[The hypotriglyceridemic effects of polyunsaturated fatty acids: pathogenetic hypothesis]

A large number of experimental and clinical studies focused the attention on the role played by omega-3 polyunsaturated fatty acids on the primary prevention of vascular diseases of atherosclerotic origin, especially influencing plasma triglycerides decrease. Aim of the present work was to investigate whether a relationship between triglyceride synthesis and human energy metabolism could exist, in order to explain the hypotriglyceridemic effect of omega-3 fatty acids that could be due to any thermogenic action. Eight male subjects aged 45 years (from 20 to 62) were studied, selected on the basis of high levels of triglycerides (536.7 +/- 204.3 mg/dl), normal or high levels of total serum cholesterol (219.4 +/- 51.2 mg/dl), normal or low HDL-cholesterol (33.6 +/- 6.3 mg/dl) and moderate obesity (BMI 30.3 +/- 1.7). Anthropometric parameters (body weight, height, waist to hip ratio), body composition measurements (fat free mass, fat mass), biochemical parameters were evaluated before and 10-days after PUFAs supplementation (student t paired test) at the compressive dose of 60 mg/kg BW bis in die. At the end of the observation significant decrease of triglycerides was documented (p < 0.005), while total and HDL-cholesterol did not vary significantly, although improved values were noticed. No change in anthropometric, body composition and energy metabolism parameters was demonstrated, except for respiratory quotient and substrates oxidation: a significant increment of respiratory quotient value (p < 0.05) due both to augmented carbohydrates oxidation (p < 0.05) and correspondent lipid oxidation reduction (p < 0.05) and correspondent lipid oxidation reduction (p < 0.05) without any change in the daily total calorie consumption. In conclusion, from a clinical point of view it is possible to hypothesize, even if in a small number of subjects, that PUFAs hypotriglyceridemic effect could derive from a reduced substrate availability, due to the higher carbohydrate oxidation. In other terms, considering the metabolic cascade of triglyceride synthesis, the augmented drug-induced carbohydrate consumption could provoke a reduced availability of products of intermediate metabolism useful to triglycerides hepatic synthesis.