The pathophysiology of hyperinsulinemia in CPSS is partly similar to that in cirrhosis and is linked to several mechanisms: absence of hepatic insulin metabolism after its secretion into the mesenteric and portal system [22,70]; excessive insulin secretion in response to peripheral hyperglycemia due to absence of hepatic first pass [19,71]; and insulin resistance due to the negative-feedback of hyperinsulinemia on insulin receptor-binding proteins [71]. Here, INS is linked to Hyperglycemia.