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母体膳食蔗糖或果葡糖浆对 CD36、瘦素和胃饥饿素介导的肥胖胎儿编程的潜在影响。

Potential effect of maternal dietary sucrose or fructose syrup on CD36, leptin, and ghrelin-mediated fetal programming of obesity.

机构信息

Department of Nutrition and Dietetics, Faculty of Health Sciences, Hacettepe University, Sıhhiye 06100, Ankara, Turkey.

出版信息

Nutr Neurosci. 2020 Mar;23(3):210-220. doi: 10.1080/1028415X.2018.1491151. Epub 2018 Jul 1.

DOI:10.1080/1028415X.2018.1491151
PMID:29961406
Abstract

The influence of HFCS (high fructose corn syrup - free fructose) and sucrose (bound fructose) on fetal appetite signals is unknown. This study aimed to determine the effects of HFCS or sucrose on the peptide-mediated appetite regulation in fetal programming of obesity. Sprague Dawley female rats were administered feed and plain water (control) or water containing maltodextrin (vehicle), sucrose, fructose, or HFCS (20%, w/v) for 12 weeks before mating and throughout pregnancy and lactation ( = 31; = 207). Maternal chow-feed consumption in the HFCS and sucrose groups and sugar-added drink consumption in the HFCS group were higher compared to the vehicle and control groups ( < 0.05). The total body fat accumulated in sucrose, fructose, and HFCS groups in dams and pups was higher than those in the vehicle and control groups ( < 0.05). The HFCS groups showed lower plasma leptin levels and higher ghrelin levels. Soluble CD36 levels in plasma and tongue samples were high in HFCS groups of dams and pups ( < 0.05). Rather than bound fructose, the free fructose from the maternal diet contributes to the programming of obesity through the disruption of leptin, ghrelin, and CD36 expression involved in appetite regulation.

摘要

HFCS(高果糖玉米糖浆-无游离果糖)和蔗糖(结合果糖)对胎儿食欲信号的影响尚不清楚。本研究旨在确定 HFCS 或蔗糖对肥胖胎儿编程中肽介导的食欲调节的影响。在交配前 12 周以及整个妊娠和哺乳期,给予 Sprague Dawley 雌性大鼠饲料和白开水(对照)或含麦芽糖糊精(载体)、蔗糖、果糖或 HFCS(20%,w/v)的水(n = 31;n = 207)。与载体和对照组相比,HFCS 和蔗糖组的母鼠饲料消耗和 HFCS 组的加糖饮料消耗较高(<0.05)。与载体和对照组相比,蔗糖、果糖和 HFCS 组的母体和幼体总体脂积累较高(<0.05)。HFCS 组的血浆瘦素水平较低,胃饥饿素水平较高。母鼠和幼鼠 HFCS 组的血浆和舌样本中可溶性 CD36 水平较高(<0.05)。不是结合果糖,而是来自母体饮食的游离果糖通过破坏与食欲调节相关的瘦素、胃饥饿素和 CD36 表达,导致肥胖的发生。

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