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In the hepatic response to fasting, PGC-1[alpha] has been shown to coordinate the induction of gluconeogenic enzymes by coactivating such liver-enriched transcription factors as hepatocyte nuclear factor 4[alpha] (HNF4[alpha]) and forkhead box O1 protein (FOXO1), as well as the glucocorticoid receptor (3).
Both primary and secondary pollutants affected hepatocyte nuclear factor 4[alpha] signaling, which plays a role in the function of organs such as the kidney, liver, and intestine.
About 70% of MODY cases result from a mutation in the hepatocyte nuclear factor 1-[alpha] (HNF1[alpha]) gene.