Dept. of Nutritional Sciences
School of Env & Biological Sci
Inst for Food, Nutrition and Health
61 Dudley Road
New Brunswick, NJ 08901
Oxidative damage, mitochondrial function, DNA repair, metabolic disease
Obesity and related complications such as fatty liver disease, diabetes pose a growing threat to population health in theUnited States and around the world. A greater understanding of the dietary factors and cellular mechanisms that lead to the development of obesity is essential to devising preventive and therapeutic strategies to combat these metabolic diseases. Oxidative stress such as that induced by consumption of high-fat diets is thought to be a causal factor in the development of obesity. Oxidative stress induces damage to cellular components, including DNA, which, if left unrepaired, can lead to mutations and tumorigenesis. Oxidative DNA lesions are repaired by the base-excision repair pathway which is initiated by DNA glycosylases such as 8-oxoguanine DNA glycosylase (OGG1). OGG1 recognizes and excises the most commonly formed oxidative DNA lesion, 8-oxo-G. We have reported that mice deficient in OGG1 are susceptible to obesity and fatty liver, indicating an unexpected by critical role for this DNA repair pathway in the development of metabolic disease. Additionally, preliminary data indicate that OGG1 may also play a role in the development of inflammatory bowel disease, especially ulcerative colitis. The overarching goals of the Sampath lab are to delineate the mechanisms that link oxidative DNA damage to obesity, metabolic syndrome, and inflammatory conditions and to identify dietary factors contributing to the development or prevention of DNA damage.