Hepatogenous diabetes: Knowledge, evidence, and skepticism

Figure 2 Complex pathophysiological mechanisms likely to play important roles in the development of hepatogenous diabetes. Neurohormonal alterations, endotoxemia, and chronic inflammation induced by cirrhosis and portal hypertension all contribute to the development of insulin resistance and β-cell dysfunction. These changes may be further modulated by other concomitant abnormalities, such as gut dysbiosis, hyperammonemia, sarcopenia, adiposity, and myosteatosis. NH₃: Ammonia; AGE: Advanced glycation end products; HIF: Hypoxia inducible factor; HCV: Hepatitis C virus; NAFLD: Non-alcoholic fatty liver disease; LPS: Lipopolysaccharides; IL-6: Interleukin-6; TNF: Tumour necrosis factor; UPP: Ubiquitin proteasome pathways.