Project 1

Due to excess intake of dietary calories and a sedentary lifestyle in modern society, obesity has risen at an alarming rate in the US (adult obesity prevalence reached to 42.4% in 2017-2018 according to CDC statistics). As a result, extra energy stored as lipids in various cells and tissues can negatively affect cell metabolism and homeostasis.

Obesity occurs when excess energy intake is stored as different lipid species in adipose tissue. Thus, intake of different types of caloric components is critical in determining the composition of stored lipids and lipid-mediated responses in obesity. Recent studies have linked overconsumption of high-fat diets to the epidemic of obesity. Dietary fatty acids (FA) are either saturated (e.g. 16:0 palmitic acid, PA; 18:0 stearic acid, SA) or unsaturated (e.g. monounsaturated 18:1 oleic acid, OA; polyunsaturated 18:2 linoleic acid, LA). Polyunsaturated FA include n-6 (omega-6, e.g. LA) and n-3 (omega-3, e.g. docosapentaenoic acid, DPA; eicosapentaenoic acid, EPA) FA, depending on the double bond position counting from the methyl end of the carbon chain. Given the different FA components in various high-fat diets (HFD), it is of interest to determine whether and how FA composition in HFD influences obesity and obesity-associated diseases.

Obesity is associated with increased cancer risk and mortality. Specifically, recent epidemiologic studies confirmed that excess body fat significantly increases the risk of at least 13 types of cancer, including breast, colon, liver and ovary cancer. While obesity is usually defined as a body mass index (BMI) of 30 or more, BMI alone cannot predict cancer susceptibility in obese individuals. In this project, we will dissect how different HFDs influence obesity-associated cancer through regulating immune cell metabolism and function.