Treatment with a hormone from the body that has cardiovascular benefits can provide multisystem protection from the negative consequences of the metabolic syndrome, such as insulin resistance, nonalcoholic fatty liver disease and fat-tissue inflammation. This finding comes from a new study that will be presented Saturday at The Endocrine Society’s 92nd Annual Meeting in San Diego.
The hormone, called angiotensin 1-7, was effective in an established animal model of the metabolic syndrome, said Yonit Marcus, MD and Naftali Stern, MD, of Tel Aviv University Faculty of Medicine in Tel Aviv, Israel. This syndrome refers to a group of metabolic risk factors linked to overweight.
“No specific form of medical therapy for the metabolic syndrome presently exists, and good tools to curb the illnesses associated with the obesity epidemic are nowhere in sight,” Stern said. “These results, if applicable in humans, may have a huge public health impact.”
The metabolic syndrome affects about 25 percent of adults and increases the likelihood of developing heart disease, stroke, diabetes and liver damage. This cluster of cardiovascular risk factors includes excess belly fat, abnormal cholesterol, and high blood glucose (sugar) and blood pressure.
In the body, the hormone angiotensin II normally helps control blood pressure, but when overactive, as can occur in obesity and diabetes, it makes the body less sensitive to the effect of insulin. The product of angiotensin II metabolism, angiotensin 1-7, opposes many of the negative effects of excess angiotensin II, including high blood pressure, kidney disease, heart failure and abnormal heart rhythms, according to Stern.
Stern, with researchers from Tel Aviv University and from the Weizmann Institute of Science in Rehovat, Israel, studied the effects of angiotensin 1-7 on rats fed a diet rich with high fructose sugar. In this model, rats eventually develop characteristics similar to those of the human metabolic syndrome.
For six months the researchers pumped a continuous infusion of angiotensin 1-7 into six rats. They gave no treatment to nine rats, which served as the control group.
By the end of six months, rats given angiotensin 1-7 weighed less and had less fat mass than did controls, the authors reported. Also, the angiotensin-treated rats had lower triglycerides (blood fats), smaller increases in blood sugar, less insulin resistance and lower blood levels of aldosterone. This hormone, when elevated, can cause high blood pressure.
Compared with controls, the treated rats also had reduced deposition of fat in the liver (“fatty liver”) and less fat-tissue inflammation. This inflammation is a possible “key process that explains the association between obesity and cardiovascular disease,” Stern said.
It appears, Stern said, that angiotensin 1-7 has an anti-inflammatory effect on fat tissue.
