Improvement in glucose metabolism in adult male offspring of maternal mice fed diets supplemented with inulin via regulation of the hepatic long noncoding RNA profile

Abstract

Maternal overnutrition during pregnancy and lactation is an important risk factor for the later development of metabolic disease, especially diabetes, among mothers and their offspring. As a fructan-type plant polysaccharide, inulin has prebiotic functions and is widely used as a natural antidiabetic supplement. However, to date, the mechanism of maternal inulin treatment in the livers of offspring has not been addressed, especially with respect to long noncoding RNAs (lncRNAs).In this study, female C57BL6/J mice were fed either a high-fat diet (HFD) with or without inulin supplementation or a standard rodent diet (SD) during gestation and lactation. After the offspring were weaned, they were fed a SD for 5 weeks.At 8 weeks of age, the glucose metabolism indexes of the offspring were assessed, and their livers were collected to assay lncRNA and mRNA profiles to investigate the effects of early maternal inulin intervention on offspring. Our results indicate that male offspring from HFD-fed dams displayed glucose intolerance and an insulin resistance phenotype at 8 weeks of age. Early maternal inulin intervention improved glucose metabolism in male offspring of mothers fed a HFD during gestation and lactation. The lncRNA and mRNA profile data revealed that compared with the offspring from HFD dams, offspring from the early inulin intervention dams had 99 differentially expressed hepatic lncRNAs and 529 differentially expressed mRNAs. The differentially expressed lncRNA-mRNA coexpression analysis demonstrated that early maternal inulin intervention may change hepatic

Dietary inulin supplementation promote hepatic gluconeogenesis in goats

“…The observed reduction in blood insulin content and the consistent levels of glucagon and glucose in this study suggest that inulin attenuates insulin secretion from pancreatic β-cells Miao et al reported that 3.33 and 1.67 g/kg/day inulin supplementation signi cantly reduced blood glucose and insulin levels in gestational diabetes mellitus mice [24]. Similar results were reported by Zhang et al [25]that blood glucose and insulin levels in high-fat mice were signi cantly reduced when supplemented with 2 g/kg of inulin. However, blood glucose concentrations were comparable between the two groups in this study, suggesting that goats maintained a stable range of blood glucose to maintain their body and cellular function when inulin was supplemented.…”

“…However, blood glucose concentrations were comparable between the two groups in this study, suggesting that goats maintained a stable range of blood glucose to maintain their body and cellular function when inulin was supplemented. The discrepancy in the blood glucose content might be due to the difference in the variety and physiological stage, and the health status of animals [25,26].…”

Higher gestational weight gain delays wound healing and reduces expression of long non‐coding RNA KLRK1‐AS1 in neonatal endothelial progenitor cells

“…Elevated expression of lncRNA MEG3 induces endothelial dysfunction in HUVECs of IVF‐born offspring (Jiang et al., 2021 ). In rats, overnutrition of pregnant dams alters hepatic lncRNAs in male offspring (Zhang et al., 2021 ). Moreover, accumulating evidence suggests that lncRNAs are involved in the regulation of placental development and function (McAninch et al., 2017 ), which may have the potential to influence fetal development and program the fetus for diseases.…”

Preventive Epigenetic Mechanisms of Functional Foods for Type 2 Diabetes

“…For instance, the parental intake of five functional food oils has been shown to modulate miRNA expression in both the parent and offspring [47]. In addition, functional foods have also been shown to modulate the expression of lncRNA in parents and offspring [38,[48][49][50]. Essentially, in T2D, changes in the expression of non-coding RNAs have been observed in genes involved in insulin secretion and glucose metabolism, leading to alterations in their function [51,52].…”