Abstract
Herein, we investigate whether: (1) the administration of glucose or a lipid emulsion is useful in liver transplantation (LT) using steatotic (induced genetically or nutritionally) or non-steatotic livers from donors after brain death (DBDs); and (2) any such benefits are due to reductions in intestinal damage and consequently to gut microbiota preservation. In recipients from DBDs, we show increased hepatic damage and failure in the maintenance of ATP, glycogen, phospholipid and growth factor (HGF, IGF1 and VEGFA) levels, compared to recipients from non-DBDs. In recipients of non-steatotic grafts from DBDs, the administration of glucose or lipids did not protect against hepatic damage. This was associated with unchanged ATP, glycogen, phospholipid and growth factor levels. However, the administration of lipids in steatotic grafts from DBDs protected against damage and ATP and glycogen drop and increased phospholipid levels. This was associated with increases in growth factors. In all recipients from DBDs, intestinal inflammation and damage (evaluated by LPS, vascular permeability, mucosal damage, TLR4, TNF, IL1, IL-10, MPO, MDA and edema formation) was not shown. In such cases, potential changes in gut microbiota would not be relevant since neither inflammation nor damage was evidenced in the intestine following LT in any of the groups evaluated. In conclusion, lipid treatment is the preferable nutritional support to protect against hepatic damage in steatotic LT from DBDs; the benefits were independent of alterations in the recipient intestine.
Highlights
At present, some 80% of grafts are taken from donors after brain death (DBDs)
The BD + liver transplantation (LT) group resulted in exacerbated hepatic damage and endothelial cell damage, measured by von Willebrand factor (vWF) and hyaluronic acid (HA) levels, in both steatotic and non-steatotic grafts, when compared with the results of the LT group
We studied the relevance of the treatment with lipids or glucose for hepatic damage in nonsteatotic and steatotic LT from DBDs
Summary
Brain death (BD) markedly reduces tolerance of preservation/reperfusion injury among liver grafts and reduces graft survival [1,2]. In clinical liver transplantation (LT), the shortage of hepatic graft donors, and the increase in waiting lists for LT, has led centers to relax their criteria for the acceptance of organs from marginal donors, such as steatotic liver grafts. Up to 50% of deceased donor livers are estimated to be steatotic and steatosis is recognized to be a key donor variable when it comes to predicting post-transplant outcomes [3]. It is important to note that hepatic steatosis represents a greater risk of organ dysfunction and primary non-function when compared to non-steatotic livers [2]. Many steatotic livers, especially those with severe fatty infiltration, are excluded from consideration for LT, which exacerbates the critical shortage of liver donors [1]
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