Clinical diagnosis
Case 256
【Discussion】
When blood glucose concentration elevates after food ingestion, insulin is secreted from pancreas by its stimulation. Insulin functions blood glucose to transport to liver, muscle and adipose tissue for energy source and storage. Insulin simulates liver to produce glycogen from glucose, and to suppress neo-glucose formation and to produce triglyceride. Namely, in normal liver, insulin has two functions to suppress neo-glucose formation and produce glycogen and triglyceride (1, 2).
Fatty liver means accumulation of fat literally, more precisely, accumulation of triglycerides by insulin. When hepatic cells function normally, irrespective of fat deposit in liver or not, blood glucose does not elevate. However, insulin resistant liver can occur especially in case of saturated fatty food ingestion and/or obesity. Insulin resistant liver implies loss of a function to suppress neo-glucose formation from glycogen, inducing to produce glucose, leading type 2 diabetes mellitus (1, 2). Meanwhile, liver preserves another function to produce triglycerides, the term of insulin selective resistant liver indicates that insulin does not work for liver to suppress neo-formation of glucose but work to continue to produce triglycerides. In other words, insulin selective resistant liver might be in a state that too much storage of glycogen induces liver unable to process glucose, leading diabetes mellitus and hyperlipidemia continuing to produce triglycerides.
When fatty liver is detected on CT, we might recognize fatty liver has two types; normal function or selective insulin resistant (3-5). The key for its differentiation is whether type II diabetes mellitus is associated or not.
Hepatic segment S4 is known to often occur pseudo lesion because S4 has the area sites where systemic veins inflows rather than portal branch blood flow: cystic vein, paraumbilical vein and right gastric vein (pyloro-duodeno-pancreatic vein) (3-5). The pseudo-lesion at S4 irrigated by right gastric vein is visualized as localized spared fatty liver or localized fatty liver on CT. The reason why the opposite image emerges is yet to be clarified.
In our case with type II diabetes mellitus, CT showed marked fatty area at S4 in the whole fatty liver, indicating she has selective insulin resistant liver. Lower density area at S4 is irrigated by right gastric vein which includes pancreatic vein branch with more concentration of insulin. When the area is exposed more insulin concentration, more accumulation of triglycerides and more glucose production, leading to focal area with more fatty change.
(In case of fatty liver with normal liver function (no insulin resistance), the irrigated area with more insulin concentration by right gastric vein including pancreatic sub-branch remains spared fatty liver, because of more fatty concentration rather than right gastric vein, where insulin functions to produce glycogen with repressing to produce neo-glucose despite triglyceride production.)
【Summary】
We presented a thirty-four-year-old female with liver dysfunction. Laboratory test revealed AST 77 IU/L, ALT 66 IU/L, ALP 124 IU/L. CT and MRI depict the focal area at S4 with more fatty accumulation in the fatty liver. It was borne in mind that there are two types of fatty liver: with normal function and insulin selective resistant. Insulin functions to come to lower the blood insulin level, inducing to deliver energy source to muscle, fat tissue and liver. Insulin works to transform glucose to glycogen, suppress to neo-produce glucose and produce triglycerides in normal liver. Meanwhile, in insulin resistant liver, insulin does not suppress to produce neo-glucose, inducing hyperglycosemia and causing diabetes mellitus II type. Further, triglyceride production is continued to produce, indicating hyper lipidemia. Pseudo-lesion at S4 caused by irrigation by right gastric vein comes to spared fatty liver on normal liver function because portal vein contains more fat rather than right gastric vein. Meanwhile, pseudo-lesion at S4 caused by irrigation by right gastric vein on insulin selective resistant liver comes to more fat accumulation at S4 because insulin concentration of right gastric vein is greater, inducing production of both neo-glucose production and triglycerides.
【References】
1.Kitade H, et al. Nonalcoholic Fatty Liver Disease and Insulin Resistance: New Insights and Potential New TreatmentsNutrients. 2017 Apr; 9(4): 387.
2.Yki-Järvinen, H, et al. The fatty liver and insulin resistance. Curr Mol Med. 2005 May;5(3):287-95
3.Matsui O, et al. Pseudolesion in segment IV of the liver at CT during arterial portography - correlation with aberrant gastric venous drainage. Radiology. 1994;193:31–35. [PubMed]
4.Yoshimitsu K, et al. Anatomy and clinical importance of cholecystic venous drainage: Helical CT observations during injection of contrast medium into the cholecystic artery. AJR Am J Roentgenol. 1997;169:505–510. [PubMed]
5.Terayama N, et al. Focal sparing of fatty liver in segment II associated with aberrant left gastric vein. Br J Radiol. 2004;77:150–152
2022.2.1