Growth factors expression genes involved in liver development in gestational protein-restricted male mice offspring

The DOHaD experimental research has shown that gestational protein restriction is related to the rise prevalence of metabolic dysfunction in adult life. The liver is the largest internal organ providing essential metabolic, exocrine, and endocrine functions, and changes in the hepatogenic process can be related to the genesis of observed metabolic impairment. Between e10–15, the liver bud originating from the endoderm undergoes accelerated growth as it is vascularized and colonized by hematopoietic cells to become the significant fetal hematopoietic organ. This growth is regulated by paracrine signals from hepatic mesenchyme and by genes that act intrinsically in the hepatoblast. Autophagy can be important in a low protein environment organogenesis where intracellular components may be degraded in lysosomes to release substrates for energy production and to synthesize new macromolecules.