Department of Medicine, Division of Endocrinology, University Hospital Center of Sherbrooke, University of Sherbrooke, Sherbrooke, Quebec, Canada; and.
Department of Medicine, Division of Endocrinology, University Hospital Center of Sherbrooke, University of Sherbrooke, Sherbrooke, Quebec, Canada; and Clinical Research Center, University Hospital Center of Sherbrooke, Sherbrooke, Quebec, Canada.
Am J Physiol Endocrinol Metab. 2015 Jul 1;309(1):E55-62. doi: 10.1152/ajpendo.00016.2015. Epub 2015 May 12.
Acetylcholine (Ach) has vasodilatory actions. However, data are conflicting about the role of Ach in regulating blood flow in subcutaneous adipose tissue (ATBF). This may be related to inaccurate ATBF recording or to the responder/nonresponder (R/NR) phenomenon. We showed previously that healthy individuals are R (ATBF increases postprandially by >50% of baseline BF) or NR (ATBF increases ≤50% postprandially). Our objective was to assess the role of the cholinergic system on ATBF in R and NR subjects. ATBF was manipulated by in situ microinfusion of vasoactive agents (VA) in AT and monitored by the (133)Xenon washout technique (both recognized methods) at the VA site and at the control site. We tested incrementally increasing doses of Ach (10(-5), 10(-3), and 10(-1) mol/l; n = 15) and Ach receptor antagonists (Ra) before and after oral administration of 75-g glucose using atropine (muscarinic Ra; 10(-4) mol/l, n = 13; 10(-5) mol/l, n = 22) and mecamylamine (nicotinic Ra; 10(-3) mol/l, n = 15; 10(-4) mol/l, n = 10). Compared with baseline [2.41 (1.36-2.83) ml·100 g(-1)·min(-1)], Ach increased ATBF dose dependently [3.32 (2.80-5.09), 6.46 (4.36-9.51), and 10.31 (7.98-11.52), P < 0.0001], with no difference between R and NR. Compared with control side, atropine (both concentrations) had no effect on fasting ATBF; only atropine 10(-4) mol/l decreased post-glucose ATBF [iAUC: 1.25 (0.32-2.91) vs. 1.98 (0.64-2.94); P = 0.04]. This effect was further apparent in R. Mecamylamine had no impact on fasting and postglucose ATBF in R and NR. Our results suggest that the cholinergic system is implicated in ATBF regulation, although it has no role in the blunting of ATBF response in NR.
乙酰胆碱（Ach）具有血管扩张作用。然而，关于 Ach 在调节皮下脂肪组织（ATBF）血流中的作用，数据存在矛盾。这可能与不准确的 ATBF 记录或应答者/无应答者（R/NR）现象有关。我们之前曾表明，健康个体是 R（餐后 ATBF 增加超过基础 BF 的 50%）或 NR（餐后 ATBF 增加≤50%）。我们的目的是评估胆碱能系统在 R 和 NR 受试者中对 ATBF 的作用。通过在 AT 中局部微输注血管活性物质（VA）来操纵 ATBF，并通过（133）氙洗脱技术（两者均为公认的方法）在 VA 部位和对照部位监测 ATBF。我们使用阿托品（毒蕈碱受体拮抗剂；10(-4)mol/l，n=13；10(-5)mol/l，n=22）和氨甲酰胆碱（烟碱受体拮抗剂；10(-3)mol/l，n=15；10(-4)mol/l，n=10）在口服 75g 葡萄糖前后，逐步测试了 Ach（10(-5)、10(-3)和 10(-1)mol/l；n=15）和 Ach 受体拮抗剂（Ra）的递增剂量。与基线相比[2.41（1.36-2.83）ml·100g(-1)·min(-1)]，Ach 呈剂量依赖性增加 ATBF[3.32（2.80-5.09），6.46（4.36-9.51）和 10.31（7.98-11.52），P<0.0001]，R 和 NR 之间无差异。与对照侧相比，阿托品（两种浓度）对空腹 ATBF 无影响；只有阿托品 10(-4)mol/l 降低了餐后葡萄糖 ATBF[iAUC：1.25（0.32-2.91）vs.1.98（0.64-2.94）；P=0.04]。这种效应在 R 中更为明显。氨甲酰胆碱对 R 和 NR 的空腹和餐后葡萄糖 ATBF 没有影响。我们的结果表明，胆碱能系统参与了 ATBF 的调节，尽管它在 NR 中对 ATBF 反应迟钝没有作用。
