No evidence of an effect of alterations in dietary fatty acids on fasting adiponectin over 3 weeks.

OBJECTIVE

Little is known about the effects of alterations in fatty acid classes on adiponectin, a hormone secreted by the adipocyte known to be important in the development of diabetes and cardiovascular disease (CVD). Any factor, including diet, that may positively influence adiponectin gene expression or increase circulating levels might be useful for improving such metabolic abnormalities. We investigated the effects of alterations in dietary fatty acid saturation on fasting serum adiponectin and associated peptides.

METHODS AND PROCEDURES

Double-blind, randomized, crossover, 2 x 3-week residential intervention trial where 18 mildly hyperlipidemic adult men were provided with a high saturated:unsaturated fat (SFA:USFA) and lower SFA:USFA treatment separated by an uncontrolled 4-week washout. Only fatty acid profile was altered between treatments. Fasting blood samples were collected on days 0, 1, 7, 14, 21, 22 of each intervention period for the measurement of adiponectin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsC-RP), leptin, and ghrelin.

RESULTS

Body weight was kept constant (+/-1 kg) throughout each treatment. There was no detectable difference in fasting adiponectin at baseline (mean day 0 + day 1) between the treatment groups (mean +/- s.d.; high(SFA:USFA) = 7.0 +/- 1.7 vs. low(SFA:USFA) = 6.7 +/- 1.4 microg/ml, P > 0.05). There were neither significant between-treatment effects of fatty acid saturation (diet x time, P > 0.05) on serum adiponectin nor any significant between-treatment effects on serum TNF-alpha, IL-6, hsC-RP, leptin, or ghrelin (P > 0.05).

DISCUSSION

Fasting serum adiponectin was not detectably affected by alterations in dietary fatty acid profile in mildly hyperlipidemic men. There was no evidence that an increase in SFA content of the diet significantly worsened fasting serum adiponectin over a 3-week intervention period.