Journal
FASEB JOURNAL
Volume 35, Issue 11, Pages -Publisher
WILEY
DOI: 10.1096/fj.202100355RRR
Keywords
ceRNA; diabetes; fetal programming; inulin; lncRNA
Categories
Funding
- National Natural Science Foundation of China [81870579, 81870545, 81570715, 81170736]
- Beijing Natural Science Foundation [7202163]
- Beijing Municipal Science & Technology Commission [Z201100005520011]
- National Key R&D Program of China [2017YFC1309603]
- National Key Research and Development Program of China [2016YFA0101002, 2018YFC2001100]
- Scientific Activities Foundation for Selected Returned Overseas Professionals of Human Resources and Social Security Ministry, Beijing Dongcheng District Outstanding Talent Funding Project [2019DCT-M-05]
- Medical Epigenetics Research Center, Chinese Academy of Medical Sciences [2017PT31036, 2018PT31021]
- Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences [2017PT32020, 2018PT32001]
- Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences [CIFMS2017-I2M-1-008]
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Maternal overnutrition is a risk factor for metabolic diseases in mothers and offspring. Inulin, a fructan-type plant polysaccharide, has prebiotic functions and is used as a natural antidiabetic supplement. Early maternal inulin intervention improved glucose metabolism in male offspring with hepatic lncRNA and mRNA expression differences compared to offspring from high-fat diet dams.
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 lncRNA expression in offspring; there lncRNAs are involved in metabolic pathways and the AMP-activated protein kinase signaling pathway. Importantly, the early maternal inulin intervention alleviated glucose metabolism by inhibiting the lncRNA Serpina4-ps1/let-7b-5p/Ppargc1a as a competing endogenous RNA in male offspring.
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