Preferential reduction in adipose tissue α-linolenic acid (18∶3ω3) during very low calorie dieting despite supplementation with 18∶3ω3

We have previously reported that the relative content of 18∶3ω3 in adipose triglyceride (TG) of women was reduced following major weight loss while on a very low calorie diet (VLCD). In an attempt to prevent this loss of 18∶3ω3 reserves, we have tested two VLCD supplemented with varying amounts of 18∶3ω3. The formula (FORM) and food VLCD (2.1–3.0 MJ or 500–700 kcal/d) contained 20 g/d of fat and provided the recommended dietary allowance for minerals and vitamins. FORM subjects (Group 1) were 5 women initial body mass index (BMI) of 36.8, 168% ideal body weight (IBW) who received 20 g/d of canola oil (1.6 g 18∶3ω3). Their mean weight loss was 23.9 kg in a 4–5 mon period. Food VLCD subjects (Group 2) were 6 women (BMI 33.9, 155% IBW) supplemented with 2 g/d of linseed oil (1.1 g 18∶3ω3). Their mean weight loss was 17.4 kg in a 2–3 mon period. Needle biopsies of adipose tissue were obtained from Group 1 before, at midpoint and after weight loss; and from Group 2 before and after weight loss. The adipose TG and serum (Group 1) were separated and their fatty acid composition determined by thin-layer and gas chromatography. In Group 1, adipose 18∶3ω3 fell from 0.65 to 0.59 wt%, then to 0.52 wt% during weight loss. In Group 2, it fell from 0.77 to 0.64 wt%. The fall in adipose 18∶3ω3 with weight loss was significant atP=0.01 (Group 1) andP<0.01 (Group 2). There were no differences between responses to the 1.1 g/d or 1.6 g/d 18∶3ω3 supplements. The relative content of 18∶3ω3 in serum free fatty acids from Group 1 was reduced after major weight loss. Thus, in both groups the ω3 supplementation did not help to maintain adipose tissue 18∶3ω3 during rapid weight loss, and its decrement may affect circulating lipid pools. As adipose 18∶2ω6 did not change with weight loss, this reduction in the ratio of ω6 precursor to ω3 precursor could eventually alter the balance of their products as well. This work was presented in part at the North American Society for the Study of Obesity, Sacramento, California, 1991.