The interleukin‐6 (IL‐6) output from subcutaneous, abdominal adipose tissue was studied in nine healthy subjects before, during and for 3 h after 1 h two‐legged bicycle exercise at 60 % maximal oxygen consumption. Seven subjects were studied in control experiments without exercise. The adipose tissue IL‐6 output was measured by direct Fick technique. An artery and a subcutaneous vein on the anterior abdominal wall were catheterized. Adipose tissue blood flow was measured using the 133Xe‐washout method. In both studies there was a significant IL‐6 output in the basal state and no significant change was observed during exercise. Post‐exercise the IL‐6 output began to increase after 30 min. Three hours post‐exercise it was 58.6 ± 22.2 pg (100 g)−1 min−1. In the control experiments the IL‐6 output also increased, but it only reached a level of 3.5 ± 0.8 pg (100 g)−1 min−1. The temporal profile of the post‐exercise change in the IL‐6 output closely resembles the changes in the outputs of glycerol and fatty acids, which we have described previously in the same adipose tissue depot. The difference is that it begins to increase ≈30 min before the glycerol and fatty acid outputs begin to increase. Thus, we suggest that the enhanced IL‐6 production post‐exercise in abdominal, subcutaneous adipose tissue may act locally via autocrine/paracrine mechanisms influencing lipolysis and fatty acid mobilization rate from this lipid depot.

Interleukin‐6 (IL‐6) was infused intravenously for 2.5 h in seven healthy human volunteers at a dose giving rise to a circulating IL‐6 concentration of ≈35 ng l−1. The metabolic effects of this infusion were studied in subcutaneous adipose tissue on the anterior abdominal wall and in the splanchnic tissues by the Fick principle after catheterizations of an artery, a subcutaneous vein draining adipose tissue, and a hepatic vein, and measurements of regional adipose tissue and splanchnic blood flows. In control studies without IL‐6 infusion subcutaneous adipose tissue metabolism was studied by the same technique in eight healthy subjects. The net release of glycerol and fatty acids from the subcutaneous abdominal adipose tissue remained constant in the control experiment. IL‐6 infusion gave rise to increase in net glycerol release in subcutaneous adipose tissue while the net release of fatty acids did not change significantly. In the splanchnic region IL‐6 elicited a pronounced vasodilatation, and the uptake of fatty acids and the gluconeogenic precursors glycerol and lactate increased significantly. The splanchnic net output of glucose and triacylglycerol did not change during the IL‐6 infusion. It is concluded that IL‐6 elicits lipolytic effects in human adipose tissue in vivo, and that IL‐6 also has effects on the splanchnic lipid and carbohydrate metabolism.

This study was conducted to investigate the role of splanchnic and adipose tissue in the regulation of fatty acid (FA) metabolism at rest, during 1 h of semi‐recumbent cycle exercise at 60 % of maximal power output and 3 h of recovery. In six post‐absorptive healthy volunteers catheters were placed in a radial artery, hepatic vein and a subcutaneous vein on the anterior abdominal wall. Whole body, and regional splanchnic and adipose tissue FA metabolism were measured by a constant infusion of the stable isotopes [U‐13C] palmitate and [2H5] glycerol and according to Fick's principle. The whole body rate of extracellular FA reesterification was similar at rest and during exercise (≈290 μmol min−1) and increased during recovery to a plateau of 390 μmol min−1. FA and triacylglycerol (TAG) uptake by adipose tissue was undetectable, but a constant but small glycerol uptake of ≈25 nmol (100 g)−1 min−1 was observed. From the FA taken up by the splanchnic area, 13 % was oxidized, 5–11 % converted to ketone bodies, and ≈35 % incorporated in TAG released both at rest and at the third hour of recovery from exercise. Splanchnic FA reesterification could account for 51 % and 58 % of whole body extracellular FA reesterification, of which half was accounted for by TAG released from the splanchnic area, at rest and in recovery, respectively. In conclusion, in the post‐absorptive state, adipose tissue contributes very little to extracellular FA reesterification and splanchnic reesterification can account for 50–60 %, implying that FA reesterification in other tissues is important. The extracellular FA reesterification rate does not change with exercise but is higher during recovery. Furthermore, the uptake of glycerol by adipose tissue indicates that adipose tissue can metabolize glycerol.