Blood Pressure Hormone Can Trigger Obesity

Blood Pressure Hormone

New studies made by University of Iowa researchers help give an explanation for how a hormone system mostly detailed to deal with cardiovascular disease may lessen metabolism and promote obesity. The renin-angiotensin system (RAS) controls blood pressure and is predominant for cardiovascular well being. Most of the medicinal drugs used to treat hypertension (high blood pressure) and heart failure block or inhibit the RAS.

Increasing proof suggests that the RAS also performs a role in controlling energy stability and metabolic rate and for that reason could also be important in weight problems. But, depending on the place in the body this hormone approach is working, it may as well have opposing effects on weight gain.

When the RAS is increased in the brain, it raises energy expenditure through increasing resting metabolism, leading to weight reduction. Nonetheless, improved activity of the RAS circulating within the body or the peripheral RAS, which happens during weight problems in humans and experimental animals,  has the opposite effect, lowering resting metabolism and increasing weight gain.

Angiotensin

According to the senior author of the study and the UI assistant professor of pharmacology Justin Grobe, PhD, At a very simplistic level, you can think of the brain RAS as the gas pedal on metabolism and the peripheral (circulating) RAS as the brake, with angiotensin as the driver.

These new findings, released in the Aug. 9 issue of the journal Cell Reports, suggest that in mice, circulating angiotensin reduces resting metabolic rate via activating its less common receptor (angiotensin II type 2 receptor or AT2) principally on subcutaneous fat cells.

A more particular understanding of how the RAS acts in tissue-specific and receptor-precise methods to have an impact on energy balance may ultimately be priceless in developing new ways to deal with weight problems and the health problems associated with it.

Grobe and his colleagues, together with study author Nicole Littlejohn, PhD, studied genetically modified mice which have a hyper-activated brain RAS. These mice have improved resting metabolic rate and weight loss as compared to control mice despite having equivalent meals and physical activity.

The researchers learned that the expanded resting metabolic rate in mice is because of improved heat production (thermogenesis) within the pads of subcutaneous fat on the animals’ hips. This type of fat is ordinarily regarded “healthy.” In contrast, the abdominal fat surrounding the internal organs, which is believed to be “unhealthy,” didn’t exhibit elevated thermogenesis.

When the researchers activated AT2 receptors on the subcutaneous fat cells, the mice gained weight without altering feeding behavior, suggesting that activating AT2 receptors decreases resting metabolic rate. Activating AT2 mimics what would happen when the peripheral RAS is accelerated.

Specially, the team found that activating AT2 receptors reduces the quantity of UCP1 protein made in the subcutaneous fats cells. This protein is important for non-shivering heat production. Diminished quantities of UCP1 interfere with the ability of the fat cells to make heat.

According to Grobe If the fat cell is the thermogenic tissue (generating heat by burning calories), you can either have a bigger engine or you can push the gas pedal harder to create a larger effect. Our study shows that angiotensin is modulating the size of the engine (amount of UCP1), not how hard the gas pedal is being pushed.

He further added, In multiple ways, activation of the AT2 receptor [by increasing the peripheral RAS] is interfering with the capacity of the cell to make heat. It is very consistent with the clinical observation that peripheral angiotensin goes up during obesity. This is probably at least one of the mechanisms by which that excess angiotensin is perpetuating obesity. Because it is telling the body to slow down its metabolism as the body gets bigger.

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Reference: Science Daily

Written By: Dr. Marie Gabrielle Laguna Bedia