New York, May 6 (IANS) Researchers have identified the enzyme responsible for obesity-related hypertension that can lead to severe health issues such as heart attacks, kidney failure, organ damage, and weakened or ruptured blood vessels.

Obese individuals have an increased risk of diabetes and cardiovascular disease, including hypertension and the findings show promise of new treatment options.
“By comparing genetically obese rats to lean rats, we discovered that obese animals were deficient in the amino acid arginine due to elevated activity of the enzyme arginase, which breaks down this molecule,” said lead study author William Durante, professor at University of Missouri School of Medicine.
Although arginase is present throughout the body, it is primarily found in the liver. Its role is to assist in the breakdown of ammonia, which is eventually flushed out during urination.
However, Durante’s team found significantly increased arginase activity within blood vessels and in the blood of obese rats compared to lean animals.
“The problem with this development is that arginase depletes arteries and blood of arginine, which is needed to generate nitric oxide,” Durante said.
“Nitric oxide is a gas formed from arginine that relaxes blood vessels and lowers arterial blood pressure. The destruction of arginine by arginase reduces nitric oxide levels, leading to the constriction of blood vessels and high blood pressure,” he pointed out.
Using two methods to correct the arginine deficiency, Durante’s team first supplemented the diet of obese animals with the amino acid L-arginine which is commonly found in red meat, poultry, fish and dairy products.
The second method involved using drugs that block the activity of arginase. Although both approaches restored nitric oxide production and reversed hypertension in obese rats, the use of arginase-inhibiting drugs may be a better solution.
“Blocking arginase activity offers a more specific approach in treating hypertension, because you are directly targeting the underlying biochemical defect in obesity,” Durante said.
The study appeared in the journal Obesity.

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