UCD Conway Institute researchers and their collaborators in France, the United States and Ireland have shown how genetic predisposition and specific environmental factors such as dietary fat intake interact to influence our risk of chronic disease. The results of the study involving over seventeen hundred French men and women are published in the current issue of the Journal of Nutrition and the December issue of the American Journal of Clinical Nutrition.
Scientists use the term metabolic syndrome to describe a cluster of health abnormalities such as abdominal obesity, abnormal blood lipid levels, hyperglycaemia and hypertension that can predispose a person to type 2 diabetes, stroke and heart disease. Although it is thought that metabolic syndrome stems from the interplay of both environmental and genetic factors, this group believe that metabolic stressors (high-fat diet, obesity, etc.) and low-grade, chronic inflammation may play a prominent role.
Led by Conway Fellow, Prof Helen Roche and senior postdoctoral scientist Dr Catherine Phillips, the researchers looked in particular at two proteins released during the early stages of the inflammatory process called signal transducer and activator of transcription 3 (STAT3) and complement component 3 (C3). Different alterations of these proteins have been previously identified in humans and occur as a result of changes to the genes encoding STAT3 and C3.
Commenting on the findings, Prof Roche says, “Further research concerning how saturated fats can amplify the negative effects of genetic background and how omega-3 polyunsaturated fatty acids can improve the protective effects of genetic background might lead to personalised or targeted strategies for prevention and treatment of conditions such as abdominal obesity, the metabolic syndrome & diabetes”.
The research is supported by the European Commission, Framework Programme 6 (LIPGENE).
