Background: A decreased content of n-3 fatty acids in erythrocyte membrane of type 1 diabetic patients, which is inversely related to plasma levels of HbA(1c), has been reported previously. Our aim in this study was to observe the changes after a low-dose n-3 fatty acid (330 mg/day docosahexaenoic acid and 630 mg/day eicosapentanoic acid) dietary intervention in the lipid composition of cell membrane and metabolic control (measured according to plasma HbA(1c) levels). Since changes in both parameters may alter transmembrane sodium transport or influence parameters measuring target organ damage, we also studied the neural conduction quality and activity of four sodium transporters.
Methods: Eighteen type 1 diabetic patients were randomly assigned to continue their usual diet (control group) or to supplement their diet with a daily low dose of n-3 fatty acids (supplemented group). The changes between baseline and end values of the following parameters were compared: HbA(1c), lipid and phospholipid composition of cell membrane, activity of four ion carriers and neural conduction quality.
Results: The dietary supplementation caused statistically significant changes in membrane lipid composition, particularly an increase of C22:6 (n-3) and the total n-3 fatty acid (respectively +0.90+/-1.14% vs. -0.44+/-1.23% and +1.36+/-1.62% vs. -0.5+/-1.80%, p<0.05). After the dietary supplementation, we also observed a significant decrease of HbA(1c) (-2.00+/-1.9% vs. -0.13+/-0.48%, p<0.05), without significant changes in the dose of insulin required, an increase in the motor conduction velocity by the median nerve (+2.12 +/-1.35 m/s vs. -0.8+/-2.34 m/s, p<0.05) and a decrease of the V(max) of the Na(+)-Li(+) countertransport (-96.6+/-111.2 vs. +58.1+/-81.3 micromol/l cell/h(-1), p<0.01).
Conclusion: A low-dose omega-3 fatty acid dietary supplementation may change the fatty acid composition of the cell membrane and improve the metabolic control of diabetes. Using this dose, we also observed a decrease of the maximal rate of Na(+)-Li(+) countertransport and a slight improvement of neural conduction.