Behenic acid alleviates inflammation and insulin resistance in gestational diabetes mellitus by regulating TLR4/NF-κB signaling pathway
Kerong Liu,
Ying Gu,
Xingnan Pan,
Sha Chen,
Jie Cheng,
Le Zhang,
Minkai Cao
Affiliations
Kerong Liu
Department of Endocrinology, Affiliated Children’s Hospital of Jiangnan University (Wuxi Children’s Hospital), Wuxi 214023, Jiangsu, China
Ying Gu
Department of Obstetrics and Gynecology, Affiliated Women’s Hospital of Jiangnan University (Wuxi Maternity and Child Health Care Hospital), Wuxi 214002, Jiangsu, China
Xingnan Pan
Department of Pediatric, Affiliated Children’s Hospital of Jiangnan University (Wuxi Children’s Hospital), Wuxi 214023, Jiangsu, China
Sha Chen
Department of Obstetrics and Gynecology, Affiliated Women’s Hospital of Jiangnan University (Wuxi Maternity and Child Health Care Hospital), Wuxi 214002, Jiangsu, China
Jie Cheng
Center for Reproductive Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200135, China; Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai 200135, China; Corresponding author
Le Zhang
Department of Neonatology, Affiliated Children’s Hospital of Jiangnan University (Wuxi Children’s Hospital), Wuxi 214023, Jiangsu, China; Corresponding author
Minkai Cao
Department of Obstetrics and Gynecology, Affiliated Women’s Hospital of Jiangnan University (Wuxi Maternity and Child Health Care Hospital), Wuxi 214002, Jiangsu, China; Corresponding author
Summary: Gestational diabetes mellitus (GDM) is a distinct form of diabetes that poses a significant threat to the health of both pregnant women and fetuses. The objective of this study was to investigate the impact of behenic acid (BA) on glucose metabolism, inflammation, and insulin resistance in GDM mice, and to elucidate the underlying molecular mechanism. Here, we demonstrated that daily administration of 10 mg/mL BA during pregnancy effectively ameliorated abnormal glucose metabolism in GDM mice and their offspring and improved birth outcomes in the offspring. Moreover, BA promoted the proliferation of islet β cells, restored their normal function, and augmented glucose uptake by skeletal muscle cells. Mechanistically, BA mitigated inflammation and insulin resistance in GDM mice by inhibiting activation of the TLR4/NF-κB signaling pathway. Our study provides compelling evidence supporting the efficacy of BA in improving GDM, suggesting its potential use as a dietary supplement for preventing and treating GDM.
