Adiponectin Helps Clear Away Apoptotic Cells

in Health & Medicine, News Releases, School of Medicine
January 25th, 2007

Contact: Gina M. Digravio, 617-638-8491 | gina.digravio@bmc.org

(Boston) – Researchers at the Boston University School of Medicine (BUSM) have found that a protein produced by fat cells has the ability to clear dead cells from the body, reducing inflammation that leads to autoimmune diseases, diabetes and heart disease.

The finding, reported in a paper in the Jan. 25 issue of The Journal of Clinical Investigation, may help in the understanding of these diseases and could lead to the development of new drugs to help treat or prevent them.

“Understanding how fat controls inflammation is a key to understanding how fat contributes to many disease processes,’’ said Kenneth Walsh, Director of Molecular Cardiology at the Whitaker Cardiovascular Institute at BUSM and senior author of the paper. “This study has figured out one of the mechanisms by which fat controls inflammation.’’

In animal studies, Walsh’s group showed that the protein, adiponectin, was able to reduce inflammation by helping macrophages or “eater cells’’ remove dead cells from the body, an essential feature of immune system function. Such dead cells are produced by the billions each day as the body’s cells are renewed.

“Adiponectin facilitates that process by forming a bridge between the dead cells and the macrophages that will consume them,’’ Walsh said.

The research could prove important, particularly now that the link between obesity and diabetes and cardiovascular disease has been made clear. “Obesity is becoming more and more prevalent in our society and in developing nations,’’ Walsh said. “And it goes hand in hand with diabetes and other diseases, including cardiovascular disease. It’s a major health issue.’’

Fat produces both pro-inflammatory and anti-inflammatory proteins. The right amount of fat protects the body from starvation and infection, but too much fat produces excessive pro-inflammatory proteins. These can induce inflammation that can lead to diabetes, heart disease and autoimmune disorders, according to Walsh. “The fat from lean, healthy people makes large amounts of protective anti-inflammatory proteins such as adiponectin.” “When you’re too fat, the pro-inflammatory proteins win out,’’ he said. “You make lower amounts of adiponectin.’’

In Walsh’s experiments, autoimmune mice given adiponectin showed diminished symptoms of autoimmunity. And autoimmune mice bred to lack adiponectin had more symptoms.

Autoimmune mice given adiponectin saw their inflammatory antibodies reduced by up to 80 to 90 percent, the paper showed.

The study “demonstrates that adiponectin can facilitate the removal of early (dead) cells by macrophages and modulate the processes of inflammation and autoimmunity,’’ the paper concludes.

It also demonstrates a link between obesity and systemic inflammation by showing that adiponectin functions to promote the clearance of dead cell debris, the paper adds.

“Because the accumulation of cell corpses can cause inflammation and immune system dysfunction, these findings suggest a new mechanism by which (low adiponectin level) can contribute to the development of diabetes, atherosclerosis and other compex diseases where chronic inflammation is a contributing feature,’’ the paper says.

The research, funded by the National Institute of Aging, could shed new light on the aging process, which is associated with immune system dysfunction, Walsh said, and could lead to the development of new drugs to elevate adiponectin levels and suppress autoimmune diseases as well as cardiovascular diseases.

“It tells scientists that we should be looking at impaired clearance of apoptotic cells as having a more causal role in diabetes and cardiovascular disease,’’ he said. “It’s a new way of thinking about cardiovascular disease and diabetes.’’

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