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Eating High-Fat Meal Raises Blood’s Proinflammatory Factors; Vitamins E, C Counter Response

SAN FRANCISCO — In a series of studies designed to define the role of dietary macronutrients in the initiation of arterial inflammation that predisposes a person to atherosclerosis, University at Buffalo researchers have found that a high intake of glucose, or eating a high-fat, high-calorie fast-food meal causes an increase in the blood’s inflammatory components.

 However, they also have shown that the antioxidant vitamins E and C can nullify this inflammatory response.

 Results of the research were presented here today (June 16, 2002) at the annual meeting of the American Diabetes Association. “A meal high in calories and fat caused an increase in inflammatory markers that lasted three to four hours,” said Paresh Dandona, M.D., professor of medicine, head of the UB School of Medicine and Biomedical Sciences’ Division of Endocrinology, and senior author on the studies.

 “We think the influx of macronutrients may alter cell behavior and that genes are activated to produce more powerful enzymes and mediators that are potentially more damaging to the lining of blood vessels. Obese persons may have an ongoing abnormality of the white blood cells and the lining of blood vessels.” (Calories, fat, protein, carbohydrates and water, the major components of any food, are considered macronutrients.) “On the other hand, we found that one way to render an ‘unsafe’ meal ‘safe’ is to include antioxidant vitamins,” Dandona said.

 “The proinflammatory effect of glucose is stopped if right at the outset you give vitamins E and C.” The “meal” study was conducted with nine normal subjects who ate a 900-calorie breakfast — an egg-and-ham sandwich and hash browns from a fast-food restaurant — after an overnight fast. Blood samples were taken before eating and at one, two and three hours after eating to determine the concentration of oxygen free radicals, which can begin the inflammation cascade by injuring blood vessel linings, and of several blood mediators of inflammation.

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