Dysmetabolic comorbidities and non-alcoholic fatty liver disease: a stairway to metabolic dysfunction-associated steatotic liver disease
0
Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. This term does not describe the pathogenetic mechanisms and complications associated with NAFLD. The new definition, Metabolic Dysfunction-associated Steatotic Liver disease (MASLD), emphasizes the relationship between NAFLD and cardiometabolic comorbidities. Cardiovascular disease features, such as arterial hypertension and atherosclerosis, are frequently associated with patients with MASLD. Furthermore, these patients have a high risk of developing neoplastic diseases, primarily hepatocellular carcinoma, but also extrahepatic tumors, such as esophageal, gastric, and pancreatic cancers. Moreover, several studies showed the correlation between MASLD and endocrine disease. The imbalance of the gut microbiota, systemic inflammation, obesity, and insulin resistance play a key role in the development of these complications. This narrative review aims to clarify the evolution from NAFLD to the new nomenclature MASLD and evaluate its complications.
Keywords
INTRODUCTION
The most common cause of chronic liver disease (CLD) in the world is Non-alcoholic fatty liver disease (NAFLD), especially in Western countries. NAFLD was defined by the presence of Steatotic Liver Disease (SLD) without significant alcohol consumption or other chronic liver diseases[1]. Significant alcohol consumption is defined as an intake of > 21 drinks and > 14 drinks per week in two years in men and women, respectively[2]. However, the World Health Organization (WHO) defined a risk factor of health status for every alcohol level[3]. Indeed, low alcohol consumption could induce the progression from liver steatosis to non-alcoholic steatohepatitis (NASH) and fibrosis. For example, in a rat model, the combination of sweeteners, such as fructose and alcohol, is responsible for changes in the liver and in the serum characterizing type 2 diabetes mellitus (T2DM)[4]. Usually, NAFLD includes a broad spectrum of liver damage, possibly due to hepatocytic damage, inflammatory processes, and fibrosis[5]. The worldwide prevalence of NAFLD is around 25%-30% in the adult population. The highest prevalence rates have been reported in Latin America, the Middle East, and North Africa. The NAFLD diffusion is a consequence of the worldwide overweight “pandemic”. Indeed, WHO estimated that obesity affects more than 2 billion people worldwide[6]. The cause of this development is an unhealthy lifestyle. Western diet, over-consumption of alcohol, sedentary lifestyle, and smoking are the main risk factors of overweight[7]. These factors are strongly influenced by socio-demographic factors (such as gender, age, ethnicity, and socioeconomic status)[8]. The highest prevalence of obesity is observed in countries across America and Europe[9]. However, the prevalence has increased in developing countries in the last years, from 8% in 1980 to 13% in 2013, respectively[10]. The NAFLD mortality rate is 12.60 per 1,000 patients/year. The leading cause of death in patients with NAFLD is represented by cardiovascular events triggered by overweight/obesity, and by hepatic complications only when inflammation (NASH) and fibrosis develop[11]. Subsequently, the definition of NAFLD was considered inaccurate to reflect its pathogenesis. Moreover, it did not allow the correct stratification of patients for management when alcohol consumption is associated with increased caloric intake[4]. In 2020, the new nomenclature of metabolic dysfunction-associated fatty liver disease (MAFLD) was proposed[12,13]. MAFLD was defined by the presence of SLD associated with inclusion criteria: T2DM, overweight/obesity (body mass index, BMI ≥ 25 kg/m2), or the presence of metabolic dysregulation[1]. Additionally, MAFLD co-exists with other chronic liver diseases and is independent of alcoholic intake[12]. The disease progression is faster in MAFLD than in NAFLD due to dysmetabolic comorbidities. Indeed, recent evidence underlined that MAFLD was related to a higher rate of fibrosis and NASH[13]. Therefore, there are several limitations in the MAFLD term: the different etiologies and the inappropriate use of the term “fatty”. After four rounds of the Delphi survey, the definition of Metabolic Dysfunction-associated Steatotic Liver disease (MASLD) was chosen to replace NAFLD. MASLD was defined as SLD with at least one of five cardiometabolic risk factors without excessive alcohol intake (less than 140-30 g/week and 210-420 g/week for females and males, respectively)[14]. The diagnostic criteria of NAFLD and MASLD are summarized in Figure 1.
Figure 1. Diagnostic criteria of NAFLD, MAFLD and MASLD. MASLD: Metabolic Dysfunction-associated Steatotic Liver disease; NAFLD: Non-alcoholic fatty liver disease; MAFLD: Metabolic Dysfunction-associated fatty liver disease.
Aim
This recent change in nomenclature has created serious questions about its use. This narrative review aims to clarify the evolution from NAFLD to the new nomenclature MASLD and evaluate its complications.
THE CHANGE IN NOMENCLATURE
The main limitation of the term NAFLD is the difficulty of emphasizing the role of metabolic dysfunction in the pathogenesis of the disease. For this reason, a new term, MAFLD, has been proposed, which takes into account the metabolic and hepatic comorbidities associated with liver steatosis. In this way, it better captures both the hepatic and extrahepatic aspects of the patient compared to NAFLD[15]. Several studies have shown that patients with MAFLD have a worse hepatic profile compared to patients with NAFLD, which seems to be correlated not only with the presence of metabolic comorbidities but also hepatic[15-18]. Therefore, excluding patients with other hepatic etiologies in NAFLD would result in a failure to manage metabolic features in subjects who instead require multi-specialty approaches. A retrospective study analyzed the general characteristics of 175 patients with hepatic steatosis diagnosed by liver biopsy. Among these, 43.8% met only the criteria for MAFLD and 4.9% only those for NAFLD. Patients with only MAFLD had a higher BMI compared to those with NAFLD, and hepatic and metabolic comorbidities were not present in patients with NAFLD alone. Histologically, 48.1% of patients with MAFLD showed advanced-stage fibrosis[16]. These results were confirmed by another study conducted on 765 patients with hepatic steatosis. The percentage of patients with significant fibrosis was 93.9% in patients with MAFLD and 73% in patients with NAFLD[17]. Furthermore, another study observed not only an increase in fibrosis but also in biochemical indices of liver damage in patients with MAFLD alone compared to patients with NAFLD alone[18]. MAFLD, compared to NAFLD, is associated with both an increased severity of hepatic conditions and an increased risk of extrahepatic manifestations associated with metabolic comorbidities. In this regard, Huang et al. observed an increased risk of cardiovascular disease (CVD) in patients with MAFLD alone compared to patients with NAFLD alone[18]. The increased risk of CVD in MAFLD was confirmed by a study performed on 8,962,813 patients without previous CVD with a follow-up of ten years, which demonstrated the presence of 182,423 new cardiovascular events in MAFLD patients[19]. In addition, MAFLD is associated with an increased prevalence of renal comorbidities compared to NAFLD. In a study performed on 12,571 individuals, of whom 30.2% had MAFLD and 36.2% had NAFLD, patients with MAFLD had a lower estimated glomerular filtration rate and a higher prevalence of chronic kidney disease (CKD) compared to patients with NAFLD[20]. Finally, MAFLD, in addition to increasing the risk of hepatic and extrahepatic manifestations, is associated with increased mortality compared to NAFLD. In fact, a study conducted on 7,761 patients showed an increased risk of all-cause mortality and cardiovascular mortality in MAFLD patients compared to subjects with NAFLD[21]. Although MAFLD offers a better clinical framework for patients, the term “fatty” is considered stigmatizing. For this reason, the replacement of the term fatty with “steatotic” has been proposed, thus introducing the term MASLD. However, MASLD determines a semantic improvement, but it has different diagnostic criteria compared to MAFLD. In fact, the MASLD definition includes patients with a lower metabolic risk and excludes patients with other chronic liver diseases. However, this approach could be limiting in a real-life context[22]. In this regard, a recent study has highlighted how MASLD has a higher capture of lean patients compared to MAFLD[23]. Probably due to these differences, MASLD tends to fairly reproduce the NAFLD scenario, while MAFLD probably captures hepatic and extrahepatic outcomes more accurately. A recent study compared the clinical characteristics of patients with NAFLD, MAFLD, and MASLD. It was observed that in terms of hepatic, renal damage, and metabolic comorbidities, MAFLD was associated with worse outcomes than NAFLD, while MASLD presented clinical features overlapping with NAFLD[24]. Additionally, MAFLD is associated with higher cardiovascular, T2DM, and cancer-related mortality than MASLD[25]. These results may be related to MASLD involving a larger number of patients with a healthier metabolic profile compared to MAFLD and the exclusion of patients with hepatic comorbidities. In this context, Wang et al. have proposed to divide the MASLD patients into pure MASLD, MetALD (MASLD associated with increased alcohol consumption), and combinatorial MASLD (with other hepatic comorbidities) to avoid excluding patients with coexistent liver pathologies and facilitate their clinical management[26]. Overall, these nomenclatures are applicable to various types of patients in clinical practice.
EPIDEMIOLOGY OF MASLD
To our knowledge, there are no studies evaluating the epidemiology of MASLD in the general population, but only in individuals with risk factors. According to Perazzo et al., epidemiological data from NAFLD and MAFLD in the general population can apply to the MASLD definition. In a cohort of 10,651 individuals without SLD diagnosis, the prevalence of NAFLD, MAFLD, and MASLD was 34.7%, 34.9%, and 33.4%, respectively[1]. Subsequently, Song et al. assessed the prevalence of specific SLD subtypes among 1,016 randomly selected individuals with SLD diagnosed by proton magnetic resonance spectroscopy. NAFLD, MAFLD, and MASLD prevalence were 25.7%, 25.9%, and 26.7%, respectively[27]. In another study, among 15,453 subjects, the prevalence of NAFLD, MAFLD, and MASLD was 11.6%, 15.2%, and 10.7%, respectively[28]. In a single-center cohort study of 745 patients, with SLD diagnosis based on magnetic resonance imaging derived proton density fat fraction (MRI-PDFF), the prevalence of NAFLD, MAFLD, and MASLD was 81%, 84%, and 84%, respectively. However, among 104 patients with SLD diagnosed with liver biopsy, the prevalence changes (99% NAFLD, 100% both MAFLD and MASLD)[17]. These studies showed no significant difference in prevalence between MASLD, NAFLD and MAFLD in the general population[1,27-29]. However, these results in a target population might change. For example, the prevalence of MASLD and MAFLD in lean patients is different. Among 170 patients with lean NAFLD, 142 (83.5%) satisfied the MASLD criteria, while only 84 (49.4%) had MAFLD. Despite this, it should be considered that lean NAFLD is a relatively rare case compared to the overwhelming majority of obese patients[30]. Therefore, more clinical trials on the target population are needed. Table 1 summarizes the epidemiological studies regarding NAFLD, MAFLD, and MASLD.
Epidemiological studies about NAFLD, MAFLD and MASLD
| Authors | Patients | NAFLD prevalence | MAFLD prevalence | MASLD prevalence |
| Perazzo et al., 2023[1] | 10,651 patients without SLD diagnosis | 34.7% | 34.9% | 33.4% |
| Song et al., 2023[27] | 1,016 patients without SLD diagnosis | 25.7% | 25.9% | 26.7% |
| He et al., 2023[28] | 15,453 patients without SLD diagnosis | 11.6% | 15.2% | 10.7% |
| Yang et al., 2023[29] | 717 patients (SLD diagnosed with MRI-PDFF) 104 patients (SLD diagnosed with liver biopsy) | 81% 99% | 84% 100% | 84% 100% |
| De et al., 2023[30] | 170 patients with lean NAFLD | n.a. | 49.4% | 83.5% |
RISK FACTORS OF MASLD
Age, gender, tobacco, ethnicity, and genetic factors
Various risk factors, such as older age, male gender, tobacco, ethnicity, and genetic factors, are involved in the development of MASLD[1,31,32]. The prevalence of MASLD in males is higher than in females
Cardiovascular and metabolic features
Low levels of high-density lipoproteins (HDL) and an increase in glucose levels, homeostatic model assessment, triglycerides and BMI are positively correlated with hepatic steatosis, fibrosis progression, and the outcome of patients, including mortality. In this regard, it is necessary to assess the medical records and the historical data (especially the daily alcohol intake) of patients and then the clinical-laboratory parameters already mentioned[1,47-49]. The predominant cardiovascular risk factor of MASLD is BMI >
GUT MICROBIOTA IN MASLD
Gut microbiota in health and disease
Gut microbiota is a complex ecosystem comprising approximately 1014 bacteria, with Firmicutes and Bacteroidetes as predominant phyla. Its eubiosis maintains the health status[64]. However, its imbalance (dysbiosis) has been linked to the development of T2DM, IBD, CKD, and liver diseases[65]. The microbiota's role in metabolizing choline, phosphatidylcholine, and carnitine leads to trimethylamine-N-oxide, which is associated with atherosclerosis and increased mortality in CVD and CKD[66]. Gut dysbiosis is correlated with the development of colorectal cancer (CRC)[67]. Indeed, CRC patients have a higher abundance of Bacteroidetes but a lower abundance of Firmicutes phyla[68]. IBDs are linked to Proteobacteria/Firmicutes imbalance[69,70].
Gut microbiota in MASLD pathogenesis
Recent research focuses on the role of gut dysbiosis in CLD, including MASLD[71,72]. Pre-clinical studies indicate that Bacteroidetes are linked to MASLD development, and targeted interventions can mitigate disease progression[73]. Qiao et al. evaluate how the higher abundance of Bacteroides xylanisolvens in the intestinal tract of attenuated mice reduced MASLD progression[74,75]. A recent study showed how a high-fat diet (HFD) induced MASLD, altering Firmicutes/Bacteroidetes ratio. Additionally, treatment with a butyrate-producing bacterium, Kineothrix alysoides, mitigated liver fat accumulation by restoring gut eubiosis[76]. Further investigations explored the association between gut microbiota and MASLD complications, revealing specific bacterial strains' potential therapeutic effects: Bacteroides vulgatus reduced atherosclerotic lesion formation, while Bacteroides uniformis reduced cholesterol and triglyceride levels, alleviating hepatic steatosis severity[77,78]. Dysbiosis promotes the fermentation of complex carbohydrates, leading to SCFAs production[79-81]. Furthermore, lactate produced by Lactobacillus and Bifidobacterium genera prolongs post-meal satiety by providing a substrate for neuronal cells[82,83]. Gut imbalance and altered BA homeostasis may contribute to metabolic dysregulation in T2DM and obesity[84-85]. Additionally, oxygen-free radicals modulated by the bacterial microflora could overcome antioxidant barriers that cause cellular damage, inflammation, and even apoptosis. Excessive generation of oxygen free radicals caused by gut dysbiosis and translocation of bacterial endotoxin to the liver is closely related to the pathogenesis of NAFLD and dysmetabolic comorbidities that promote the progression into MASLD[86]. Liver damage is linked to an altered intestinal epithelial barrier. In a pre-clinical study, an HFD-induced gut dysbiosis with intestinal vascular barrier damage led to bacterial translocation into the portal circulation. Genetic manipulation of the β-catenin pathway and obeticholic acid treatment prevented barrier disruption[87]. In another study, mice with liver cirrhosis exhibited increased gut permeability, bacterial translocation, and FXR receptor modulation. Treatment with FXR agonists improved the epithelial barrier, reducing bacterial translocation and liver damage[88]. Figure 2 summarizes the pathway that involves the gut microbiota in MASLD pathogenesis.
Figure 2. Gut microbiota and MASLD pathogenesis. MASLD: Metabolic Dysfunction-associated Steatotic Liver Disease; BAs: Bile Acids; BMI: Body Mass Index; FFA: Free Fatty Acids; HDL-C: High-Density Lipoproteins Cholesterol.
MASLD COMPLICATIONS
Relationship between liver steatosis and metabolic comorbidities
The new nomenclature MASLD emphasizes the relationship between NAFLD and metabolic comorbidities. Recent studies reveal a 46.7% prevalence of MASLD in T2DM patients, while the cardiovascular event rate was 2.03 per 100 person-years in MASLD individuals[89,90]. In MASLD, intrahepatic toxic lipid accumulation induces endothelial dysfunction and atherogenic dyslipidemia, marked by reduced HDL and elevated low-density lipoproteins and triglycerides levels[91]. The liver produces inflammatory biomarkers that usually increase in MASLD patients[92]. Visceral adiposity in MASLD alters hormone metabolism, adipokine production, and insulin-related factors, fostering systemic inflammation and insulin resistance. Elevated insulin-like growth factor 1 levels correlate with CRC risk. Adiponectin and leptin, reduced in obese MASLD patients, influence CRC progression[93-95]. Gut dysbiosis could also mediate MASLD-associated carcinogenesis, probably through increased intestinal permeability in both the small and large intestine, leading to bacterial translocation, systemic inflammation, and tumorigenesis, as shown in CRC[96]. Increased permeability of the small intestine is known in patients with CLD. In a recent study, small intestinal permeability was assessed by a double sugar (lactulose:rhamnose) assay in patients with CLD and in healthy controls. Small intestinal permeability was significantly higher in the CLD group than in healthy controls[97]. Furthermore, in a recent study, the bacterial composition in the small intestine was evaluated through biopsies during double-balloon enteroscopy. As reported by the Authors, Proteobacteria and Firmicutes phyla were abundant in the jejunum and proximal ileum, while Firmicutes and Bacteroidetes phyla were abundant in the distal ileum[98].
MASLD and non-dysmetabolic diseases
MASLD is linked to non-dysmetabolic diseases, including CKD, IBD, endocrinopathies, and lung diseases. MASLD patients exhibit a higher prevalence of CKD, potentially associated with hyperuricemia or T2DM[99]. Studies indicate a correlation between hypothyroidism severity and MASLD, while limited evidence is available on hyperthyroidism. Low prolactin levels are associated with MASLD in women[100]. NAFLD is related to decreased adult lung function and obstructive sleep apnea syndrome development[101], while data on MASLD are lacking. MASLD patients have a higher risk of developing sarcopenia due to nutritional disorders, gut dysbiosis, and insulin resistance[102,103]. A mutual relationship between sarcopenia and insulin resistance exists due to mammalian target complex 1 rapamycin (mTORC1) action in skeletal muscle. Hyperinsulinemia activates mTORC1, but prolonged activation causes a negative feedback signal, leading to mTORC1 inhibition, autophagy, and increased protein degradation[104].
Hepatocellular carcinoma and cholangiocarcinoma
Hepatocellular carcinoma (HCC) ranks among the most prevalent solid tumors globally and stands as the third leading cause of mortality worldwide. Major culprits for HCC include hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, alcohol abuse, exposure to aflatoxin, and schistosomiasis[105]. Notably, NAFLD has emerged as a significant contributor to HCC development in recent years[106]. Particularly in the United States, NAFLD has become the fastest-growing cause of HCC among liver transplant recipients and candidates. A similar trend was observed in Europe, South Korea, and Southeast Asia, where NAFLD-related HCC cases have risen over the last two decades[107]. Notably, HCC associated with NAFLD tends to occur at an older age compared to viral-induced cases, often diagnosed at later stages, leading to poorer survival rates compared to those linked to viral or alcoholic hepatitis[108]. Importantly, NAFLD-related HCC may develop without liver cirrhosis, with a significantly higher prevalence observed in individuals with non-cirrhotic NASH compared to other liver diseases[109]. The pathogenesis of HCC in NAFLD involves insulin resistance and metabolic dysfunction, triggering the release of free fatty acids and subsequent oxidative stress, along with the secretion of proinflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α. Obesity exacerbates this process by inducing chronic inflammation, activating oncogenic transcription factors like STAT3, and fostering gut dysbiosis with hepatocarcinogenesis promotion[110]. The transition from NAFLD to MAFLD has highlighted its role as a primary cause of HCC[111]. Furthermore, HCC development in MAFLD is closely linked to the degree of fibrosis and can occur in non-cirrhotic livers[112]. The recent shift to the terminology of MASLD has prompted a reassessment of HCC risk, revealing higher risks for first-degree relatives of MASLD patients[113]. The scientific research has highlighted the role of non-coding RNAs, specifically microRNAs/small regulatory RNAs (miRNAs/miRs), in liver diseases. MiR-21-5p, implicated in MASLD progression to hepatocarcinogenesis, activates peroxisome replication, inducing lipid peroxidation and inflammation-fibrosis. Inhibiting miR-21-5p may offer therapeutic potential in HCC[114]. Additionally, gut dysbiosis contributes to HCC by increasing hepatic exposure to bacterial metabolites, activating toll-like receptor-4, and promoting fibrosis, emphasizing the therapeutic potential of gut microbiota modulation[115]. Cholangiocarcinoma (CCA), an aggressive neoplasm of the bile ducts, accounts for approximately 3%-5% of all gastrointestinal cancers. The prognosis of CCA is poor because 95% of patients die within five years. According to a recent meta-analysis of seven case-control studies, NAFLD was significantly associated with an increased risk of CCA for both subtypes[116]. On the other hand, a more recent analysis showed that NAFLD is associated with an elevated risk of both total cholangiocarcinoma and intrahepatic cholangiocarcinoma (iCCA) but without a significant association with extrahepatic cholangiocarcinoma (eCCA)[117]. Furthermore, CCA arising from NASH patients has a severe prognosis compared to that from NAFLD[118]. In recent years, the association between MAFLD and CCA was evaluated. In this regard, emerging risk factors like obesity, T2DM, and MAFLD were primarily associated with iCCA, while traditional risk factors such as biliary cysts, liver cirrhosis, HBV, and HCV infections were associated with both iCCA and eCCA[119]. Moreover, a recent study involving 173 patients who underwent liver resection for iCCA found a high prevalence of MAFLD, significantly correlated with changes in body composition such as sarcopenia and visceral obesity[120]. The association between MASLD and CCA, especially with iCCA, has been proposed, supported by findings in mice models, demonstrating that MASLD exacerbates cholangitis and iCCA development[121,122]. Additionally, overexpression of osteopontin in the tumor stroma of MASLD patients with iCCA has been observed, suggesting its potential as a predictive biomarker and therapeutic target[123]. Nevertheless, further studies are needed to elucidate the specific relationship between MASLD and CCA. Hepatic and extrahepatic complications of MASLD have been reported in Figure 3.
Figure 3. Hepatic and extrahepatic complications of MASLD. MASLD: Metabolic Dysfunction-associated Steatotic Liver disease, CVD: Cardiovascular Disease; CKD: Chronic Kidney Disease; HCC: Hepatocellular Carcinoma; CCA: Cholangiocarcinoma; IBD: Inflammatory Bowel Disease.
CONCLUSIONS
MASLD has been defined as SLD with at least one of the five cardiometabolic risk factors without excessive alcohol intake. Furthermore, it is a multi-factorial disease with a significant public health impact. Indeed, risk factors and complications necessitate the involvement of several medical specialists. Moreover, given the recent proposal of this new nomenclature, there is an urgent need to perform further clinical studies on large cohorts of patients. At the same time, future research should implement the use of new diagnostic tools and robust biomarkers for early detection of MASLD, especially in patients at risk. In this regard, the application of new algorithms and artificial intelligence could help in clinical practice. Nevertheless, further evidence is needed to clarify the clinical impact of MASLD in real-world settings.
DECLARATIONS
Authors’ contributions
Wrote, reviewed, and edited the manuscript: Colaci C, Gambardella ML
Provided figures and tables: Colaci C, Gambardella ML
Reviewed and approved the final manuscript as submitted: Colaci C, Gambardella ML, Scarlata GGM, Boccuto L, Scarpellini E
Read and approved the final manuscript: Boccuto L, Colica C, Luzza F, Scarpellini E, Mendez-Sanchez N, Abenavoli L
Conceptualized and designed the review: Abenavoli L
Availability of data and materials
Not applicable.
Financial support and sponsorship
None.
Conflicts of interest
All authors declared that there are no conflicts of interest.
Ethical approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Copyright
© The Author(s) 2024.
REFERENCES
1. Perazzo H, Pacheco AG, Griep RH. Collaborators. Changing from NAFLD through MAFLD to MASLD: Similar prevalence and risk factors in a large Brazilian cohort. J Hepatol 2024;80:e72-4.
2. Chalasani N, Younossi Z, Lavine JE, et al. American Gastroenterological Association; American Association for the Study of Liver Diseases; American College of Gastroenterologyh. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American gastroenterological association, American association for the study of liver diseases, and American college of gastroenterology. Gastroenterology 2012;142:1592-609.
3. World Health Organization. No level of alcohol consumption is safe for our health. Available from: https://www.who.int/europe/news/item/04-01-2023-no-level-of-alcohol-consumption-is-safe-for-our-health [Last accessed on 28 Mar 2024].
4. Alwahsh SM, Xu M, Schultze FC, et al. Combination of alcohol and fructose exacerbates metabolic imbalance in terms of hepatic damage, dyslipidemia, and insulin resistance in rats. PLoS One 2014;9:e104220.
5. Eshraghian A, Nikeghbalian S, Dehghani M, et al. Nonalcoholic steatohepatitis is the most rapidly growing indication for liver transplantation in Iranian patients. Exp Clin Transplant 2022;20:487-94.
6. World Health Organization. World obesity day 2022-accelerating action to stop obesity. Available online: https://www.who.int/news/item/04-03-2022-world-obesity-day-2022-accelerating-action-to-stop-obesity [Last accessed on 23 Jan 2024].
7. Keramat SA, Alam K, Gow J, Biddle SJH. Impact of Disadvantaged neighborhoods and lifestyle factors on adult obesity: evidence from a 5-year cohort study in Australia. Am J Health Promot 2021;35:28-37.
8. Sun Y, Wang S, Sun X. Estimating neighbourhood-level prevalence of adult obesity by socio-economic, behavioural and built environment factors in New York City. Public Health 2020;186:57-62.
9. Boutari C, Mantzoros CS. A 2022 update on the epidemiology of obesity and a call to action: as its twin COVID-19 pandemic appears to be receding, the obesity and dysmetabolism pandemic continues to rage on. Metabolism 2022;133:155217.
10. Ng M, Fleming T, Robinson M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the global burden of disease study 2013. Lancet 2014;384:766-81.
11. Angulo P, Kleiner DE, Dam-Larsen S, et al. Liver fibrosis, but no other histologic features, is associated with long-term outcomes of patients with nonalcoholic fatty liver disease. Gastroenterology 2015;149:389-97.e10.
12. Eslam M, Sanyal AJ, George J. International Consensus Panel. MAFLD: a consensus-driven proposed nomenclature for metabolic associated fatty liver disease. Gastroenterology 2020;158:1999-2014.e1.
13. Ramírez-Mejía MM, Qi X, Abenavoli L, Romero-Gómez M, Eslam M, Méndez-Sánchez N. Metabolic dysfunction: The silenced connection with fatty liver disease. Ann Hepatol 2023;28:101138.
14. Rinella ME, Lazarus JV, Ratziu V, et al. NAFLD Nomenclature consensus group. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology 2023;78:1966-86.
15. Alharthi J, Gastaldelli A, Cua IH, Ghazinian H, Eslam M. Metabolic dysfunction-associated fatty liver disease: a year in review. Curr Opin Gastroenterol 2022;38:251-60.
16. Cheng YM, Wang CC, Kao JH. Metabolic associated fatty liver disease better identifying patients at risk of liver and cardiovascular complications. Hepatol Int 2023;17:350-6.
17. Yamamura S, Eslam M, Kawaguchi T, et al. MAFLD identifies patients with significant hepatic fibrosis better than NAFLD. Liver Int 2020;40:3018-30.
18. Huang SC, Su HJ, Kao JH, et al. Clinical and histologic features of patients with biopsy-proven metabolic dysfunction-associated fatty liver disease. Gut Liver 2021;15:451-8.
19. Lee H, Lee YH, Kim SU, Kim HC. Metabolic dysfunction-associated fatty liver disease and incident cardiovascular disease risk: a nationwide cohort study. Clin Gastroenterol Hepatol 2021;19:2138-47.e10.
21. Kim D, Konyn P, Sandhu KK, Dennis BB, Cheung AC, Ahmed A. Metabolic dysfunction-associated fatty liver disease is associated with increased all-cause mortality in the United States. J Hepatol 2021;75:1284-91.
22. Ramírez-Mejía MM, Eslam M, Méndez-Sánchez N. Letter to the EDITOR: THE MAFLD and MASLD conundrum: is it reinvention of the wheel? J Hepatol 2024;79:S0168-8278(24)00158.
23. Ramírez-Mejía MM, Jiménez-Gutiérrez C, Eslam M, George J, Méndez-Sánchez N. Breaking new ground: MASLD vs. MAFLD-which holds the key for risk stratification? Hepatol Int 2024;18:168-78.
24. Chen L, Tao X, Zeng M, Mi Y, Xu L. Clinical and histological features under different nomenclatures of fatty liver disease: NAFLD, MAFLD, MASLD and MetALD. J Hepatol 2024;80:e64-6.
25. Zhao Q, Deng Y. Comparison of mortality outcomes in individuals with MASLD and/or MAFLD. J Hepatol 2024;80:e62-4.
26. Wang CC, Cheng YM, Kao JH. Letter to the editor: statement of steatotic liver disease-A great leap toward the global standardization. Hepatology 2024;79:E7-8.
27. Song SJ, Lai JC, Wong GL, Wong VW, Yip TC. Can we use old NAFLD data under the new MASLD definition? J Hepatol 2024;80:e54-6.
28. He L, Zheng W, Qiu K, Kong W, Zeng T. Changing from NAFLD to MASLD: The new definition can more accurately identify individuals at higher risk for diabetes. J Hepatol 2024;80:e85-7.
29. Yang A, Zhu X, Zhang L, Ding Y. Transitioning from NAFLD to MAFLD and MASLD: Consistent prevalence and risk factors in a Chinese cohort. J Hepatol 2024;80:e154-5.
30. De A, Bhagat N, Mehta M, Taneja S, Duseja A. Metabolic dysfunction-associated steatotic liver disease (MASLD) definition is better than MAFLD criteria for lean patients with NAFLD. J Hepatol 2024;80:e61-2.
31. Hutchison AL, Tavaglione F, Romeo S, Charlton M. Endocrine aspects of metabolic dysfunction-associated steatotic liver disease (MASLD): Beyond insulin resistance. J Hepatol 2023;79:1524-41.
32. Wang Y, Huang Y, Antwi SO, Taner CB, Yang L. Racial disparities in liver disease mortality trends among black and white populations in the United States, 1999-2020: an analysis of CDC WONDER database. Am J Gastroenterol 2024;119:682-9.
33. Comitato R, Saba A, Turrini A, Arganini C, Virgili F. Sex hormones and macronutrient metabolism. Crit Rev Food Sci Nutr 2015;55:227-41.
34. Yuan Q, Wang H, Gao P, et al. Prevalence and risk factors of metabolic-associated fatty liver disease among 73,566 individuals in Beijing, China. Int J Environ Res Public Health 2022;19:2096.
35. Chen YL, Li H, Li S, et al. Prevalence of and risk factors for metabolic associated fatty liver disease in an urban population in China: a cross-sectional comparative study. BMC Gastroenterol 2021;21:212.
36. Chen Q, Zhao L, Mei L, et al. Association of sex hormones with hepatic steatosis in men with chronic hepatitis B. Dig Liver Dis 2022;54:378-84.
37. Liu L, Fu Q, Li T, et al. Gut microbiota and butyrate contribute to nonalcoholic fatty liver disease in premenopause due to estrogen deficiency. PLoS One 2022;17:e0262855.
38. Eng PC, Forlano R, Tan T, Manousou P, Dhillo WS, Izzi-Engbeaya C. Non-alcoholic fatty liver disease in women - Current knowledge and emerging concepts. JHEP Rep 2023;5:100835.
39. Anderson WD, Soh JY, Innis SE, et al. Sex differences in human adipose tissue gene expression and genetic regulation involve adipogenesis. Genome Res 2020;30:1379-92.
40. Jang YS, Joo HJ, Park YS, Park EC, Jang SI. Association between smoking cessation and non-alcoholic fatty liver disease using NAFLD liver fat score. Front Public Health 2023;11:1015919.
41. Cui Y, Zhu Q, Lou C, et al. Gender differences in cigarette smoking and alcohol drinking among adolescents and young adults in Hanoi, Shanghai, and Taipei. J Int Med Res 2018;46:5257-68.
42. Vespasiani-Gentilucci U, Valenti L, Romeo S. Usefulness of PNPLA3 variant for predicting hepatic events in steatotic liver disease: a matter of ethnicity or baseline risk? Liver Int 2023;43:2052-4.
43. Romeo S, Kozlitina J, Xing C, et al. Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease. Nat Genet 2008;40:1461-5.
44. Wagenknecht LE, Palmer ND, Bowden DW, et al. Association of PNPLA3 with non-alcoholic fatty liver disease in a minority cohort: the insulin resistance atherosclerosis family study. Liver Int 2011;31:412-6.
45. Huang G, Wallace DF, Powell EE, Rahman T, Clark PJ, Subramaniam VN. Gene variants implicated in steatotic liver disease: opportunities for diagnostics and therapeutics. Biomedicines 2023;11:2809.
46. Goffredo M, Caprio S, Feldstein AE, et al. Role of TM6SF2 rs58542926 in the pathogenesis of nonalcoholic pediatric fatty liver disease: a multiethnic study. Hepatology 2016;63:117-25.
47. Semmler G, Balcar L, Wernly S, et al. Insulin resistance and central obesity determine hepatic steatosis and explain cardiovascular risk in steatotic liver disease. Front Endocrinol 2023;14:1244405.
48. Fernández-Barrena MG, Avila MA. Frontiers in fatty liver: recent advances in pathogenic mechanisms, assessment of patients' prognosis and pharmacotherapy: MASLD: new pathogenic mechanisms, risk assessment tools and drug therapies. J Physiol Biochem 2023;79:811-3.
49. Yang T, Yin J, Li J, Wang Q. The influence of different combinations of cardiometabolic risk factors on the prevalence of MASLD and risk of advanced fibrosis deserves attention. J Hepatol 2024;80:e82-5.
50. Balogun O, Wang JY, Shaikh ES, et al. Effect of combined tobacco use and type 2 diabetes mellitus on prevalent fibrosis in patients with MASLD. Hepatol Commun 2023;7:e0300.
51. Forlano R, Stanic T, Jayawardana S, et al. A prospective study on the prevalence of MASLD in people with type-2 diabetes in the community. Cost effectiveness of screening strategies. Liver Int 2024;44:61-71.
52. Ciardullo S, Vergani M, Perseghin G. Nonalcoholic fatty liver disease in patients with type 2 diabetes: screening, diagnosis, and treatment. J Clin Med 2023;12:5597.
53. Yang G, Liu R, Rezaei S, Liu X, Wan YY. Uncovering the gut-liver axis biomarkers for predicting metabolic burden in mice. Nutrients 2023;15:3406.
54. Heller B, Reiter FP, Leicht HB, et al. Salt-intake-related behavior varies between sexes and is strongly associated with daily salt consumption in obese patients at high risk for MASLD. Nutrients 2023;15:3942.
55. Pei E, Wang H, Li Z, Xie X, Cai L, Lin M. Endoplasmic reticulum stress inhibitor may substitute for sleeve gastrectomy to alleviate metabolic dysfunction-associated steatotic liver disease. Clin Res Hepatol Gastroenterol 2023;47:102229.
56. Hepburn C, von Roenn N. Nutrition in liver disease - a review. Curr Gastroenterol Rep 2023;25:242-9.
57. Zhang X, Daniel CR, Soltero V, et al. A study of dietary patterns derived by cluster analysis and their association with metabolic dysfunction-associated steatotic liver disease severity among Hispanic patients. Am J Gastroenterol 2024;119:505-11.
58. Tamilmani P, Sathibabu Uddandrao VV, Chandrasekaran P, et al. Linalool attenuates lipid accumulation and oxidative stress in metabolic dysfunction-associated steatotic liver disease via Sirt1/Akt/PPRA-α/AMPK and Nrf-2/HO-1 signaling pathways. Clin Res Hepatol Gastroenterol 2023;47:102231.
59. Chen VL, Song MW, Suresh D, Wadhwani SI, Perumalswami P. Effects of social determinants of health on mortality and incident liver-related events and cardiovascular disease in steatotic liver disease. Aliment Pharmacol Ther 2023;58:537-45.
60. Kani AS, Ozercan A, Kani HT, Eren F, Sayar K, Yilmaz Y. Chronotype preference, sleep quality, and night-eating behaviors in patients with metabolic dysfunction-associated steatotic liver disease: assessing the relationship with disease severity and fibrosis. Hepatol Forum 2023;4:123-8.
61. Lai J, Luo L, Zhou T, Feng X, Ye J, Zhong B. Alterations in circulating bile acids in metabolic dysfunction-associated steatotic liver disease: a systematic review and meta-analysis. Biomolecules 2023;13:1356.
62. García-Mateo S, Martínez-Domínguez SJ, Gargallo-Puyuelo CJ, et al. Lifestyle can exert a significant impact on the development of metabolic complications and quality life in patients with inflammatory bowel disease. Nutrients 2023;15:3983.
63. Martínez-Domínguez SJ, García-Mateo S, Gargallo-Puyuelo CJ, et al. Inflammatory bowel disease is an independent risk factor for metabolic dysfunction-associated steatotic liver disease in lean individuals. Inflamm Bowel Dis 2023;Online ahead of print:izad175.
64. Gomaa EZ. Human gut microbiota/microbiome in health and diseases: a review. Antonie Van Leeuwenhoek 2020;113:2019-40.
65. Chen Y, Zhou J, Wang L. Role and mechanism of gut microbiota in human disease. Front Cell Infect Microbiol 2021;11:625913.
66. Rutsch A, Kantsjö JB, Ronchi F. The gut-brain Axis: how microbiota and host inflammasome influence brain physiology and pathology. Front Immunol 2020;11:604179.
68. Wong SH, Yu J. Gut microbiota in colorectal cancer: mechanisms of action and clinical applications. Nat Rev Gastroenterol Hepatol 2019;16:690-704.
69. Shan Y, Lee M, Chang EB. The gut microbiome and inflammatory bowel diseases. Annu Rev Med 2022;73:455-68.
70. Laserna-Mendieta EJ, Clooney AG, Carretero-Gomez JF, et al. Determinants of reduced genetic capacity for butyrate synthesis by the gut microbiome in crohn's disease and ulcerative colitis. J Crohns Colitis 2018;12:204-16.
71. Milano W, De Biasio V, Di Munzio W, Foggia G, Capasso A. Obesity: The new global epidemic pharmacological treatment, opportunities and limits for personalized therapy. Endocr Metab Immune Disord Drug Targets 2020;20:1232-43.
72. Sumida Y, Yoneda M. Current and future pharmacological therapies for NAFLD/NASH. J Gastroenterol 2018;53:362-76.
73. Chiu CC, Ching YH, Li YP, et al. Nonalcoholic fatty liver disease is exacerbated in high-fat diet-fed gnotobiotic mice by colonization with the gut microbiota from patients with nonalcoholic steatohepatitis. Nutrients 2017;9:1220.
74. Qiao S, Bao L, Wang K, et al. Activation of a specific gut bacteroides-folate-liver axis benefits for the alleviation of nonalcoholic hepatic steatosis. Cell Rep 2020;32:108005.
76. Choi KJ, Yoon MY, Kim JE, Yoon SS. Gut commensal Kineothrix alysoides mitigates liver dysfunction by restoring lipid metabolism and gut microbial balance. Sci Rep 2023;13:14668.
77. Yoshida N, Emoto T, Yamashita T, et al. Bacteroides vulgatus and Bacteroides dorei Reduce Gut Microbial Lipopolysaccharide Production and Inhibit Atherosclerosis. Circulation 2018;138:2486-98.
78. López-Almela I, Romaní-Pérez M, Bullich-Vilarrubias C, et al. Bacteroides uniformis combined with fiber amplifies metabolic and immune benefits in obese mice. Gut Microbes 2021;13:1-20.
79. Koh A, De Vadder F, Kovatcheva-Datchary P, Bäckhed F. From dietary fiber to host physiology: short-chain fatty acids as key bacterial metabolites. Cell 2016;165:1332-45.
80. Iruzubieta P, Medina JM, Fernández-López R, Crespo J, de la Cruz F. A role for gut microbiome fermentative pathways in fatty liver disease progression. J Clin Med 2020;9:1369.
81. de la Cuesta-Zuluaga J, Mueller NT, Álvarez-Quintero R, et al. Higher fecal short-chain fatty acid levels are associated with gut microbiome dysbiosis, obesity, hypertension and cardiometabolic disease risk factors. Nutrients 2018;11:51.
82. Wu Y, He H, Cheng Z, Bai Y, Ma X. The role of neuropeptide y and peptide yy in the development of obesity via gut-brain axis. Curr Protein Pept Sci 2019;20:750-8.
83. Jiao N, Baker SS, Chapa-Rodriguez A, et al. Suppressed hepatic bile acid signalling despite elevated production of primary and secondary bile acids in NAFLD. Gut 2018;67:1881-91.
84. Chávez-Talavera O, Tailleux A, Lefebvre P, Staels B. Bile acid control of metabolism and inflammation in obesity, type 2 diabetes, dyslipidemia, and nonalcoholic fatty liver disease. Gastroenterology 2017;152:1679-94.e3.
85. Liang Y, Chen H, Liu Y, et al. Association of MAFLD with diabetes, chronic kidney disease, and cardiovascular disease: a 4.6-year cohort study in China. J Clin Endocrinol Metab 2022;107:88-97.
86. Mouries J, Brescia P, Silvestri A, et al. Microbiota-driven gut vascular barrier disruption is a prerequisite for non-alcoholic steatohepatitis development. J Hepatol 2019;71:1216-28.
87. Sorribas M, Jakob MO, Yilmaz B, et al. FXR modulates the gut-vascular barrier by regulating the entry sites for bacterial translocation in experimental cirrhosis. J Hepatol 2019;71:1126-40.
88. Chan WL, Chong SE, Chang F, et al. Long-term clinical outcomes of adults with metabolic dysfunction-associated fatty liver disease: a single-centre prospective cohort study with baseline liver biopsy. Hepatol Int 2023;17:870-81.
89. Ramírez-Mejía MM, Méndez-Sánchez, N. What is in a name: from NAFLD to MAFLD and MASLD-unraveling the complexities and implications. Curr Hepatology Rep 2023;22:221-7.
90. Nazir S, Jankowski V, Bender G, Zewinger S, Rye KA, van der Vorst EPC. Interaction between high-density lipoproteins and inflammation: function matters more than concentration! Adv Drug Deliv Rev 2020;159:94-119.
91. Heeren J, Scheja L. Metabolic-associated fatty liver disease and lipoprotein metabolism. Mol Metab 2021;50:101238.
92. Mantovani A, Petracca G, Beatrice G, et al. Non-alcoholic fatty liver disease and increased risk of incident extrahepatic cancers: a meta-analysis of observational cohort studies. Gut 2022;71:778-88.
93. Pati S, Irfan W, Jameel A, Ahmed S, Shahid RK. Obesity and cancer: a current overview of epidemiology, pathogenesis, outcomes, and management. Cancers 2023;15:485.
94. Umar MI, Hassan W, Murtaza G, et al. The adipokine component in the molecular regulation of cancer cell survival, proliferation and metastasis. Pathol Oncol Res 2021;27:1609828.
95. Jiménez-Cortegana C, García-Galey A, Tami M, et al. Role of leptin in non-alcoholic fatty liver disease. Biomedicines 2021;9:762.
96. Deng Y, Zhao Q, Gong R. Association between metabolic associated fatty liver disease and chronic kidney disease: a cross-sectional study from NHANES 2017-2018. Diabetes Metab Syndr Obes 2021;14:1751-61.
97. Raj AS, Shanahan ER, Tran CD, et al. Dysbiosis of the duodenal mucosal microbiota is associated with increased small intestinal permeability in chronic liver disease. Clin Transl Gastroenterol 2019;10:e00068.
98. Vuik F, Dicksved J, Lam SY, et al. Composition of the mucosa-associated microbiota along the entire gastrointestinal tract of human individuals. United European Gastroenterol J 2019;7:897-907.
99. Ruan Z, Lu T, Chen Y, et al. Association between psoriasis and nonalcoholic fatty liver disease among outpatient US adults. JAMA Dermatol 2022;158:745-53.
100. Wang H, Gao Q, He S, et al. Self-reported snoring is associated with nonalcoholic fatty liver disease. Sci Rep 2020;10:9267.
101. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: executive summary: a report of the American college of Cardiology/American heart association task force on clinical practice guidelines. Hypertension 2018;71:1269-324.
102. Cruz-Jentoft AJ, Bahat G, Bauer J, et al. Writing Group for the European Working Group on Sarcopenia in Older People 2 (EWGSOP2); and the Extended Group for EWGSOP2. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing 2019;48:16-31.
103. Kumar R, Prakash SS, Priyadarshi RN, Anand U. Sarcopenia in chronic liver disease: a metabolic perspective. J Clin Transl Hepatol 2022;10:1213-22.
104. Mohammadi-Motlagh HR, Sadeghalvad M, Yavari N, et al. β cell and autophagy: what do we know? Biomolecules 2023;13:649.
105. Mazzotta AD, Bonci D. Advancements in hepatocellular carcinoma diagnosis and treatment: liquid biopsy and surgical as precision treatment. Hepatoma Res 2024;10:8.
106. Li J, Zou B, Yeo YH, et al. Prevalence, incidence, and outcome of non-alcoholic fatty liver disease in Asia, 1999-2019: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol 2019;4:389-98.
107. Pais R, Fartoux L, Goumard C, et al. Temporal trends, clinical patterns and outcomes of NAFLD-related HCC in patients undergoing liver resection over a 20-year period. Aliment Pharmacol Ther 2017;46:856-63.
108. Lin L, Li Z, Yan L, Liu Y, Yang H, Li H. Global, regional, and national cancer incidence and death for 29 cancer groups in 2019 and trends analysis of the global cancer burden, 1990-2019. J Hematol Oncol 2021;14:197.
109. Stine JG, Wentworth BJ, Zimmet A, et al. Systematic review with meta-analysis: risk of hepatocellular carcinoma in non-alcoholic steatohepatitis without cirrhosis compared to other liver diseases. Aliment Pharmacol Ther 2018;48:696-703.
110. Zunica ERM, Heintz EC, Axelrod CL, Kirwan JP. Obesity management in the primary prevention of hepatocellular carcinoma. Cancers 2022;14:4051.
111. Abenavoli L, Scarlata GGM, Scarpellini E, et al. Metabolic-dysfunction-associated fatty liver disease and gut microbiota: from fatty liver to dysmetabolic syndrome. Medicina 2023;59:594.
112. Norero B, Dufour JF. Should we undertake surveillance for HCC in patients with MAFLD? Ther Adv Endocrinol Metab 2023;14:20420188231160389.
113. Fassio E, Barreyro FJ, Pérez MS, et al. Hepatocellular carcinoma in patients with metabolic dysfunction-associated fatty liver disease: Can we stratify at-risk populations? World J Hepatol 2022;14:354-71.
114. Aspichueta P, Zeisel MB. miR-21p-5p coordinates biological pathways to promote MASLD progression. Liver Int 2023;43:2343-5.
115. Abenavoli L, Scarlata GGM, Paravati MR, Boccuto L, Luzza F, Scarpellini E. Gut microbiota and liver transplantation: immune mechanisms behind the rejection. Biomedicines 2023;11:1792.
116. Wongjarupong N, Assavapongpaiboon B, Susantitaphong P, et al. Non-alcoholic fatty liver disease as a risk factor for cholangiocarcinoma: a systematic review and meta-analysis. BMC Gastroenterol 2017;17:149.
117. Corrao S, Natoli G, Argano C. Nonalcoholic fatty liver disease is associated with intrahepatic cholangiocarcinoma and not with extrahepatic form: definitive evidence from meta-analysis and trial sequential analysis. Eur J Gastroenterol Hepatol 2021;33:62-8.
118. De Lorenzo S, Tovoli F, Mazzotta A, et al. Non-alcoholic steatohepatitis as a risk factor for intrahepatic cholangiocarcinoma and its prognostic role. Cancers 2020;12:3182.
119. Pascale A, Rosmorduc O, Duclos-Vallée JC. New epidemiologic trends in cholangiocarcinoma. Clin Res Hepatol Gastroenterol 2023;47:102223.
120. Lurje I, Uluk D, Pavicevic S, et al. Body composition is associated with disease aetiology and prognosis in patients undergoing resection of intrahepatic cholangiocarcinoma. Cancer Med 2023;12:17569-80.
121. Takahashi Y, Dungubat E, Kusano H, Fukusato T. Pathology and Pathogenesis of metabolic dysfunction-associated steatotic liver disease-associated hepatic tumors. Biomedicines 2023;11:2761.
122. Maeda S, Hikiba Y, Fujiwara H, et al. NAFLD exacerbates cholangitis and promotes cholangiocellular carcinoma in mice. Cancer Sci 2021;112:1471-80.
Cite This Article
Export citation file: BibTeX | RIS
OAE Style
Colaci C, Gambardella ML, Scarlata GGM, Boccuto L, Colica C, Luzza F, Scarpellini E, Mendez-Sanchez N, Abenavoli L. Dysmetabolic comorbidities and non-alcoholic fatty liver disease: a stairway to metabolic dysfunction-associated steatotic liver disease. Hepatoma Res 2024;10:16. http://dx.doi.org/10.20517/2394-5079.2023.134
AMA Style
Colaci C, Gambardella ML, Scarlata GGM, Boccuto L, Colica C, Luzza F, Scarpellini E, Mendez-Sanchez N, Abenavoli L. Dysmetabolic comorbidities and non-alcoholic fatty liver disease: a stairway to metabolic dysfunction-associated steatotic liver disease. Hepatoma Research. 2024; 10: 16. http://dx.doi.org/10.20517/2394-5079.2023.134
Chicago/Turabian Style
Colaci, Carmen, Maria Luisa Gambardella, Giuseppe Guido Maria Scarlata, Luigi Boccuto, Carmela Colica, Francesco Luzza, Emidio Scarpellini, Nahum Mendez-Sanchez, Ludovico Abenavoli. 2024. "Dysmetabolic comorbidities and non-alcoholic fatty liver disease: a stairway to metabolic dysfunction-associated steatotic liver disease" Hepatoma Research. 10: 16. http://dx.doi.org/10.20517/2394-5079.2023.134
ACS Style
Colaci, C.; Gambardella ML.; Scarlata GGM.; Boccuto L.; Colica C.; Luzza F.; Scarpellini E.; Mendez-Sanchez N.; Abenavoli L. Dysmetabolic comorbidities and non-alcoholic fatty liver disease: a stairway to metabolic dysfunction-associated steatotic liver disease. Hepatoma. Res. 2024, 10, 16. http://dx.doi.org/10.20517/2394-5079.2023.134
About This Article
Special Issue
Copyright
Data & Comments
Data
0
Cite This Article 0 clicks
Like This Article 1
likes
Comments
Comments must be written in English. Spam, offensive content, impersonation, and private information will not be permitted. If any comment is reported and identified as inappropriate content by OAE staff, the comment will be removed without notice. If you have any queries or need any help, please contact us at support@oaepublish.com.