Bilirubin, a Cardiometabolic Signaling Molecule (Sep 22, 2018)

Saturday, September 22, 2018

Hello folks,

It is time for the next article which I am sharing on my website. Today we are going to discuss the following article published in the October issue of American Heart Association’s Hypertension Journal.

Title of the Article: Bilirubin, a Cardiometabolic Signaling Molecule

Authors: Terry D. Hinds Jr, David E. Stec

The link: https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.118.11130

My interpretation and analysis: Bilirubin has long been believed to be a waste product of red blood cell metabolism. It is produced by the catabolism of the heme pigment, and binds to albumin in the blood in the unconjugated form. Then it travels to the liver, gets conjugated with glucuronic acid, and secreted with bile into the intestines as conjugated bilirubin.

The unconjugated bilirubin (UCB) is the yellow pigment that is responsible for the yellow appearance of the skin and eyes, when a patient has jaundice. Previously considered just to be a waste product, new research shows that UCB has many protective effects against cardiovascular and metabolic disease.

One of the most protective features of UCB is to act as an antioxidant to protect the tissues against reactive oxygen species (ROS) by increasing nitric oxide (NO) bioavailability, especially in the heart and kidneys. UCB treatment has been shown in mice to reduce body weight, body fat and increase lean body mass. It also decreases fasting blood glucose levels, thereby preventing diabetes mellitus, and also protects against stroke. Some of these protective features are mediated by augmentation of PPARꭤ activity, whereas some are independent of PPARꭤ activity, such as opposing angiotensin-II-dependent hypertension. More studies are needed to elucidate these effects in greater detail.

UCB has effects on the lipid profile as well. It causes lowering of total cholesterol, LDL cholesterol and oxidized LDL. Biliverdin reductase (BVR) is the enzyme responsible for the formation of UCB from biliverdin, and studies have shown that loss of BVR is associated with worse cellular outcomes.

It is worthwhile mentioning that the protective effects are limited to UCB and conjugated bilirubin does not have any of these effects.

The future in my opinion: I feel that these preliminary results into the beneficial effects of UCB are promising, but they need more validation in the future. It is not unthinkable that at some point in future, we can utilize drug therapy to pharmacologically increase a patient’s UCB levels in order to protect against diabetes mellitus, hypertension, chronic kidney disease, obesity and hyperlipidemia. Please share with me how, in your opinion, this research can impact future therapeutic protocols?

I thank you for taking the time to visit my website. We have a lot of work to do to defeat the menace of hypertension. Please join me in my quest to eradicate this disease from our planet. This is the best gift we can give to our future generations.

Kashif J. Piracha, MD
Houston, Texas
United States

 

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