Maternal fructose consumption down-regulates Lxra expression via miR-206-mediated regulation

Yamazaki, Mirai; Munetsuna, Eiji; Yamada, Hiroya; Ando, Yoshitaka; Mizuno, Genki; Fujii, Ryosuke; Nouchi, Yuki; Kageyama, Itsuki; Teshigawara, Atsushi; Ishikawa, Hiroaki; Suzuki, Kôji; Shimono, Yohei; Hashimoto, Shuji; Ohashi, Koji

doi:10.1016/j.jnutbio.2020.108386

Cited by 25 publications

(25 citation statements)

References 42 publications

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“…Figure 1A,B shows data obtained from 60‐day‐old rats. No significant changes were observed in the biochemical parameters between both groups (Figure 1A), as reported previously 17 . In addition, no significant differences were observed in blood glucose and insulin levels between both groups in iv‐GTT (Figure 1B).…”

Section: Resultssupporting

confidence: 85%

Section: Resultsmentioning

confidence: 98%

“…While caloric intake was not significantly different between the groups (Additional file 1: Figure S1). 17 No significant difference was observed between the offspring of the control mothers and those of the fructose-fed mothers. 17 We investigated the effect of maternal fructose consumption on the serum triglyceride, TNFα, total cholesterol, and HDL cholesterol levels (Figure 1A,C), as well as on the insulin sensitivity (Figure 1B,D) of the rat offspring.…”

Section: Caloric Intake and Weight Changes In The Fructose Groupmentioning

confidence: 90%

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Maternal fructose intake predisposes rat offspring to metabolic disorders via abnormal hepatic programming

et al. 2021

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Given that fructose consumption has increased by more than 10‐fold in recent decades, it is possible that excess maternal fructose consumption causes harmful effects in the next generation. This study attempted to elucidate the mechanism of the harmful effects of excessive maternal fructose intake from the perspective of offspring liver function. Female rats during gestation and lactation were fed water containing fructose, and their offspring were fed normal water. We attempted to elucidate the mechanism of fructose‐induced transgenerational toxicity by conducting a longitudinal study focusing on hepatic programming prior to disease onset. Impaired Insulin resistance and decreased high‐density lipoprotein‐cholesterol levels were observed at 160 days of age. However, metabolic disorders were not observed in 60‐day‐old offspring. Microarray analysis of 60‐day‐old offspring livers showed the reduction of hepatic insulin‐like growth factor‐1 (Igf1) mRNA expression. This reduction continued until the rats were aged 160 days and attenuated Igf1 signaling. Hepatic microRNA‐29 (miR‐29a) and miR‐130a, which target Igf1 mRNA, were also found to be upregulated. Interestingly, these miRNAs were upregulated in the absence of metabolic disorder. In this study, we found that maternal fructose intake resulted in dysregulated expression of Igf1 and its target miRNAs in the offspring liver, and that these offspring were more likely to develop metabolic disorders. Abnormal hepatic programming induced by an imbalanced maternal nutritional environment is maintained throughout life, implying that it may contribute to metabolic disorders.

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Section: Resultssupporting

confidence: 85%

Section: Resultsmentioning

confidence: 98%

Section: Caloric Intake and Weight Changes In The Fructose Groupmentioning

confidence: 90%

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Maternal fructose intake predisposes rat offspring to metabolic disorders via abnormal hepatic programming

et al. 2021

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“…Our NGS results suggest that epigenetic regulation may be involved in the developmental programming of various adult diseases in an organ-specific manner. Additionally, maternal fructose exposure altered the miR-206 expression level in offspring liver that increased promoter methylation at Lxra gene [ 70 , 71 ]. Gut microbiota and their metabolites have shown the ability of epigenetic programming of multiple host tissues [ 72 ].…”

Section: Fructose and Gut Microbiotamentioning

confidence: 99%

The Impact of Gut Microbiome on Maternal Fructose Intake-Induced Developmental Programming of Adult Disease

Hsu

Chan

et al. 2022

Nutrients

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Excessive or insufficient maternal nutrition can influence fetal development and the susceptibility of offspring to adult disease. As eating a fructose-rich diet is becoming more common, the effects of maternal fructose intake on offspring health is of increasing relevance. The gut is required to process fructose, and a high-fructose diet can alter the gut microbiome, resulting in gut dysbiosis and metabolic disorders. Current evidence from animal models has revealed that maternal fructose consumption causes various components of metabolic syndrome in adult offspring, while little is known about how gut microbiome is implicated in fructose-induced developmental programming and the consequential risks for developing chronic disease in offspring. This review will first summarize the current evidence supporting the link between fructose and developmental programming of adult diseases. This will be followed by presenting how gut microbiota links to common mechanisms underlying fructose-induced developmental programming. We also provide an overview of the reprogramming effects of gut microbiota-targeted therapy on fructose-induced developmental programming and how this approach may prevent adult-onset disease. Using gut microbiota-targeted therapy to prevent maternal fructose diet-induced developmental programming, we have the potential to mitigate the global burden of fructose-related disorders.

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“…Promoter methylation at this gene is increased in male offspring, whereas it is decreased in female offspring after maternal fructose exposure. Lxra expression may also be affected by maternal fructose-induced changes in miR-206 expression in offspring liver [ 36 ].…”

Section: Maternal Fructose and Offspring Glucose And Lipid Metabolismmentioning

confidence: 99%

Maternal Fructose Diet-Induced Developmental Programming

Thompson

DeBosch

2021

Nutrients

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Developmental programming of chronic diseases by perinatal exposures/events is the basic tenet of the developmental origins hypothesis of adult disease (DOHaD). With consumption of fructose becoming more common in the diet, the effect of fructose exposure during pregnancy and lactation is of increasing relevance. Human studies have identified a clear effect of fructose consumption on maternal health, but little is known of the direct or indirect effects on offspring. Animal models have been utilized to evaluate this concept and an association between maternal fructose and offspring chronic disease, including hypertension and metabolic syndrome. This review will address the mechanisms of developmental programming by maternal fructose and potential options for intervention.

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Maternal fructose consumption down-regulates Lxra expression via miR-206-mediated regulation

Cited by 25 publications

References 42 publications

Maternal fructose intake predisposes rat offspring to metabolic disorders via abnormal hepatic programming

Maternal fructose intake predisposes rat offspring to metabolic disorders via abnormal hepatic programming

The Impact of Gut Microbiome on Maternal Fructose Intake-Induced Developmental Programming of Adult Disease

Maternal Fructose Diet-Induced Developmental Programming

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