Figure 9
PPARγ serves a key part in the regulation of adipocyte differentiation, adipogenesis and lipid metabolism, which are affected by maternal LCD in offspring adipose tissue. Maternal LCD triggers offspring adipose PPARγ pathway through activating ZFP423, CCAAT/enhancer-binding protein α (CEBPα) and SREBP1. Activated PPARγ binds to retinoid X receptor (RXR), enhancing its downstream target adipogenesis enzymes (Fabp3 and Lpl) and conversely inducing SREBP1 and CEBPα to increase circulation TGs.
Schematic illustration of the effect of maternal low chromium on offspring through PPARγ pathway.

PPARγ serves a key part in the regulation of adipocyte differentiation, adipogenesis and lipid metabolism, which are affected by maternal LCD in offspring adipose tissue. Maternal LCD triggers offspring adipose PPARγ pathway through activating ZFP423, CCAAT/enhancer-binding protein α (CEBPα) and SREBP1. Activated PPARγ binds to retinoid X receptor (RXR), enhancing its downstream target adipogenesis enzymes (Fabp3 and Lpl) and conversely inducing SREBP1 and CEBPα to increase circulation TGs.

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