RBM15 suppresses hepatic insulin sensitivity of offspring of gestational diabetes mellitus mice via m6A-mediated regulation of CLDN4

• Published in: Molecular medicine (Cambridge, Mass.) Vol. 29; no. 1; pp. 23 - 16
• Main Authors: Fang, Jie, Wu, Xiafei, He, Jie, Zhang, Hanwen, Chen, Xuyang, Zhang, Hua, Novakovic, Boris, Qi, Hongbo, Yu, Xinyang
• Format: Journal Article
• Language: English
• Published: England BioMed Central 20.02.2023; BMC
• Subjects: Animals; Claudin-4 - metabolism; CLDN4; Diabetes, Gestational - genetics; Diabetes, Gestational - metabolism; Female; Gestational diabetes mellitus (GDM); Humans; Insulin Resistance; Liver - metabolism; Metabolic syndrome; Metabolic Syndrome - metabolism; Methyltransferases - metabolism; Mice; N6-methyladenosine (m6A); Pregnancy; RBM15; RNA - metabolism; RNA modifications; RNA, Messenger - metabolism; RNA-Binding Proteins - genetics; RNA-Binding Proteins - metabolism; Gestational diabetes mellitus (GDM); N6-methyladenosine (m6A); CLDN4; RBM15; Metabolic syndrome; RNA modifications

Gestational diabetes Mellitus (GDM) is a common pregnancy-specific disease with high morbidity, which is linked to a high risk of obesity and diabetes in offspring. N6-methyladenosine modification of RNA is emerging as an important epigenetic mechanism that is widely manifested in many diseases. Thi...