Renaud Helen J, Klaassen Curtis D, Csanaky Iván L
Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas
Drug Metab Dispos. 2016 Mar;44(3):366-9. doi: 10.1124/dmd.115.064766. Epub 2016 Jan 7.
There is wide variation in how patients respond to therapeutics. Factors that contribute to pharmacokinetic variations include disease, genetics, drugs, age, and diet. The purpose of this study was to determine the effect of calorie restriction on the expression of Abcb1a in the intestine and whether calorie restriction can alter the absorption of an Abcb1a substrate (i.e., digoxin) in mice. Ten-week-old C57BL/6 mice were given either an ad libitum diet or a 25% calorie-restricted diet for 3 weeks. To determine digoxin absorption, mice were administered [(3)H]-labeled digoxin by oral gavage. Blood and intestine with contents were collected at 1, 2, 4, and 12 hours after digoxin administration. Concentrations of [(3)H]-digoxin in plasma and tissues were determined by liquid scintillation. Calorie restriction decreased plasma digoxin concentrations (about 60%) at 1, 2, and 4 hours after administration. Additionally, digoxin concentrations in the small intestine of calorie-restricted mice were elevated at 4 and 12 hours after administration. Furthermore, calorie restriction increased Abcb1a transcripts in the duodenum (4.5-fold) and jejunum (12.5-fold). To confirm a role of Abcb1a in the altered digoxin pharmacokinetics induced by calorie restriction, the experiment was repeated in Abcb1a/b-null mice 4 hours after drug administration. No difference in intestine or plasma digoxin concentrations were observed between ad libitum-fed and calorie-restricted Abcb1a/b-null mice. Thus, these findings support the hypothesis that calorie restriction increases intestinal Abcb1a expression, leading to decreased absorption of digoxin in mice. Because Abcb1a transports a wide variety of therapeutics, these results may be of important clinical significance.
患者对治疗药物的反应存在很大差异。导致药代动力学差异的因素包括疾病、基因、药物、年龄和饮食。本研究的目的是确定热量限制对小鼠肠道中Abcb1a表达的影响,以及热量限制是否会改变Abcb1a底物(即地高辛)的吸收。给10周龄的C57BL/6小鼠自由饮食或25%热量限制饮食,持续3周。为了测定地高辛的吸收情况,通过口服灌胃给小鼠施用[³H]标记的地高辛。在地高辛给药后1、2、4和12小时收集血液和含内容物的肠道。通过液体闪烁法测定血浆和组织中[³H] - 地高辛的浓度。热量限制使给药后1、2和4小时的血浆地高辛浓度降低(约60%)。此外,热量限制小鼠小肠中的地高辛浓度在给药后4和12小时升高。此外,热量限制使十二指肠(4.5倍)和空肠(12.5倍)中的Abcb1a转录本增加。为了证实Abcb1a在热量限制诱导的地高辛药代动力学改变中的作用,在给药4小时后在Abcb1a/b基因敲除小鼠中重复该实验。自由饮食和热量限制的Abcb1a/b基因敲除小鼠之间在肠道或血浆地高辛浓度上未观察到差异。因此,这些发现支持以下假设:热量限制增加肠道Abcb1a表达,导致小鼠对地高辛的吸收减少。由于Abcb1a转运多种治疗药物,这些结果可能具有重要的临床意义。