2018
DOI: 10.1016/j.jnutbio.2018.07.006
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Maternal diet-induced obesity during suckling period programs offspring obese phenotype and hypothalamic leptin/insulin resistance

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Cited by 53 publications
(41 citation statements)
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“…Transcriptomic assessment of baboon fetal livers born to mothers fed high-fat/high-fructose diet indicated dysregulation of the TCA cycle, glycolysis, changes in Wnt/β-catenin signaling, and marked lipid accumulation 15 . Epigenome-wide methylation changes 16 and hypothalamic leptin and insulin resistance are postulated to be contributing factors 17 . These studies provide evidence that maternal obesity is a risk factor for offspring metabolic programming.…”
Section: Ghmentioning
confidence: 99%
“…Transcriptomic assessment of baboon fetal livers born to mothers fed high-fat/high-fructose diet indicated dysregulation of the TCA cycle, glycolysis, changes in Wnt/β-catenin signaling, and marked lipid accumulation 15 . Epigenome-wide methylation changes 16 and hypothalamic leptin and insulin resistance are postulated to be contributing factors 17 . These studies provide evidence that maternal obesity is a risk factor for offspring metabolic programming.…”
Section: Ghmentioning
confidence: 99%
“…The meta-analysis conducted by Ribaroff et al [ 20 ] on 171 experimental studies identified that the exposure to high fat diet during the lactation period was a key modulator of bodyweight of the offspring at weaning and in adulthood, with a significantly greater effect on offspring fat mass than when WD exposure occurred during pregnancy alone [ 21 ]. High exposure to a WD during the breastfeeding phase is also associated with hyperinsulinemia, hyperglycemia, pancreatic islet hypertrophy, insulin resistance, hyperphagia, and overweight in male offspring [ 22 ]. Indeed, the development of dys-metabolic and non-alcoholic hepatic steatosis phenotype observed in offspring exposed to maternal obesity in the postpartum period has been suggested to be induced by factors in breast milk which probably modify the brain centers of energetic homeostasis [ 21 ].…”
Section: Introductionmentioning
confidence: 99%
“…It has been reported that insulin resistance and chronic inflammation contribute to hepatic lipid accumulation (43). There are also suggested effects of maternal HF diet and GTE intake on the formation of predispositions to hepatic lipid accumulation in offspring (44)(45)(46). Therefore, further study is necessary to clarify the mechanism underlying the preventive effects of maternal GTE intake on hepatic lipid accumulation.…”
Section: Discussionmentioning
confidence: 99%