Current Knowledge about the Effect of Nutritional Status, Supplemented Nutrition Diet, and Gut Microbiota on Hepatic Ischemia-Reperfusion and Regeneration in Liver Surgery

Abstract

Ischemia-reperfusion (I/R) injury is an unresolved problem in liver resection and transplantation. The preexisting nutritional status related to the gut microbial profile might contribute to primary non-function after surgery. Clinical studies evaluating artificial nutrition in liver resection are limited. The optimal nutritional regimen to support regeneration has not yet been exactly defined. However, overnutrition and specific diet factors are crucial for the nonalcoholic or nonalcoholic steatohepatitis liver diseases. Gut-derived microbial products and the activation of innate immunity system and inflammatory response, leading to exacerbation of I/R injury or impaired regeneration after resection. This review summarizes the role of starvation, supplemented nutrition diet, nutritional status, and alterations in microbiota on hepatic I/R and regeneration. We discuss the most updated effects of nutritional interventions, their ability to alter microbiota, some of the controversies, and the suitability of these interventions as potential therapeutic strategies in hepatic resection and transplantation, overall highlighting the relevance of considering the extended criteria liver grafts in the translational liver surgery.

Keywords: gut microbiota; ischemia-reperfusion injury; liver transplantation; nutritional status; partial hepatectomy; supplemented nutrition.

Figure 1

Gut microbiota and hepatic I/R. The dotted box summarizes the mechanisms involved in hepatic I/R injury and how some of these have been altered in the liver by changes in the gut microbiota. ALD, alcoholic liver disease; ATP, adenosine triphosphate; Cyt c, cytochrome c; EC, endothelial cell; ET, endothelin; HCC, hepatocellular carcinoma; ICAM, intracellular cell adhesion molecule; IL, interleukin; INF, interferon; KC, Kupffer cell; LTB4, leucotriene B4; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; NO, nitric oxide; PAF, platelet activating factor; ROS, reactive oxygen species; SC, stellate cell; TNF, tumor necrosis factor; VCAM, vascular cell adhesion molecule; and X/XOD, xanthine/xanthine oxidase.