Characterization of the mechanisms underlying omega-3 fatty acids effects on energy balance

Abstract

Recent studies from our laboratory have shown that increased body content of omega 3 (n-3) fatty acids, through the intake of a diet rich in fish oil or expression of fat-1 desaturase which converts omega 6 to n-3, protect mice from diet induced obesity, inflammation and glucose intolerance. Interestingly, such protection from obesity induced by n-3 fatty acids occur independently of changes in food intake, indicating a likely involvement of energy expenditure as a underlying cause. Herein we will test the hypothesis that n-3 fatty acids enhance energy expenditure in mice through the modulation of uncoupling protein-1 (UCP-1) dependent and independent thermogenesis. To test this hypothesis we will perform two different protocols: first we will assess the effects of different concentrations of n-3 fatty acids on C57BL/6J mice body weight, energy balance, adiposity, energy expenditure, sympathetic activity to brown and white adipose tissue, mitochondrial content and function, hypothalamus-pituitary-thyroid status, body temperature, and brown and white adipose tissues morphology, contents of UCP1, deiodinase type 2, SERCA 1 e 2, and other thermogenesis- related proteins. In the second protocol, we will evaluated the same parameters in wild-type and UCP-1 deficient mice fed with a regular high-fat diet or a fish oil enriched diet to investigate the contribution of nonshivering thermogenesis to the increase in energy expenditure induced by n-3 fatty acids. (AU)