Extended Data Fig. 10: A graph model depicting the role of adipokine Serpina3c in maternal exercise-mediated amelioration of HFD-induced metabolic disorders in offspring mice.
From: Maternal exercise prevents metabolic disorders in offspring mice through SERPINA3C
During maternal exercise in pregnancy, increased expression and secretion of Serpina3c in maternal WAT were observed. Maternal Serpina3c can be transported to enter the fetal circulation and further act on fetal preadipocytes, facilitating the demethylation of the Klf4 gene promoter through the Cathepsin G/Integrin β1/PI3K/OGT/Tet1 signaling axis to increase Klf4 gene expression. Moreover, Klf4 can also maintain the protein stability of Serpina3c in adipocytes. This establishes a positive feedback loop between Serpina3c and Klf4 in the white adipose tissues of offspring mice, effectively suppressing WATs inflammation induced by HFD feeding and enhancing glucose tolerance and insulin sensitivity. Consequently, the above process mitigates metabolic disturbances caused by HFD feeding in offspring mice. WATs, white adipose tissues. Figure created with BioRender.com.
