Effects of systemic inflammation due to hepatic ischemia-reperfusion injury upon lean or obese visceral adipose tissue.

Ligia Fernanda Ferraz,Alessandra Gambero,Raquel De Cássia Santos,Cintia Rabelo E Paiva Caria,Marcelo Lima Ribeiro

doi:10.1590/acb370105

Abstract

ABSTRACTPurpose:To evaluate how the induction of liver damage by ischemia and reperfusion affects the adipose tissue of lean and obese mice.Methods:Lean and diet-induced obese mice were subjected to liver ischemia (30 min) followed by 6 h of reperfusion. The vascular stromal fraction of visceral adipose tissue was analyzed by cytometry, and gene expression was evaluated by an Array assay and by RT-qPCR. Intestinal permeability was assessed by oral administration of fluorescein isothiocyanate (FITC)-dextran and endotoxemia by serum endotoxin measurements using a limulus amebocyte lysate assay.Results:It was found that, after liver ischemia and reperfusion, there is an infiltration of neutrophils, monocytes, and lymphocytes, as well as an increase in the gene expression that encode cytokines, chemokines and their receptors in the visceral adipose tissue of lean mice. This inflammatory response was associated with the presence of endotoxemia in lean mice. However, these changes were not observed in the visceral adipose tissue of obese mice.Conclusions:Liver ischemia and reperfusion induce an acute inflammatory response in adipose tissue of lean mice characterized by an intense chemokine induction and leukocyte infiltration; however, inflammatory alterations are already present at baseline in the obese adipose tissue and liver ischemia and reperfusion do not injure further.

Highlights

Several liver surgical procedures that include resections or transplants, as well as the occurrence of generalized shock, result in periods of liver ischemia
The present study evaluates the effects of systemic inflammatory response triggered by liver ischemia-reperfusion injury (IRI) on visceral adipose tissue (VAT)
High morbidity and mortality occur because liver ischemia and reperfusion modify the function of many remote organs, such as lung, kidney, intestine, pancreas, adrenals and heart due metabolic and oxidative changes, and inflammatory responses triggered after reperfusion[12]

Summary

Introduction

Several liver surgical procedures that include resections or transplants, as well as the occurrence of generalized shock, result in periods of liver ischemia. The consequences of ischemia and subsequent reperfusion can range from transient liver dysfunction to total organ damage associated to a systemic inflammation that can result in multiple organ failure[1]. It is widely known that adipose tissue is responsible for the production of inflammatory mediators in obesity, collectively called adipokines, which contribute to the establishment of chronic, systemic and low-grade inflammation that occurs in. In other conditions, such as Crohn’s disease, mesenteric adipose tissue becomes hyperplastic and it creeps around the inflamed segments of the small intestine, releasing proinflammatory mediators[4]. Adipocyte death followed by stem cell activation and tissue remodeling is observed when adipose tissue is exposed to hypoxia, as seen in plastic surgery, for example[5]. Little information is available about the repercussions of systemic inflammation induced by liver IRI upon adipose tissue

Methods

Results

Conclusion