Glucagon‐like peptide‐1 is involved in fasting and postprandial blood flow regulation of subcutaneous adipose tissue

Aims Glucagon‐like peptide 1 (GLP‐1) is a gastrointestinal hormone with pleiotropic functions, including vasodilatory and vasculoprotective effects. As GLP‐1 increases after a meal, it could be involved in adipose tissue blood flow (ATBF) regulation. In one‐third of healthy people, the postprandial ATBF response to meals is blunted. Whether this responder/non‐responder phenomenon stems from an incretin defect is not known. Thus, we aimed to assess the implication of GLP‐1 in ATBF regulation and responder/non‐responder status. Materials and Methods ATBF at the anterior abdominal wall was recorded using the 133 Xenon washout technique. Fasting and post‐oral glucose ATBF were assessed during local microinfusion of a GLP‐1 receptor antagonist exendin(9‐39). Physiological ATBF was recorded at the control saline site. Anthropometric and metabolic parameters were measured as well. Results Twenty‐seven healthy individuals (8 men) participated, and 14 responders (ATBF increase >50% of baseline values) and 13 non‐responders were identified. Compared to the control site, exendin(9‐39) significantly decreased fasting (0.16 [0.41; 0.04] vs. 0.04 [0.17; 0.14] mL 100 g −1 min −1 ; p = 0.001) and post‐glucose ATBF (iAUC: 45.2 [9.0; 150.9] vs. 49.8 [13.3; 216.6] mL 100 g −1 min −1 ; p < 0.001). Exendin(9‐39) led to comparable relative suppression of post‐glucose ATBF in responders and non‐responders (20.9 [45.6; 12.2] vs. 15.1 [66.5; −0.1] %; p = 0.84). In non‐responders, post‐glucose triacylglycerols (TAG) were significantly higher. Conclusions GLP‐1 seems to be involved in ATBF regulation, which is reduced when GLP‐1 action is blocked in situ, but has no role in the blunting of ATBF response in non‐responders. Blunted postprandial ATBF may be implicated in higher postprandial circulating TAG levels.