Nonalcoholic fatty liver disease (NAFLD) is characterized by fat deposition in hepatocytes, and a strong association with nutritional factors. Dietary fatty acids are classified according to their biochemical properties, which confer their bioactive roles. Monounsaturated fatty acids have a dual role in various human and murine models. In contrast, polyunsaturated fatty acids exhibit antiobesity, anti steatosic and anti-inflammatory effects. The combination of these forms of fatty acids—according to dietary type, daily intake and the proportion of n-6 to n-3 fats—can compromise hepatic lipid metabolism. A chemosensory rather than a nutritional role makes bioactive fatty acids possible biomarkers for NAFLD. Bioactive fatty acids provide health benefits through modification of fatty acid composition and modulating the activity of liver cells during liver fibrosis. More and better evidence is necessary to elucidate the role of bioactive fatty acids in nutritional and clinical treatment strategies for patients with NAFLD.

Hepatic steatosis is characterized by triglyceride accumulation within hepatocytes in response to a high calorie intake, and it may be related to intestinal microbiota disturbances. The prebiotic inulin is a naturally occurring polysaccharide with a high dietary fiber content. Here, we evaluate the effect of inulin on the intestinal microbiota in a non-alcoholic fatty liver disease model. Mice exposed to a standard rodent diet or a fat-enriched diet, were supplemented or not, with inulin. Liver histology was evaluated with oil red O and H&E staining and the intestinal microbiota was determined in mice fecal samples by 16S rRNA sequencing. Inulin treatment effectively prevents liver steatosis in the fat-enriched diet group. We also observed that inulin re-shaped the intestinal microbiota at the phylum level, were Verrucomicrobia genus significantly increased in the fat-diet group; specifically, we observed that Akkermansia muciniphila increased by 5-fold with inulin supplementation. The family Prevotellaceae was also significantly increased in the fat-diet group. Overall, we propose that inulin supplementation in liver steatosis-affected animals, promotes a remodeling in the intestinal microbiota composition, which might regulate lipid metabolism, thus contributing to tackling liver steatosis.

In the metabolic dysfunction-associated steatotic liver disease (MASLD) scenario, more and more evidence has emerged indicating that MASLD patients can develop portal hypertension (PH), which has a direct impact on the prognosis of the disease and represents a significant challenge during the clinical approach. There are different explanations for early PH pathophysiology in patients with MASLD, among which are dysbiosis, microthrombosis, impairments in inflammatory mediators, sinusoid-level alterations in the liver architecture, genetic factors, and so on. Currently, we have evidence in animal models and humans demonstrating that all these factors could be modulated or modified; unfortunately, we are far from translating these results into clinical scenarios. The early PH phenomenon only occurs in 20% patients with MASLD. This review aims to describe the current evidence from the pathophysiological and treatment point of view, as well as the implications in the clinical care of patients with MASLD presenting early PH. Although the presence of PH in these patients has a significant clinical impact, the traditional diagnostic approach may not be the best option; other diagnostic tools have been studied, and perhaps, at some point, they can be added to the treatment algorithms of these patients.

Background: The triglyceride–glucose index (TyG) and a combination of body mass index (BMI) and waist circumference (WC) have been proposed as predictive scores for liver steatosis (LS). The aim of this study was to determine the diagnostic accuracy of these indices compared with controlled attenuation parameters (CAPs) and other predictive scores of LS. Methods: A retrospective analysis of patients who attended a check-up unit in 2021 was performed. LS was determined by CAP. Anthropometric and biochemical parameters for calculating TyG, TyG-BMI, TyG-WC, fatty liver index, and hepatic steatosis index were obtained. ROC curve was used to establish the best cut-off point of each TyG index for LS detection. The accuracy was determined for all patients, as well as for overweight and diabetic patients. Results: Medical records of 855 patients with a median age of 48 [IQR, 44–54] years and a BMI of 25.7 [IQR 23.4–28.1] kg/m² were included. According to CAP, LS prevalence was 31.8% (n = 272). TyG-BMI and TyG-WC show better AUCs compared with CAP (0.82, 0.81), FLI (0.96, both), and HSI (0.93, 0.85). For diabetic patients, TyG-WC shows an AUC of 0.70. Meanwhile, TyG-BMI shows better accuracy (0.75) compared with CAP. Conclusions: TyG-BMI and TyG-WC showed a superior predictive accuracy for detecting LS compared with the TyG index.

Background: Non-alcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of metabolic syndrome. Recently, the term metabolic dysfunction-associated fatty liver disease (MAFLD) has been proposed and adapted to body mass index (BMI). This study describes the impact on prevalence of the application of both criteria in overweight and lean patients. Methods: Patients who were evaluated for liver steatosis by transient elastography were included and divided according to BMI (≥25 kg/m² and <25 kg/m²) and classified as NAFLD or MAFLD, according to metabolic abnormalities. Differences in prevalence were evaluated applying both criteria. A multivariate analysis was performed to evaluate independent associations of metabolic abnormalities and liver steatosis in lean patients. Results: 3847 patients were included. In overweight patients (61%), the prevalence NAFLD was 63.6% and 65.3% for MAFLD (p = 0.22). In contrast, the prevalence of MAFLD was lower (7.9% vs. 18.3%, p ≤ 0.001) in lean patients. In this group, higher age, fasting glucose, triglycerides, and waist circumference showed independent association with liver steatosis. Conclusion: The application of NAFLD/MAFLD criteria did not show prevalence differences in overweight patients. With MAFLD criteria, the prevalence is lower in lean patients, but patients with high risk of progression of liver disease for steatosis were identified, according to their metabolic abnormalities.