APOB and Hepatic steatosis: It was revealed that in CD patients the serine kinases phosphorylating serine sites on insulin receptors, such as JNK and IKK-β, are activated, which results in insulin resistance (25), and in return, insulin resistance acts synergistically with hypercortisolism to upregulate lipogenesis, causing central obesity and hepatic steatosis (26).The main abnormality related to IGM is increased assembly and secretion of VLDL, apoB, and TG (27, 28).