Reversal of obese phenotype by dietary LC n-3 PUFA administered as either triglycerides or phospholipids.

To induce obesity, dyslipidemia and glucose intolerance, mice were fed a cHF diet between three and seven months of age, and then for nine more weeks on different diets (all containing 2 g metformin per kg diet). cHF+ω3TG and cHF+ω3PL diets were supplemented with ∼30 g DHA/EPA per kg diet. No significant differences between metformin-supplemented cHF diet and the cHF diet alone were observed with regard to any of the parameters shown above (e.g. cHF alone - weight gain: 46.0±2.0 g; epididymal WAT: 2160±204 mg; plasma triglycerides: 1.11±0.05 mmol/l; AUC glucose: 3395±231 mmol x 180 min; and plasma insulin: 400±47 pmol/l; not shown). Body weight gain was calculated as the difference in body weight between the beginning of the experiment and after eight weeks of treatment. Food intake was monitored weekly during weeks 2 to 8 of the dietary treatment. Glucose homeostasis was assessed by a glucose tolerance test in mice fasted overnight after eight weeks of treatment.Data are means±SEM (n = 8–9).a,bSignificant differences (ANOVA) compared with cHF and cHF+ω3TG, respectively. AU, arbitrary units; AUC, area under the glucose curve; FBG, fasting blood glucose; HMW: total, ratio of high molecular weight to total adiponectin; NEFA, non-esterified fatty acids; WAT, white adipose tissue.