Postprandial response of adiponectin, interleukin-6, tumor necrosis factor-α, and C-reactive protein to a high-fat dietary load

ObjectiveCirculating levels of adiponectin are low in obesity and metabolic disorders associated with increasing fat mass including insulin resistance and dyslipidemia. Body fat stores may be positively related to intake of dietary fat, but little is known of mechanisms by which serum adiponectin may be regulated through diet. We investigated acute effects of a high-fat load and changes in fatty acid saturation on circulating adiponectin and associated mediators of inflammation including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP).MethodsA high-fat test meal (59 ± 4 g fat; 71% of energy as fat) containing a high (∼71:29) or low (∼55:45) ratio of saturated:unsaturated fatty acids was given at breakfast on two occasions. Blood samples were collected at 0 (baseline), 1, 3, and 6 h for measurement of adiponectin, IL-6, TNF-α, and high-sensitivity CRP. A fat-exclusion lunch, snack, and dinner were also given and blood samples collected at 10 and 24 h.ResultsEighteen healthy, lean men completed the trial. There was no evidence of acute change in circulating adiponectin in response to the lipid bolus or a differential effect of fatty acid saturation on adiponectin, high-sensitivity CRP, or IL-6 (P > 0.05). IL-6 increased over 6 h on both treatments (time, P < 0.05). TNF-α decreased on the high saturated:unsaturated fatty acid treatment (treatment by time, P < 0.05). There were no significant correlations between circulating adiponectin and insulin on either dietary treatment in these normoglycemic subjects.ConclusionAcute changes in the content of saturated and unsaturated fatty acids had no adverse effect on postprandial circulation of the adipose-related factors adiponectin, IL-6, TNF-α, or high-sensitivity CRP.