A new study revealed that a potent antioxidant can improve immune dysfunction and oxidative stress caused by a high-fat diet.
In the United States, the average daily intake of trans-fat is approximately 5.8 grams, with saturated fat constituting approximately 11-12 percent of the diet. Additionally, fast food meals total approximately 55 percent of the diet for the average American. High-fat diets have been linked to immune dysfunction, including diminished numbers and function of white blood cells known as lymphocytes, increased susceptibility to infection and the development of oxidative stress, which damages cells.
In this new study, researchers investigated the mechanism in which high-fat diets suppress lymphocyte function in mice. The researchers evaluated the gene expression from lymphocytes in the small intestines to understand the role of oxidative stress in lymphocyte signaling. The study also evaluated the effect of the antioxidant lipoic acid on these changes. Lipoic acid is a unique antioxidant in that it is both fat and water soluble, and can regenerate other antioxidants such as glutathione, vitamin C and vitamin E.
The results of the study confirmed that a high-fat diet induced oxidative stress and immune suppression in the small intestine. Treatment with lipoic acid reversed the high-fat-diet-induced immune suppression and reduced the oxidative stress. Specifically, lipoic acid was shown to improve the transcription of genes important for B-lymphocyte receptors, which are receptors for white blood cells that mature in the bone marrow, as well as T-lymphocyte differentiation and free radical scavenging mechanisms.
The researchers stated, “The present study indicates that a high-fat diet can induce chronic oxidative stress, suppress signal transduction of gut-associated lymphocytes, and lead to an inhibition of mucosal immunity.”
Reference:
Cui J, Le G, Yang R, Shi Y. Lipoic acid attenuates high fat diet-induced chronic oxidative stress and immunosuppression in mice jejunum: A microarray analysis. Cell Immunol. 2009 Aug 11. Published Online Ahead of Print.