Fighting fat with fat improve adiposity with N-acyl taurines

Obesity is an ever-growing epidemic that results in immense health care costs due to its comorbidities of cardiovascular disease, diabetes and more. Obesity is a chronic disease characterized by excessive fat deposition that results in the impairment of health. Adipose tissue, commonly known as body fat, plays a central role in the development of obesity. Excessive dietary caloric intake and sedentary lifestyle lead to an imbalance of energy intake and usage, ultimately leading to a tremendous increase in adipose tissue. In healthy conditions, adipose tissue can expand and store the excess calories as fat, however, a constant excess energy surplus leads to an exhausted adipose tissue storage capacity that may lead to fat deposited in other tissues. A hallmark of obesity is the inflammatory response of adipose tissue that actively contributes to the worsening of metabolic health by the release of harmful molecules that negatively affect whole body metabolism. Strategies to improve adipose tissue function and reduce its inflammation are of great importance to combat obesity and its consequences. Alterations to diet can improve obesity, either through reduction of calories, or by incorporating functional foods that are precursors to biologically active molecules, which can offer benefits over pharmaceuticals due to their safety and lower risk of side effects. Specific types of fatty acids (FA) have been shown to reduce inflammation and are considered to be better for health (e.g., polyunsaturated FA). We will study how these FA are converted in the body to an understudied metabolite N-acyl taurines (NATs). NATs are a widely unknown type of fat that is evolutionary conserved from marine sponges and crayfish to mice and humans and has beneficial effects on insulin sensitivity, liver fat accumulation and systemic inflammation. We will explore whether those benefits are due to an effect on the adipose tissue function and inflammatory cells, using both cell culture and animal models of obesity. First, we will determine if NATs are involved in the fat storage or release process of the adipose tissue. Then we will also test if NATs contribute to the communication of adipocytes and inflammatory cells and finally assess if we can translate these results and determine their anti-inflammatory potential in a mouse model of obesity. Obesity is also one of the major risk factors for the development of the pregnancy complication gestational diabetes mellitus (GDM) that not only affects the mother but also can impact the unborn child negatively. Therefore, back in Austria we will further test whether these NATs can be also efficient to reduce inflammation upon inflammatory pregnancy disorders like GDM.

No additional funding sources recorded.