Abstract
For decades, parenteral nutrition (PN) has been a successful method for intravenous delivery of nutrition and remains an essential therapy for individuals with intolerance of enteral feedings or impaired gut function. Although the benefits of PN are evident, its use does not come without a significant risk of complications. For instance, parenteral nutrition-associated liver disease (PNALD)—a well-described cholestatic liver injury—and atrophic changes in the gut have both been described in patients receiving PN. Although several mechanisms for these changes have been postulated, data have revealed that the introduction of enteral nutrition may mitigate this injury. This observation has led to the hypothesis that gut-derived signals, originating in response to the presence of luminal contents, may contribute to a decrease in damage to the liver and gut. This review seeks to present the current knowledge regarding the modulation of what is known as the “gut–liver axis” and the gut-derived signals which play a role in PN-associated injury.
Highlights
Parenteral nutrition (PN) is the method of nutritional delivery that bypasses the gastrointestinal tract and intravenously administers key elements of nutrition, such as amino acids, glucose, vitamins, minerals, and lipids
The purpose of this review is to present the relevant basic science and clinical research focusing on the gut–liver crosstalk in the context of total parenteral nutrition (TPN)-associated injury (Figure 1)
This was demonstrated in a study published by Javid et al, who concluded that the level of conjugated bilirubin, which is classically elevated in parenteral nutrition-associated liver disease (PNALD), normalized after initiation of full enteral nutrition in a cohort of 12 infants on PN for a duration of 5 ± 1 months
Summary
Parenteral nutrition (PN) is the method of nutritional delivery that bypasses the gastrointestinal tract and intravenously administers key elements of nutrition, such as amino acids, glucose, vitamins, minerals, and lipids. Some individuals receive adjunctive or short-term delivery of parenteral nutrition during hospitalization, perioperative management, or home care [3,4], others may require long-term administration of PN as a life-sustaining therapy, such as those with intestinal failure [7] In these individuals, regardless of the underlying etiology of disease, the gut is unable to maintain proper homeostasis of fluids, electrolytes, and nutrients. Recent animal and human data reveal that an alteration in gut-derived signals may occur with administration of TPN in the absence of enteral nutrition, leading to gut and liver injury This hypothesis is driven by the observation that hepatic injury is decreased if even a small percentage of nutrition can be provided enterally [8,16]. 7 alpha-hydroxylase; GLP-2: Glucagon-like peptide 2; FGF19: Fibroblast growth factor 19; FGFR4: Fibroblast growth factor receptor 4; FXR: Farnesoid X receptor; TGR5: Takeda G-protein-coupled receptor 5
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