Bile Acids May Treat Heart Disease

Heart disease treatments may be possible from bile acids

/ Author:  / Reviewed by: Joseph V. Madia, MD

(RxWiki News) Bile acids in the gut may be more important than for just processing dietary fat. They may also be a key to treating heart disease by exerting an anti-inflammatory effect.

A new theory suggests that a modified bile acid named INT-777 may prevent a build up of plaque inside artery walls that causes heart disease.

"Eat lean meat to reduce plaque build up in arteries."

Dr. Thijs Pols and Mitsunori Nomura, researchers from Ecole Polytechnique Fédérale de Lausanne's Laboratory of Integrative Systems Physiology in Switzerland, conducted experiments in mice, finding that the bile acid offered a protective effect.

INT-777 is able to activate a receptor in the membrane of gut cells called TGR5, which enhances the secretion of a hormone called Glucagon-Like Peptide-1 (GLP-1). GLP-1 is induced by feeding, and stimulates insulin secretion in response to glucose. It already is used in diabetes drugs.

During the study treated mice prone to a build up of fatty plaques inside their arteries received INT-777, which was found to significantly reduce plaque formation.

This is because those plaques contain inflammatory cells called macrophages that are generated in the bone marrow. Investigators replaced the bone marrow of the mice with that from wild healthy mice, or mice engineered to lack TGR5. Only the mice that received marrow from the healthy mice showed a substantial reduction in plaque formation after the INT-777 treatment. This accounted for the anti-inflammatory effect.

Though the bile acid offers significant protection, it is unlikely to interfere with immune response, which means it may not only benefit the heart, but also patients with other disorders such as metabolic syndrome.

The next step is clinical trials in humans to test the safety and effectiveness of INT-777.

The pre-clinical study was recently published in journal Cell Metabolism.

Reviewed by: 
Review Date: 
December 9, 2011
Last Updated:
December 14, 2011