# Gut Dysbiosis, Malnutrition and Sarcopenia in Liver Cirrhosis: A Narrative Review

**Authors:** Marian-Vlad Lăpădat, Claudia Georgeta Iacobescu, Ion Daniel Baboi, Maria Nedelcu, Lavinia Alice Bălăceanu, Valeria Ioana Grigorescu, Ion Dina

PMC · DOI: 10.3390/diseases14030090 · 2026-03-02

## TL;DR

This review explores how gut problems, poor nutrition, and muscle loss are connected in liver cirrhosis patients, affecting their health and outcomes.

## Contribution

The paper provides a comprehensive synthesis of the interplay between gut dysbiosis, malabsorption, and sarcopenia in liver cirrhosis.

## Key findings

- Gut dysbiosis and intestinal dysfunction contribute to malnutrition and muscle wasting in cirrhosis.
- Sarcopenia is strongly linked to poor prognosis and transplant outcomes in cirrhotic patients.
- The gut-liver-muscle axis represents a key area for future therapeutic interventions.

## Abstract

Liver cirrhosis represents the end stage of chronic liver disease arising from diverse etiologies and is characterized by persistent hepatic injury, architectural distortion, extensive fibrosis, and nodular regeneration. While decompensated cirrhosis is commonly associated with overt, life-threatening complications such as hepatic encephalopathy, hepatorenal syndrome and gastrointestinal bleeding, less apparent manifestations—including sarcopenia and metabolic disturbances—have emerged as major determinants of prognosis. Sarcopenia, defined by the progressive loss of skeletal muscle mass and function, is highly prevalent in cirrhotic patients and is closely linked to frailty, increased morbidity, mortality, and adverse liver transplantation outcomes. Increasing data support the role of gastrointestinal dysfunction in the pathogenesis of sarcopenia in liver cirrhosis. In chronic liver disease, intestinal dysfunction is exacerbated by portal hypertension, which promotes increased intestinal permeability and bacterial translocation. Furthermore, gut dysbiosis, a key feature of advanced liver disease, contributes to impaired digestion, malabsorption of macro- and micronutrients, increased intestinal permeability, malnutrition and systemic inflammation. These alterations promote negative energy balance, reduce muscle protein synthesis and enhance muscle catabolism, thereby accelerating muscle wasting. Despite increasing recognition of the individual roles of gut dysbiosis, malabsorption, and sarcopenia in cirrhosis, their complex interrelationship has not been comprehensively addressed. This narrative review synthesizes current evidence on the interplay between gut dysbiosis, malabsorption and sarcopenia in patients with liver cirrhosis. We discuss underlying pathophysiological mechanisms, clinical implications and potential therapeutic strategies, while highlighting existing knowledge gaps and future research directions. Improved understanding of the gut-liver-muscle axis may offer novel opportunities for early intervention and optimization of outcomes in this high-risk patient population.

## Linked entities

- **Diseases:** hepatic encephalopathy (MONDO:0001711), hepatorenal syndrome (MONDO:0001382)

## Full-text entities

- **Genes:** MSTN (myostatin) [NCBI Gene 2660] {aka GDF8, MSLHP}
- **Diseases:** hematological abnormalities (MESH:D006402), proinflammatory cytokines (MESH:D000080424), neurocognitive dysfunction (MESH:D019965), hypersplenism (MESH:D006971), endocrine dysfunction (MESH:D004700), systemic disorder (MESH:D009422), mitochondrial dysfunction (MESH:D028361), frailty (MESH:D000073496), micronutrient deficiencies (MESH:D007153), gastrointestinal dysfunction (MESH:D005767), HCC (MESH:D006528), portal hypertension (MESH:D006975), bone marrow suppression (MESH:D001855), muscle wasting (MESH:D009133), systemic (MESH:D015619), alcohol (MESH:D000437), Dysbiosis (MESH:D064806), cirrhotic (MESH:D000094724), Muscle depletion (MESH:D019042), muscle weakness (MESH:D018908), hepatic insufficiency (MESH:D048550), Malnutrition (MESH:D044342), bacterial peritonitis (MESH:D010538), skeletal muscle condition (MESH:D005207), intestinal dysfunction (MESH:D007410), gastrointestinal bleeding (MESH:D006471), Sarcopenia (MESH:D055948), Child-Pugh C (MESH:C562515), infections (MESH:D007239), bleeding (MESH:D006470), impaired (MESH:D060825), absorption (MESH:C564600), injury to (MESH:D014947), SIBO (MESH:D001765), splenic sequestration (MESH:D001998), malabsorption (MESH:D008286), metabolic dysregulation (MESH:D021081), portal vein thrombosis (MESH:D012170), DRM (MESH:C580316), esophagogastric varices (MESH:D014648), Inflammation (MESH:D007249), endothelial dysfunction (MESH:D014652), Thrombocytopenia (MESH:D013921), Cirrhosis of the liver (MESH:D008103), liver conditions (MESH:D017093), metabolic disturbances (MESH:D024821), fatigue (MESH:D005221), Hepatic Encephalopathy (MESH:D006501), chronic liver disease (MESH:D008107), decompensated (MESH:D006333), Endotoxemia (MESH:D019446), Cirrhosis (MESH:D005355), loss (MESH:D016388), encephalopathy (MESH:D001927), chronic (MESH:D002908), hepatorenal syndrome (MESH:D006530), coagulation abnormalities (MESH:D001778), non-alcoholic liver disease (MESH:D008108), Hyperammonemia (MESH:D022124), hepatic injury (MESH:D056486)
- **Chemicals:** prebiotics (MESH:D056692), alcohol (MESH:D000438), branched-chain amino acid (MESH:D000597), Ammonia (MESH:D000641), bile acid (MESH:D001647)
- **Species:** Homo sapiens (human, species) [taxon 9606], gut metagenome (species) [taxon 749906], Lactobacillus (genus) [taxon 1578], Enterococcus (genus) [taxon 1350], Clostridia (class) [taxon 186801], Enterobacter (genus) [taxon 547], Bifidobacterium (genus) [taxon 1678]

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Source: https://tomesphere.com/paper/PMC13024842