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FGF4, A New Potential Regulator in Gestational Diabetes Mellitus
Miaojuan Fan1,2,3, Tongtong Pan1, Wei Jin1,4
1Department of Infectious Diseases & Zhejiang Provincial Key laboratory of Liver Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Fibroblast growth factor 4 (FGF4) is elevated in gestational diabetes mellitus (GDM) and shows therapeutic potential. FGF4 treatment reduced fetal neural tube defects in GDM mouse models by inhibiting inflammation and apoptosis.
Area of Science:
- Endocrinology
- Developmental Biology
- Reproductive Medicine
Background:
- Gestational diabetes mellitus (GDM) is linked to poor maternal and neonatal outcomes.
- The precise mechanisms driving GDM pathogenesis are not fully understood.
- Identifying key regulators in GDM is crucial for developing effective interventions.
Purpose of the Study:
- To identify key fibroblast growth factors (FGFs) involved in GDM.
- To investigate the role of FGF4 in GDM development and progression.
- To explore FGF4 as a potential diagnostic and therapeutic target for GDM.
Main Methods:
- Systematic screening of placental FGFs in GDM patients and mouse models.
- Expression analysis of FGFs in GDM models.
- Administration of engineered recombinant FGF4 (rFGF4) to GDM mouse models.
- Assessment of metabolic phenotypes and fetal outcomes in treated mice.
Main Results:
- FGF4 expression was elevated in GDM patients and correlated with blood glucose levels.
- rFGF4 normalized metabolic phenotypes in diet-induced GDM mice but not in STZ-induced GDM mice.
- rFGF4 significantly reduced embryonic neural tube defects in both GDM models.
- rFGF4 inhibited pro-inflammatory signaling and neuroepithelial cell apoptosis independently of glucose regulation.
Conclusions:
- Placental FGF4 plays a significant role in GDM pathogenesis.
- FGF4 may serve as a diagnostic biomarker for GDM.
- FGF4 demonstrates therapeutic potential for mitigating GDM-associated fetal complications.
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