Since insulin itself decreases renal gluconeogenesis (among other mechanisms via a decrease in gluconeogenic substrates and diminished expression of PCK1 and G6P mRNA), it might be hypothesized that hypoglycaemia of origins other than insulin mediation (sulfonylureas, chronic liver disease, etc.)exhibits a different magnitude of renal SGN response. The gene discussed is PCK1; the disease is Hypoglycemia.