Wellness & Fitness

New therapy for weak diabetics’ bones

diabetic

A diabetic patient injects insulin as a nurse looks on. FILE PHOTO | NMG

A new therapy is promising to reverse the bone weakening effect of diabetic drugs among patients.

The development, which came as an unexpected benefit in a study done on mice, may soon relieve bones pain and minimise risk of fractures that diabetics face.

Research published last month in the Stem Cell Journal shows that a compound dubbed TNP can promote transformation of new bone.

“This is in contrast to many diabetes drugs currently in wide use that leave patients’ bones weaker. There are millions and millions of people who have osteoporosis [with or without diabetes], and it’s not something we can cure,” says Sean Morrison, a stem cell researcher at the University of Texas Southwestern in Dallas.

Osteoporosis is a condition that weakens bones, making them fragile and more likely to break, typically as a result of hormonal changes, or deficiency of calcium or vitamin D.

Dr Morrison continues: “We need new agents that promote bone formation. If the therapy (TNP) has similar effects in humans, it may even be able to stimulate bone growth after fractures or prevent bone loss due to aging.”

Researchers say that for eight weeks, they injected mice with the therapy and a placebo.

The mice were also fed with normal high-fat diet and given daily injections of either TNP, a well-known IP6K1 inhibitor, or a placebo.

IP6K1 is a gene for an enzyme called inositol hexakisphosphate kinase 1, which plays a role in fat accumulation and insulin sensitivity.

When the animals’ bones and marrow were analysed, the scientists found that mice that had received TNP had significantly more bone cells, fewer fat cells, and greater overall bone area.

The IP6K1 inhibitor apparently protected the mice from the detrimental effects of the high-fat diet.

“The study provided the surprising result that one new therapy currently being explored to lower insulin resistance promotes, rather than decreases, the formation of bone in mice,” says Darwin Prockop, a stem cell researcher at Texas A and M College of Medicine in Temple.

Inhibition of IP6K1 is a promising target for patients with both diabetes and obesity, Dr Prockop says.

The scientists will take the research higher and test their findings in a wide range of bone-related diseases and disorders. It might even help heal broken bones, they speculate.

Dr Morison says most patients successfully manage diabetes with drugs that increase their insulin sensitivity, but that comes at the cost of decreased activity among cells that produce bones.

The findings show that a high-fat diet causes mice to develop bones that contain more fat and less bone cells.

Such diet increases the levels of leptin, a hormone produced by fat cells that usually signals satiety in the brain in the bone marrow, which promotes the development of fat cells instead of bone cells.

That shows that nutrition has a direct effect on the balance of bone and fat in the bone marrow.

Dr Anutosh Chakraborty, a molecular biologist who was studying such mice said that the animals lacked the gene for inositol hexakisphosphate kinase 1 enzyme.

The scientists suspected that the lost enzyme might affect the animals stem cells found in the bone marrow that is capable of developing into both the bone cells and fat cells that make up our skeletons.

If too many fat cells develop, they take the place of bone cells, weakening the bone.

The mice were fed with genetically altered and normal mice a high-fat diet for eight weeks.

Not only did the genetically altered mice develop fewer fat cells than their normal counterparts, but their production of bone cells was higher than that of the normal mice.