Introduction

The NAFLD prevalence is estimated to be near 25% of the world population. There is a theory that inulin intake can reduce endotoxemia. This prebiotic could increase the SCFA production by bacteria with further the pro-inflammatory markers decreasing in gut-liver axis. Thus, microbiota regulation by prebiotic treatment could be a key role player in NAFLD prevention.

Aims & Methods

The aim of the study was to compare the microbiome before and after 20 days of inulin intake in patients with NAFLD and to find the correlational relationship between prebiotics treatment and liver biochemical markers.
93 patients (44 men, 49 women), and 46.64±2.52 (average age) with NAFLD (based on liver transient elastography) were examined. All patients followed the recommendations of 5 mg Inulin per os twice a day for 20 days. The study excluded any other pre-, probiotics, and antibacterial drugs during the course of treatment. Before and after the treatment the next biochemical markers were examined: lipid profile, C-reactive protein high sensitivity, ALT, AST, GGTP, bilirubin, TNF-a, and HOMA index. Determination of microbial composition was carried out by identification of total bacterial DNA, and DNA of Bacteroidetes, Firmicutes, and Actinobacteria by quantitative real-time PCR (qRT-PCR), using gene-targeted primers.

Results

The microbiome of patients with NAFLD before Inulin intake (Figure 1): Bacteroidetes - 51%, Firmicutes - 28%, Actinobacteria 6%, F/B index - 1.62. After the treatment - Bacteroidetes 45%, Firmicutes 39%, Actinobacteria 10%, F/B index 1.29.
Biochemical tests before treatment (Figure 2): GGTP 42 U/L, Triglycerides 2.72 mmol/L, HDL 1.12 mmol/L, CRP (high sensitivity) - 9 mg/L, HOMA index 3.51.
After the treatment, GGTP decreased to 29 U/L, Triglycerides to 1.26 mmol/L, and CRP to 5 mg/L.
HOMA index to 3.12. HDL level increased to 1.36.
What was unexpected - in half of the patients (46) Candida was found in the microbiome. After the treatment - in 37 of them Candida was absent. Patients did not receive any antifungal drugs.
The growth of Actinobacteria was in a negative correlational relationship with Candida.

Conclusion

Inulin could be part of therapy, directed for steatohepatitis prevention in patients with NAFLD by influencing a few risk factors:

1. Decreasing the lipids
2. Reducing pro-inflammatory agents
3. Improvement the insulin sensitivity.

Introduction

Increased intestinal permeability, mediated by zonulin, has been implicated in the pathogenesis of insulin resistance, dyslipidemia, and non-alcoholic fatty liver disease (NAFLD). Small intestinal bacterial overgrowth (SIBO) may further contribute to metabolic dysfunction through endotoxin-induced inflammation.

Aims & Methods

The aim was to determine zonulin concentrations in patients with dyslipidemia and NAFLD and analyze their relationships with metabolic parameters and the prevalence of small intestinal bacterial overgrowth (SIBO). A total of 342 patients with dyslipidemia were enrolled; NAFLD was confirmed in 152 of them based on ultrasound and steatometry. Fecal zonulin levels were measured using ELISA; SIBO was assessed by hydrogen breath test. Lipid profiles, high-sensitivity C-reactive protein (hsCRP), and HDL-C levels were also analyzed.

Results

Zonulin levels in patients with NAFLD (115±2.76 ng/g) exceeded the normal range (≤107 ng/g), compared to 87±0.28 ng/g in the dyslipidemia group without NAFLD (p<0.05). SIBO was present in 45% of dyslipidemic patients and 53.2% of those with NAFLD. A positive correlation was found between zonulin and hsCRP (r=0.65) and triglycerides (r=0.58), and a negative correlation between SIBO and HDL-C (r=–0.78) in the dyslipidemia group.

Conclusion

Elevated zonulin and increased intestinal permeability are associated with higher cardiometabolic risk in patients with NAFLD and dyslipidemia. Both zonulin and SIBO may serve as potential therapeutic targets for preventing progression of NAFLD and related metabolic disturbances.

Introduction

Nonalcoholic fatty liver disease (NAFLD) is a widespread metabolic disorder associated with intestinal dysbiosis, low-grade systemic inflammation, and small intestinal bacterial overgrowth (SIBO). Targeting the gut-liver axis through microbiome-modulating therapies may represent a promising approach to disease management.

Aims & Methods

The aim was to investigate gut microbiota alterations in NAFLD patients and assess the efficacy of microbiota-based therapy on metabolic, inflammatory, and structural liver parameters. The study included 152 NAFLD patients and 47 controls. Gut microbiota composition was evaluated using qRT-PCR, and SIBO was diagnosed via hydrogen breath testing. The therapeutic protocol included rifaximin (200 mg TID for 14 days), Saccharomyces boulardii CNCM I-745 (1 capsule BID for 30 days), and essential phospholipids (600 mg TID for 30 days). Liver function tests, inflammatory markers, and steatometry were assessed before and after treatment.

Results

Alterations in gut microbiota composition indicative of dysbiosis—including increased Firmicutes/Bacteroides ratio and Actinobacteria abundance—were identified in NAFLD. Strong correlations emerged between the F/B index and triglycerides (r = 0.78), TNF-α (r = 0.77), and between Actinobacteria and hsCRP (r = 0.66). SIBO rates declined significantly post-treatment (51% → 17%). Liver enzymes, inflammatory markers, and steatometric parameters improved substantially (p<0.05).

Conclusion

Microbiota-targeted therapy combining rifaximin, S. boulardii, and phospholipids effectively corrected dysbiosis, reduced inflammation, improved metabolic parameters, and promoted liver structural recovery in NAFLD patients. These findings support incorporating microbiome-focused interventions into routine clinical practice for NAFLD. ​

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), has emerged as one of the leading causes of chronic liver disease worldwide. MASLD is closely associated with components of metabolic syndrome, including obesity, insulin resistance, dyslipidemia, and hypertension. The role of gut microbiota dysbiosis in MASLD pathogenesis is increasingly recognized, with microbial imbalance contributing to systemic inflammation and metabolic disturbances.

Aims & Methods

The aim was to determine gut microbiota composition in patients with MASLD and evaluate the impact of probiotic therapy on metabolic, inflammatory, and lipid parameters. The study included 152 patients diagnosed with MASLD. Diagnosis was based on clinical, laboratory, and imaging findings, including ultrasound and steatometry, alongside cardiometabolic risk factors. Gut microbiota composition was evaluated using quantitative real-time PCR (qRT-PCR). Patients received a combined probiotic therapy containing Saccharomyces boulardii CNCM I-745, Lactobacillus acidophilus (LA-5), and Bifidobacterium lactis (BB-12). Changes in biochemical markers, lipid profiles, inflammatory parameters, and gut microbiota composition were assessed before and after therapy.

Results

At baseline, patients with MASLD demonstrated gut microbiota dysbiosis, characterized by an increased proportion of Firmicutes (50.3%) and Actinobacteria (15.34%), and an elevated Firmicutes/Bacteroides (F/B) index (5.02). Following probiotic therapy, significant improvements were observed: the proportions of Firmicutes and Actinobacteria decreased, the F/B index was reduced, and levels of ALT, AST, high-sensitivity C-reactive protein (hsCRP), total cholesterol, and triglycerides declined, while HDL-C levels increased. Positive correlations were identified between elevated Firmicutes and Actinobacteria and markers of cardiometabolic risk, such as hsCRP and triglycerides.

Conclusion

Gut microbiota dysbiosis is strongly associated with metabolic and inflammatory disturbances in MASLD. Combined probiotic therapy effectively corrected microbial imbalance, reduced systemic inflammation, and improved metabolic and lipid parameters. These findings support the role of microbiota-targeted interventions as an adjunctive approach in the comprehensive management of MASLD.

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), is a widespread chronic liver condition closely associated with obesity, insulin resistance, and dyslipidemia. Recent evidence points to gut microbiota dysbiosis as a key player in MASLD pathogenesis, affecting intestinal barrier function and systemic inflammation.

Aims & Methods

The aim was to investigate gut microbiota composition in patients with MASLD and assess its association with disease progression and gut barrier dysfunction. A total of 152 MASLD patients and 150 matched controls without liver pathology were examined. Diagnosis was confirmed by ultrasound and steatometry, alongside assessment of cardiometabolic risk factors. Gut microbiota composition was analyzed using real-time PCR, focusing on Bacteroidetes, Firmicutes, and Actinobacteria. Hydrogen breath testing was used to diagnose small intestinal bacterial overgrowth (SIBO), and the presence of Akkermansia muciniphila was evaluated as a marker of gut barrier integrity.

Results

MASLD patients demonstrated a significant increase in Firmicutes (50.3%) and Actinobacteria (15.3%) proportions compared to controls, with a higher Firmicutes/Bacteroidetes (F/B) ratio. SIBO was detected in 52% of MASLD patients versus 40.5% in controls (p<0.05). The presence of Akkermansia muciniphila was notably lower in MASLD patients (33%) compared to controls (63%), suggesting impaired gut barrier function. Strong positive correlations were observed between Actinobacteria abundance and the F/B index (r=0.75, p<0.05), while Akkermansia muciniphila presence negatively correlated with MASLD development (r=–0.69, p<0.05).

Conclusion

Gut microbiota dysbiosis, characterized by elevated Firmicutes and Actinobacteria and reduced Akkermansia muciniphila, is closely associated with MASLD pathogenesis. The findings highlight the potential of microbiota-targeted interventions for improving gut barrier function and modifying disease progression in MASLD patients.