in bone density was caused by an increase in mineral apposition and osteoblast surface (those are defective in type 1 diabetes patients).
Additionally, the PTH treatment suppressed osteoblast apoptosis in the diabetic mice; that could also lead to better bone density. The higher dose also reversed diabetes-induced bone loss.
Given these results in diabetic mice, the researchers conclude that intermittent PTH treatment may improve bone health in type 1 diabetes patients; it has an anabolic effect on osteoblasts, and this can increase trabecular bone volume.