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Amylin plays key role in preventing bone loss

by Ruth SoRelle, MPH

Gerald Karsenty, MD, PhD

Bone.

Most people do not think much about it until one breaks. Then they realize how much they depend on their bones to be strong and vital. It is their support.

The bone that makes up the skeleton is dynamic. Its production starts in the brain. In the laboratory of Gerard Karsenty, MD, PhD, professor of molecular and human genetics at Baylor College of Medicine, the talented French scientist and his colleagues seek to understand the origin and maintenance of this material so often taken for granted.

In a recent report in the Journal of Cell Biology, Karsenty has shown that amylin, a hormone secreted by the ß-cells in the pancreas, plays a key role in preventing bone loss.

“Bone resorption is an ongoing process. It also exemplifies the connection between metabolic hormones like leptin and amylin and the control of bone mass by showing that it can affect bone formation such as that affected by leptin and bone resorption controlled by amylin.

Karsenty demonstrated that lack of amylin production in type 1 diabetes might explain why people with this disease also experience considerable bone loss. The pancreatic ß-cells that produce insulin in normal people do not work. They produce neither insulin nor amylin.

Amylin’s normal function is to prevent the loss of bone or its resorption. Bone is not static. It goes through a constant recycling. Bones called osteoclasts clear away the old bone. Osteoblasts, another form of cell, deposit new bone, thus strengthening the all-important skeleton.

During periods of famine, bone gets short shrift as the body directs scant food resources to other organs. When food becomes plentiful, the body can take advantage to begin that dynamic process that strengthens bone. To do this, the body produces amylin. Amylin inhibits the production of the osteoclasts, keeping their numbers down so that their activities do not outpace those of the osteoblasts, which deposit new bone.

Osteoporosis presents a major health issue for type 1 diabetics whose pancreatic ß-cells are inactive, producing neither insulin nor amylin. The lack of amylin means there is no control on the production of osteoclasts. As a result, type 1 diabetics often suffer serious osteoporosis. Osteoporosis is most often found in women after menopause, when their bones become brittle and easily broken.

“If osteoporosis in diabetes is associated with the absence of amylin, this finding has therapeutic implications,” Karsenty said.

Mice that lack amylin have less bone mass than those who produce the hormone because they destroy bone more rapidly than 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 in Boston, Mass., the University of Pittsburgh School of Medicine in Pennsylvania, 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.

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