Observational Study
Copyright ©The Author(s) 2016.
World J Gastroenterol. May 7, 2016; 22(17): 4403-4410
Published online May 7, 2016. doi: 10.3748/wjg.v22.i17.4403
Figure 3
Figure 3 Putative mechanism of serum Mac-2bp changes in chronic pancreatitis and pancreatic ductal adenocarcinoma. In both chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) patients, increased pancreatic bioactive substances produced in the pancreas flow into the liver through the portal vein and evoke inflammatory changes in the liver. This liver inflammation increases hepatic Mac-2bp production and serum Mac-2bp levels (Dotted arrows). Alcohol over-intake and/or relative over-nutrition induces steatohepatits in CP and further increases hepatic Mac-2bp production (left panel solid arrows). In contrast, the cessation of alcohol over-intake and no over-nutrition in PDAC would decrease hepatic Mac-2bp production and serum Mac-2bp levels would decrease in PDAC (right panel solid arrows).