Possible New Treatment for Type 1 Diabetes-induced Osteoporosis
It is possible as a person with type 1 diabetes to develop a kind of osteoporosis; the disease can impair osteoblast activity and osteoblast death, which can ultimately cause poor bone health. Unfortunately, anti-resorptive treatments (a common osteoporosis management option) won’t work in this patient population. Researchers, therefore, have been looking into ways to treat type 1 diabetes-induced osteoporosis.
In April 2012, an article—“Amelioration of type 1 diabetes-induced osteopororsis by parathyroid hormone is associated with improved osteoblast survival”—was published in the Journal of Cellular Physiology. It is on a mice study done at Michigan State University, where researchers examined in intermittent parathyroid hormone (PTH) would stimulate bone remodeling. They were investigating that particular treatment because in healthy patients, PTH treatment does stimulate bone remodeling, and they hypothesized that it could also work in the type 1 diabetic patient population.
In the study, 8 µg/kg and 40 µg/kg intermittent PTH doses were given to both diabetic and non-diabetic mice. In non-diabetic mice, PTH treatment lowered fat pad mass and blood glucose levels; the same result was not seen in type 1 diabetic mice, however.
The higher dose of PTH (40 µg/kg) significantly increased tibial trabecular bone density in both groups of mice. Specifically in diabetic mice, the 8 µg/kg dose increased trabecular bone density. This increase was seen because the PTH treatment led to an increase in mineral apposition and osteoblast surface.
Another result of PTH treatment that could lead to better bone density for diabetics: in this study, it suppressed osteoblast apoptosis in diabetic mice. Additinoally, the higher PTH dose reversed diabetes-induced bone loss.
These results from diabetic mice are promising. The researchers concluded that intermittent PTH treatment could improve bone health in type 1 diabetics, given that it has an anabolic effect on osteoblasts.