Pencek R Richard, Koyama Yoshiharu, Lacy D Brooks, James Freyja D, Fueger Patrick T, Jabbour Kareem, Williams Phillip E, Wasserman David H
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232-0615, USA.
J Appl Physiol (1985). 2003 Sep;95(3):1132-8. doi: 10.1152/japplphysiol.01172.2002. Epub 2003 May 9.
The purpose of this study was to assess whether a prior bout of exercise enhances passive gut glucose absorption. Mongrel dogs had sampling catheters, infusion catheters, and a portal vein flow probe implanted 17 days before an experiment. Protocols consisted of either 150 min of exercise (n = 8) or rest (n = 7) followed by basal (-30 to 0 min) and a primed (150 mg/kg) intraduodenal glucose infusion [8.0 mg x kg-1x min-1, time (t) = 0-90 min] periods. 3-O-[3H]methylglucose (absorbed actively, facilitatively, and passively) and l-[14C]glucose (absorbed passively) were injected into the duodenum at t = 20 and 80 min. Phloridzin, an inhibitor of the active sodium glucose cotransporter-1 (SGLT-1), was infused (0.1 mg x kg-1 x min-1) into the duodenum from t = 60-90 min with a peripheral venous isoglycemic clamp. Duodenal, arterial, and portal vein samples were taken every 10 min during the glucose infusion, as well as every minute after each tracer bolus injection. Net gut glucose output in exercised dogs increased compared with that in the sedentary group (5.34 +/- 0.47 and 4.02 +/- 0.53 mg x kg-1x min-1). Passive gut glucose absorption increased approximately 100% after exercise (0.93 +/- 0.06 and 0.45 +/- 0.07 mg x kg-1 x min-1). Transport-mediated glucose absorption increased by approximately 20%, but the change was not significant. The infusion of phloridzin eliminated the appearance of both glucose tracers in sedentary and exercised dogs, suggesting that passive transport required SGLT-1-mediated glucose uptake. This study shows 1). that prior exercise enhances passive absorption of intraduodenal glucose into the portal vein and 2). that basal and the added passive gut glucose absorption after exercise is dependent on initial transport of glucose via SGLT-1.
本研究的目的是评估先前的一次运动是否会增强肠道对葡萄糖的被动吸收。杂种犬在实验前17天植入采样导管、输液导管和门静脉血流探头。实验方案包括150分钟的运动(n = 8)或休息(n = 7),随后是基础期(-30至0分钟)和十二指肠内葡萄糖推注(150 mg/kg)后的输注期[8.0 mg·kg⁻¹·min⁻¹,时间(t)= 0至90分钟]。在t = 20和80分钟时,将3 - O - [³H]甲基葡萄糖(通过主动、易化和被动方式吸收)和l - [¹⁴C]葡萄糖(被动吸收)注入十二指肠。在t = 60至90分钟期间,通过外周静脉等血糖钳夹将活性钠葡萄糖共转运蛋白1(SGLT - 1)的抑制剂根皮苷(0.1 mg·kg⁻¹·min⁻¹)注入十二指肠。在葡萄糖输注期间,每10分钟采集十二指肠、动脉和门静脉样本,在每次示踪剂推注注射后每分钟采集样本。与久坐组相比,运动犬的肠道葡萄糖净输出增加(5.34 ± 0.47和4.02 ± 0.53 mg·kg⁻¹·min⁻¹)。运动后肠道对葡萄糖的被动吸收增加了约100%(0.93 ± 0.06和0.45 ± 0.07 mg·kg⁻¹·min⁻¹)。转运介导的葡萄糖吸收增加了约20%,但变化不显著。根皮苷的输注消除了久坐和运动犬体内两种葡萄糖示踪剂的出现,表明被动转运需要SGLT - 1介导的葡萄糖摄取。本研究表明:1)先前的运动增强了十二指肠内葡萄糖向门静脉的被动吸收;2)运动后基础期及额外的肠道葡萄糖被动吸收依赖于葡萄糖最初通过SGLT - 1的转运。