The finding may point the way toward treatments for osteoporosis, a disease of low bone mass that usually affects post-menopausal women but that is also observed in Type 1 diabetes patients, said Dr. Gèrard Karsenty, professor of molecular and human genetics at Baylor College of Medicine (BCM) in Houston and senior author.
"If osteoporosis in diabetes is associated with the absence of amylin, this finding has therapeutic implications," he said.
Amylin, a member of the calcitonin hormone family, inhibits bone loss or resorption. It is secreted by the pancreatic ß-cells at the same as insulin. Type 1 diabetics no longer produce insulin or amylin because their ß-cells no longer function. Mice who lack amylin have less bone mass than those who produce the hormone because they destroy bone more rapidly as it is seen in classical osteoporosis said Karsenty. Perhaps, he said, finding a way to replace amylin will enable physicians in the future to prevent osteoporosis in Type I diabetes and possibly in other forms of osteoporosis.
The finding extends understanding of the connection between metabolic hormones and bone mass, he said. Previously, Karsenty and his team had demonstrated that leptin, a hormone associated with weight control, affects bone formation through a brain relay.
Researchers from BCM, Beth Israel Deaconess Medical Center, Harvard Medical School, the University of Pittsburgh School of Medicine, the University of Melbourne in Australia, Hanson Institute, in South Australia and Lund University Hospital in Sweden participated in the research.
The work was supported by the National Institutes of Health, the March of Dimes, the Children's Nutrition Research Center, the National Space Biomedical Research Institute and the National Health and Medical Research Council of Australia.
Journal
Journal of Cell Biology