Published online Oct 7, 2017. doi: 10.3748/wjg.v23.i37.6777
Peer-review started: May 19, 2017
First decision: June 22, 2017
Revised: August 31, 2017
Accepted: September 20, 2017
Article in press: September 19, 2017
Published online: October 7, 2017
Metabolic syndrome is a cluster of several clinical conditions characterized by insulin-resistance and high cardiovascular risk. Non-alcoholic fatty liver disease is the liver expression of the metabolic syndrome, and insulin resistance can be a frequent comorbidity in several chronic liver diseases, in particular hepatitis C virus infection and/or cirrhosis. Several studies have demonstrated that insulin action is not only relevant for glucose control, but also for vascular homeostasis. Insulin regulates nitric oxide production, which mediates to a large degree the vasodilating, anti-inflammatory and antithrombotic properties of a healthy endothelium, guaranteeing organ perfusion. The effects of insulin on the liver microvasculature and the effects of IR on sinusoidal endothelial cells have been studied in animal models of non-alcoholic fatty liver disease. The hypotheses derived from these studies and the potential translation of these results into humans are critically discussed in this review.
Core tip: Insulin-resistance participates in the development of endothelial dysfunction and interferes with vascular homeostasis in patients with metabolic syndrome. This has been demonstrated in large conductance vessels, promoting atherosclerosis, but also occurs at a microcirculation level, suggesting an important role for Insulin in controlling vascular resistance and, finally, organ perfusion. We offer an overview of those pre-clinical and clinical studies exploring the liver microcirculation, and discuss the importance of early vascular changes induced by insulin-resistance in non-alcoholic fatty liver disease and in the most common chronic hepatitis in which Insulin-Resistance is a comorbidity.