Abstract Title:

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

Abstract Source:

Nutr Neurosci. 2018 Jul 1:1-11. Epub 2018 Jul 1. PMID: 29961406

Abstract Author(s):

Betul Kisioglu, Reyhan Nergiz-Unal

Article Affiliation:

Betul Kisioglu


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 (n= 31; n= 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 (P<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 (P<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 (P<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.

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