Omega-3 fatty acid supplementation in obesity: The effect on adiponectin, leptin and insulin sensitivity

2011 
BACKGROUND: Obesity is associated with numerous comorbidities including type 2 diabetes mellitus, cardiovascular disease (CVD) and some cancers1,2. Obesity is independently associated with altered levels of biologically active proteins secreted by adipocytes, including the hormones adiponectin and leptin. Adiponectin has regulatory actions on energy homeostasis, fatty acid metabolism and insulin sensitivity3, whilst leptin serves as a short‐term adaptation to starvation, inhibiting feeding and increasing thermogenesis4. These adipokines are implicated in insulin resistance, hypertension and dyslipidemia, all of which are components of heart disease progression. With the high prevalence of CVD in the Western world, much attention has been given to the positive role of omega–3 fatty acids in the prevention and treatment of CVD. Current evidence suggests a dose dependent relationship exists between omega–3 fatty acid supplementation and changes in adiponectin and leptin levels5. This study aims to assess the effect of a high dose supplementation on these adipokines in overweight and obese individuals. METHODS: This pilot trial will enrol 40 participants [BMI≥25], each given 2000 mg/day of a commercially available omega–3 fatty acid preparation (4000mg marine lipid) for an 8 week period. Blood samples will be taken at baseline, 4 and 8 weeks, assessing fasting levels of leptin, adiponectin, blood lipids, markers of insulin sensitivity, liver function and fatty acid indices. Physical activity, fatigue and diet will also be monitored at intervals throughout the study. DISCUSSION: This abstract presentation will discuss preliminary data of the partially completed study not yet published . CONCLUSIONS: We propose that supplementation with omega–3 fatty acids will improve the levels of these adipokines with benefits to fatty acid indices, blood lipids and insulin sensitivity that may translate into a reduced risk of developing CVD, metabolic syndrome and diabetes.
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