Fructoholism in adults: The importance of personalised care in metabolic dysfunction-associated fatty liver disease.
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ABSTRACT:
SUBMITTER: Salavrakos M
PROVIDER: S-EPMC8666557 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ContestThe relationship between metabolic dysfunction-associated fatty liver disease (MAFLD) and liver stiffness and bone mineral density (BMD) remains unclear.ObjectivesWe aimed to investigate the association between MAFLD and liver stiffness and BMD in the United States population.MethodsA cross-sectional study among 2031 participants over 50 years old in the National Health and Nutrition Examination Survey (NHANES) 2017-2018 was performed. All patients underwent vibration controlled transient elastography (VCTE) and dual-energy x-ray absorptiometry (DXA). The linear and logistic regression model were used to analyze the association between the MAFLD and liver stiffness and osteoporosis, with adjustments for known covariates. Furthermore, the sensitive analyses were conducted to explore the relationship between MAFLD and liver stiffness and whole osteoporosis (include femoral and lumbar osteoporosis).ResultsMAFLD was prevalent in the study population, with a prevalence of 50.9% for men and 40.7% for women. The multiple linear models demonstrated positive associations between MAFLD and liver stiffness and total femur BMD, femur neck BMD, trochanter BMD, intertrochanter BMD. In multiple logistic regression models, both MAFLD and significant liver fibrosis were negatively associated with femoral osteoporosis (OR=0.41, 95% CI: 0.27 to 0.63; OR=0.67, 95% CI: 0.33-1.37, respectively). Nonetheless, when BMI was adjusted, the association between MAFLD and liver stiffness and osteoporosis became insignificant. Besides, as showed in the sensitive analyses, the relationship between MAFLD and liver stiffness and whole osteoporosis were stable.ConclusionsThese results suggest that MAFLD and liver stiffness were associated with higher femoral and lumbar bone mineral density in individuals aged over 50 years. But the results may be confounded by BMI.
| S-EPMC9280639 | biostudies-literature
Project description:The complex interplay between the gut microbiota, the intestinal barrier, the immune system and the liver is strongly influenced by environmental and genetic factors that can disrupt the homeostasis leading to disease. Among the modulable factors, diet has been identified as a key regulator of microbiota composition in patients with metabolic syndrome and related diseases, including the metabolic dysfunction-associated fatty liver disease (MAFLD). The altered microbiota disrupts the intestinal barrier at different levels inducing functional and structural changes at the mucus lining, the intercellular junctions on the epithelial layer, or at the recently characterized vascular barrier. Barrier disruption leads to an increased gut permeability to bacteria and derived products which challenge the immune system and promote inflammation. All these alterations contribute to the pathogenesis of MAFLD, and thus, therapeutic approaches targeting the gut-liver-axis are increasingly being explored. In addition, the specific changes induced in the intestinal flora may allow to characterize distinctive microbial signatures for non-invasive diagnosis, severity stratification and disease monitoring.
| S-EPMC8085382 | biostudies-literature
Project description:Metabolic dysfunction-associated fatty liver disease (MAFLD) is a new term from nonalcoholic fatty liver disease (NAFLD) and is a positive diagnosis based on histopathology, imaging, or blood biomarkers. MAFLD is one of the common causes of liver dysfunction worldwide, likely due to the increase in metabolic syndrome as well as the high burden of disease and its relationship to other extrahepatic conditions. However, effective pharmacological therapeutic agents are still lacking; current management largely focuses on weight reduction and lifestyle modification. The purpose of this review was to summarize the updated evidence of novel therapies targeting different pathogenetic pathways in MAFLD.
| S-EPMC8666366 | biostudies-literature
Project description:Metabolic dysfunction-associated fatty liver disease (MAFLD) is the most common liver disease affecting a quarter of the global population and is often associated with adverse health outcomes. The increasing prevalence of MAFLD occurs in parallel to that of metabolic syndrome (MetS), which in fact plays a major role in driving the perturbations of cardiometabolic homeostasis. However, the mechanisms underpinning the pathogenesis of MAFLD are incompletely understood. Compelling evidence from animal and human studies suggest that heightened activation of the sympathetic nervous system is a key contributor to the development of MAFLD. Indeed, common treatment strategies for metabolic diseases such as diet and exercise to induce weight loss have been shown to exert their beneficial effects at least in part through the associated sympathetic inhibition. Furthermore, pharmacological and device-based approaches to reduce sympathetic activation have been demonstrated to improve the metabolic alterations frequently present in patients with obesity, MetSand diabetes. Currently available evidence, while still limited, suggests that sympathetic activation is of specific relevance in the pathogenesis of MAFLD and consequentially may offer an attractive therapeutic target to attenuate the adverse outcomes associated with MAFLD.
| S-EPMC8073135 | biostudies-literature
Project description:Background and aimsRecently metabolic dysfunction-associated fatty liver disease (MAFLD) has been introduced and was defined as hepatic steatosis with either overweight, diabetes, and/or a combination of other metabolic risk factors. We investigated the application of the MAFLD criteria as compared with NAFLD.Approach and resultsWe performed a cross-sectional analysis within the Rotterdam Study, a large prospective population-based cohort. Participants who attended the liver ultrasound and transient elastography program between 2009 and 2014 were eligible for inclusion. Subsequently, individuals with viral hepatitis, alcohol intake >60 g/day, missing alcohol data, and/or missing body mass index were excluded. According to their NAFLD and MAFLD status based on metadata and ultrasound, participants were allocated in overlap fatty liver disease (FLD), NAFLD-only, MAFLD-only, or no FLD. Fibrosis was defined as liver stiffness ≥8.0 kPa. In our analysis, 5445 participants were included: 1866 (34.3%) had MAFLD and 1604 (29.5%) [Correction added on December 27, 2021 after first online publication: The preceding fragment was changed from "1623 (29.8%)"] had NAFLD. This resulted in 1547 (28.4%) [Correction added on December 27, 2021 after first online publication: The preceding fragment was changed from "1566 (28.8%)"] individuals with overlap FLD, 319 (5.9%) [Correction added on December 27, 2021 after first online publication: The preceding fragment was changed from "300 (5.5%)"] with MAFLD-only, 57 (1.0%) with NAFLD-only, and 3522 (64.7%) with no FLD. The MAFLD-only group was strongly associated with fibrosis (adjusted OR 5.30 [Correction added on December 27, 2021 after first online publication: The preceding fragment was changed from "OR 5.27"], p < 0.001) and log-transformed liver stiffness (adjusted beta 0.116, p < 0.001), as opposed to the NAFLD-only group, in which no cases of fibrosis were identified and no association with liver stiffness (adjusted beta 0.006, p = 0.90) was found.ConclusionsFLD is highly prevalent in the general population. However, not the NAFLD-only, but the MAFLD-only group was associated with fibrosis and higher liver stiffness-independent of demographic and lifestyle factors. We believe that using the MAFLD criteria will help improve the identification and treatment of patients with FLD at risk for fibrosis.
| S-EPMC9299928 | biostudies-literature
Project description:(1) Background: The role of adipokines such as adiponectin and visfatin in metabolic-dysfunction-associated fatty liver disease (MAFLD) and cardiovascular disease remains unclear. Therefore, we aim to assess serum adiponectin and visfatin levels in MAFLD patients and associated cardiovascular parameters. (2) Methods: A cross-sectional study involving 80 participants (40 MAFLD patients, 40 controls), recruited between January and September 2020, was conducted, using both hepatic ultrasonography and SteatoTestTM to evaluate hepatic steatosis. Echocardiographic and Doppler parameters were assessed. Serum adipokines were measured using ELISA kits. (3) Results: Adiponectin and visfatin levels were not significantly different in MAFLD vs. controls. Visfatin was associated with mean carotid intima-media thickness (p-value = 0.047), while adiponectin was associated with left ventricular ejection fraction (LVEF) (p-value = 0.039) and E/A ratio (p-value = 0.002) in controls. The association between adiponectin and E/A ratio was significant in the univariate analysis at 95% CI (0.0049-0.1331, p-value = 0.035), but lost significance after the multivariate analysis. Although LVEF was not associated with adiponectin in the univariate analysis, significant values were observed after the multivariate analysis (95% CI (-1.83--0.22, p-value = 0.015)). (4) Conclusions: No significant difference in serum adiponectin and visfatin levels in MAFLD patients vs. controls was found. Interestingly, although adiponectin levels were not associated with LVEF in the univariate analysis, a significant inversely proportional association was observed after the multivariate analysis.
| S-EPMC8584895 | biostudies-literature
Project description:The diagnosis of metabolic-associated fatty liver disease is based on the detection of liver steatosis together with the presence of metabolic dysfunction. According to this new definition, the diagnosis of metabolic-associated fatty liver disease is independent of the amount of alcohol consumed. Actually, alcohol and its metabolites have various effects on metabolic-associated abnormalities during the process of alcohol metabolism. Studies have shown improved metabolic function in light to moderate alcohol drinkers. There are several studies focusing on the role of light to moderate alcohol intake on metabolic dysfunction. However, the results from studies are diverse, and the conclusions are often controversial. This review systematically discusses the effects of alcohol consumption, focusing on light to moderate alcohol consumption, obesity, lipid and glucose metabolism, and blood pressure.
| S-EPMC8516839 | biostudies-literature
Project description:Metabolic associated fatty liver disease (MAFLD), formerly named non-alcoholic fatty liver disease is the most common liver disorder in many countries. The inflammatory subtype termed steatohepatitis is a driver of disease progression to cirrhosis, hepatocellular carcinoma, liver transplantation, and death, but also to extrahepatic complications including cardiovascular disease, diabetes and chronic kidney disease. The plasticity of macrophages in response to various environmental cues and the fact that they can orchestrate cross talk between different cellular players during disease development and progression render them an ideal target for drug development. This report reviews recent advances in our understanding of macrophage biology during the entire spectrum of MAFLD including steatosis, inflammation, fibrosis, and hepatocellular carcinoma, as well as for the extra-hepatic manifestations of MAFLD. We discuss the underlying molecular mechanisms of macrophage activation and polarization as well as cross talk with other cell types such as hepatocytes, hepatic stellate cells, and adipose tissue. We conclude with a discussion on the potential translational implications and challenges for macrophage based therapeutics for MAFLD.
| S-EPMC7201150 | biostudies-literature
Project description:Metabolic dysfunction-associated fatty liver disease (MAFLD) is characterized by deregulated hepatic lipid metabolism; however, the association between MAFLD development and mitochondrial dysfunction has yet to be confirmed. Herein, we employed high-resolution respirometry, blue native polyacrylamide gel electrophoresis-based in-gel activity measurement and immunoblot analysis to assess mitochondrial function in obesity-induced mouse models with varying degrees of MAFLD. Results showed a slight but significant decrease in hepatic mitochondrial respiration in some MAFLD mice compared to mice fed a standard diet. However, the activities and levels of mitochondrial oxidative phosphorylation complexes remained unchanged during obesity-induced MAFLD progression. These results suggest that mitochondrial function, particularly oxidative phosphorylation, was mildly affected during obesity-induced MAFLD development. Moreover, transcriptome profiling of mouse and human liver tissues with varying degrees of MAFLD revealed that the decreased activation of mitochondria-related pathways was only associated with MAFLD of a high histological grade, whereas the major regulators of mitochondrial biogenesis were not altered in mice or humans during MAFLD development. Collectively, our results suggest that impaired hepatic mitochondrial function is not closely associated with obesity-induced MAFLD. Therefore, therapeutic strategies targeting mitochondria for the treatment of MAFLD should be reconsidered.
| S-EPMC7475011 | biostudies-literature
Project description:Metabolic- (dysfunction) associated fatty liver disease (MAFLD) represents the predominant hepatopathy and one of the most important systemic, metabolic-related disorders all over the world associated with severe medical and socio-economic repercussions due to its growing prevalence, clinical course (steatohepatitis and/or hepatocellular-carcinoma), and related extra-hepatic comorbidities. To date, no specific medications for the treatment of this condition exist, and the most valid recommendation for patients remains lifestyle change. MAFLD has been associated with metabolic syndrome; its development and progression are widely influenced by the interplay between genetic, environmental, and nutritional factors. Nutrigenetics and nutrigenomics findings suggest nutrition's capability, by acting on the individual genetic background and modifying the specific epigenetic expression as well, to influence patients' clinical outcome. Besides, immunity response is emerging as pivotal in this multifactorial scenario, suggesting the interaction between diet, genetics, and immunity as another tangled network that needs to be explored. The present review describes the genetic background contribution to MAFLD onset and worsening, its possibility to be influenced by nutritional habits, and the interplay between nutrients and immunity as one of the most promising research fields of the future in this context.
| S-EPMC8156164 | biostudies-literature