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1.
Hepatol Int ; 2024 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-38878111

RESUMO

BACKGROUND: With the implementation of the 11th edition of the International Classification of Diseases (ICD-11) and the publication of the metabolic dysfunction-associated fatty liver disease (MAFLD) nomenclature in 2020, it is important to establish consensus for the coding of MAFLD in ICD-11. This will inform subsequent revisions of ICD-11. METHODS: Using the Qualtrics XM and WJX platforms, questionnaires were sent online to MAFLD-ICD-11 coding collaborators, authors of papers, and relevant association members. RESULTS: A total of 890 international experts in various fields from 61 countries responded to the survey. We also achieved full coverage of provincial-level administrative regions in China. 77.1% of respondents agreed that MAFLD should be represented in ICD-11 by updating NAFLD, with no significant regional differences (77.3% in Asia and 76.6% in non-Asia, p = 0.819). Over 80% of respondents agreed or somewhat agreed with the need to assign specific codes for progressive stages of MAFLD (i.e. steatohepatitis) (92.2%), MAFLD combined with comorbidities (84.1%), or MAFLD subtypes (i.e., lean, overweight/obese, and diabetic) (86.1%). CONCLUSIONS: This global survey by a collaborative panel of clinical, coding, health management and policy experts, indicates agreement that MAFLD should be coded in ICD-11. The data serves as a foundation for corresponding adjustments in the ICD-11 revision.

3.
Liver Int ; 44(7): 1567-1574, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38641962

RESUMO

BACKGROUND AND AIM: Metabolic dysfunction-associated steatotic liver disease (MASLD) has been proposed as an alternative for the validated definition of metabolic dysfunction-associated fatty liver disease (MAFLD). We compared the abilities of MAFLD and MASLD to predict the risk of atherosclerotic cardiovascular disease (ASCVD). METHODS: Six thousand and ninety six participants from the 2017 to 2020 National Health and Nutrition Examination Survey cohort who received a thorough medical health check-up were chosen for the study. The associations between fatty liver status and coronary risk surrogates, such as 10-year ASCVD risk and self-reported cardiovascular events, were analysed. RESULTS: MAFLD and MASLD were identified in 2911 (47.7%) and 2758 (45.2%) patients, respectively. MAFLD (odds ratio [OR]: 2.14, 95% confidence interval [CI], 1.78-2.57, p < .001) was more strongly independently associated with high ASCVD risk than MASLD (OR: 1.82, 95% CI, 1.52-2.18, p < .001) was in comparison with the absence of each condition. However, compared with MAFLD, MASLD alone was not associated with increased ASCVD risk. Multiple logistic regression revealed that MAFLD alone was significantly more strongly associated with a high risk of ASCVD (OR: 2.82; 95% CI: 1.13-7.01; p < .03) than MASLD alone. CONCLUSIONS: Although both MAFLD and MASLD were associated with different ASCVD risks, MAFLD predicted the ASCVD risk better than MASLD. The higher predictive ability of MAFLD compared to MASLD was attributed to metabolic dysfunction rather than moderate alcohol use.


Assuntos
Doenças Cardiovasculares , Inquéritos Nutricionais , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Doenças Cardiovasculares/epidemiologia , Medição de Risco , Adulto , Fatores de Risco , Estados Unidos/epidemiologia , Idoso , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Modelos Logísticos , Fatores de Risco de Doenças Cardíacas
4.
Int J Mol Sci ; 25(7)2024 Mar 26.
Artigo em Inglês | MEDLINE | ID: mdl-38612504

RESUMO

Metabolic-associated fatty liver disease (MAFLD) includes several metabolic dysfunctions caused by dysregulation in the brain-gut-liver axis and, consequently, increases cardiovascular risks and fatty liver dysfunction. In MAFLD, type 2 diabetes mellitus, obesity, and metabolic syndrome are frequently present; these conditions are related to liver lipogenesis and systemic inflammation. This study aimed to review the connection between the brain-gut-liver axis and MAFLD. The inflammatory process, cellular alterations in hepatocytes and stellate cells, hypercaloric diet, and sedentarism aggravate the prognosis of patients with MAFLD. Thus, to understand the modulation of the physiopathology of MAFLD, it is necessary to include the organokines involved in this process (adipokines, myokines, osteokines, and hepatokines) and their clinical relevance to project future perspectives of this condition and bring to light new possibilities in therapeutic approaches. Adipokines are responsible for the activation of distinct cellular signaling in different tissues, such as insulin and pro-inflammatory cytokines, which is important for balancing substances to avoid MAFLD and its progression. Myokines improve the quantity and quality of adipose tissues, contributing to avoiding the development of MAFLD. Finally, hepatokines are decisive in improving or not improving the progression of this disease through the regulation of pro-inflammatory and anti-inflammatory organokines.


Assuntos
Diabetes Mellitus Tipo 2 , Hepatopatia Gordurosa não Alcoólica , Humanos , Hepatopatia Gordurosa não Alcoólica/etiologia , Adipocinas , Encéfalo
5.
Med ; 2024 Apr 24.
Artigo em Inglês | MEDLINE | ID: mdl-38677287

RESUMO

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is highly prevalent in children and adolescents, particularly those with obesity. NAFLD is considered a hepatic manifestation of the metabolic syndrome due to its close associations with abdominal obesity, insulin resistance, and atherogenic dyslipidemia. Experts have proposed an alternative terminology, metabolic dysfunction-associated fatty liver disease (MAFLD), to better reflect its pathophysiology. This study aimed to develop consensus statements and recommendations for pediatric MAFLD through collaboration among international experts. METHODS: A group of 65 experts from 35 countries and six continents, including pediatricians, hepatologists, and endocrinologists, participated in a consensus development process. The process encompassed various aspects of pediatric MAFLD, including epidemiology, mechanisms, screening, and management. FINDINGS: In round 1, we received 65 surveys from 35 countries and analyzed these results, which informed us that 73.3% of respondents agreed with 20 draft statements while 23.8% agreed somewhat. The mean percentage of agreement or somewhat agreement increased to 80.85% and 15.75%, respectively, in round 2. The final statements covered a wide range of topics related to epidemiology, pathophysiology, and strategies for screening and managing pediatric MAFLD. CONCLUSIONS: The consensus statements and recommendations developed by an international expert panel serve to optimize clinical outcomes and improve the quality of life for children and adolescents with MAFLD. These findings emphasize the need for standardized approaches in diagnosing and treating pediatric MAFLD. FUNDING: This work was funded by the National Natural Science Foundation of China (82070588, 82370577), the National Key R&D Program of China (2023YFA1800801), National High Level Hospital Clinical Research Funding (2022-PUMCH-C-014), the Wuxi Taihu Talent Plan (DJTD202106), and the Medical Key Discipline Program of Wuxi Health Commission (ZDXK2021007).

6.
Pathogens ; 13(4)2024 Apr 19.
Artigo em Inglês | MEDLINE | ID: mdl-38668294

RESUMO

Chronic hepatitis C virus infection is an important cause of liver cirrhosis, hepatocellular carcinoma and death. Furthermore, it is estimated that about 40-70% of patients develop non-hepatic alterations in the course of chronic infection. Such manifestations can be immune-related conditions, lymphoproliferative disorders and metabolic alterations with serious adverse events in the short and long term. The introduction of new Direct-Acting Antivirals has shown promising results, with current evidence indicating an improvement and remission of these conditions after a sustained virological response.

8.
J Gastrointest Oncol ; 15(1): 368-376, 2024 Feb 29.
Artigo em Inglês | MEDLINE | ID: mdl-38482245

RESUMO

Background: Most advanced hepatocellular carcinoma (HCC) cases administered molecular targeted agents and/or anti-programmed cell death-1 (PD-1) inhibitors have no response or develop resistance. Moreover, second-line therapies still cannot provide beneficial clinical outcomes. A pilot study assessing combined regorafenib and PD-1 inhibitor as second-line treatment of advanced HCC reported promising effectiveness. Methods: The current single-center, retrospective, real-world study was carried out between January 2019 and July 2021. Advanced HCC cases were administered second-line regorafenib combined with a PD-1 inhibitor or regorafenib alone were assessed. Progression-free survival (PFS), objective response rate (ORR), and disease control rate (DCR) were determined. Results: Totally 46 HCC cases were analyzed, most of whom underwent previous systemic treatment comprising targeted therapy and immunotherapy. Tumor response was evaluated in 25 and 21 individuals in the regorafenib + PD-1 inhibitor and regorafenib monotherapy groups, respectively: ORRs were 21.7% and 8.7%, and DCRs were 47.8% and 32.6%, respectively. Median PFS was markedly longer in the regorafenib plus PD-1 inhibitor group (11.5 months) compared with the regorafenib monotherapy group (5.1 months, P=0.049). Conclusions: This study suggested regorafenib and a PD-1 inhibitor in combination may provide significant clinical benefits in HCC cases showing progression following first-line treatment. Further analysis in real-world studies with large cohorts is warranted to confirm these findings.

10.
World J Gastroenterol ; 30(7): 631-635, 2024 Feb 21.
Artigo em Inglês | MEDLINE | ID: mdl-38515945

RESUMO

In this editorial, we comment on the article by Zhang et al entitled Development of a machine learning-based model for predicting the risk of early postoperative recurrence of hepatocellular carcinoma. Hepatocellular carcinoma (HCC), which is characterized by high incidence and mortality rates, remains a major global health challenge primarily due to the critical issue of postoperative recurrence. Early recurrence, defined as recurrence that occurs within 2 years posttreatment, is linked to the hidden spread of the primary tumor and significantly impacts patient survival. Traditional predictive factors, including both patient- and treatment-related factors, have limited predictive ability with respect to HCC recurrence. The integration of machine learning algorithms is fueled by the exponential growth of computational power and has revolutionized HCC research. The study by Zhang et al demonstrated the use of a groundbreaking preoperative prediction model for early postoperative HCC recurrence. Chall-enges persist, including sample size constraints, issues with handling data, and the need for further validation and interpretability. This study emphasizes the need for collaborative efforts, multicenter studies and comparative analyses to validate and refine the model. Overcoming these challenges and exploring innovative approaches, such as multi-omics integration, will enhance personalized oncology care. This study marks a significant stride toward precise, effi-cient, and personalized oncology practices, thus offering hope for improved patient outcomes in the field of HCC treatment.


Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/diagnóstico , Carcinoma Hepatocelular/prevenção & controle , Carcinoma Hepatocelular/cirurgia , Neoplasias Hepáticas/diagnóstico , Neoplasias Hepáticas/prevenção & controle , Neoplasias Hepáticas/cirurgia , Algoritmos , Aprendizado de Máquina , Oncologia
12.
Med Sci Monit ; 30: e943417, 2024 Jan 29.
Artigo em Inglês | MEDLINE | ID: mdl-38282346

RESUMO

Metabolic dysfunction-associated fatty liver disease or metabolic dysfunction-associated steatotic liver disease (MAFLD/MASLD), is a common chronic liver condition affecting a substantial global population. Beyond its primary impact on liver function, MAFLD/MASLD is associated with a myriad of extrahepatic manifestations, including cognitive impairment. The scope of cognitive impairment within the realm of MAFLD/MASLD is a matter of escalating concern. Positioned as an intermediate stage between the normal aging process and the onset of dementia, cognitive impairment manifests as a substantial challenge associated with this liver condition. Insights from studies underscore the presence of compromised executive function and a global decline in cognitive capabilities among individuals identified as being at risk of progressing to liver fibrosis. Importantly, this cognitive impairment transcends mere association with metabolic factors, delving deep into the intricate pathophysiology characterizing MAFLD/MASLD. The multifaceted nature of cognitive impairment in the context of MAFLD/MASLD is underlined by a spectrum of factors, prominently featuring insulin resistance, lipotoxicity, and systemic inflammation as pivotal contributors. These factors interplay within the intricate landscape of MAFLD/MASLD, fostering a nuanced understanding of the links between hepatic health and cognitive function. By synthesizing the available evidence, exploring potential mechanisms, and assessing clinical implications, the overarching aim of this review is to contribute to a more complete understanding of the impact of MAFLD/MASLD on cognitive function.


Assuntos
Doenças Metabólicas , Hepatopatia Gordurosa não Alcoólica , Humanos , Encéfalo , Cognição
13.
Adv Ther ; 41(3): 967-990, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38286960

RESUMO

Liver diseases cause a significant burden on public health worldwide. In spite of great advances during recent years, there are still many challenges in the diagnosis and treatment of liver diseases. During recent years, artificial intelligence (AI) has been widely used for the diagnosis, risk stratification, and prognostic prediction of various diseases based on clinical datasets and medical images. Accumulative studies have shown its performance for diagnosing patients with nonalcoholic fatty liver disease and liver fibrosis and assessing their severity, and for predicting treatment response and recurrence of hepatocellular carcinoma, outcomes of liver transplantation recipients, and risk of drug-induced liver injury. Herein, we aim to comprehensively summarize the current evidence regarding diagnostic, prognostic, and/or therapeutic role of AI in these common liver diseases.


Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , Hepatopatia Gordurosa não Alcoólica , Humanos , Inteligência Artificial , Cirrose Hepática/complicações , Cirrose Hepática/diagnóstico , Hepatopatia Gordurosa não Alcoólica/complicações , Hepatopatia Gordurosa não Alcoólica/diagnóstico , Hepatopatia Gordurosa não Alcoólica/terapia , Neoplasias Hepáticas/diagnóstico
14.
Curr Med Res Opin ; 40(2): 303-313, 2024 02.
Artigo em Inglês | MEDLINE | ID: mdl-38006404

RESUMO

Budd-Chiari syndrome (BCS) and sinusoidal obstruction syndrome (SOS) are two major vascular disorders of the liver, of which both can cause portal hypertension related complications, but their locations of obstruction are different. BCS refers to the obstruction from the hepatic vein to the junction between the inferior vena cava and right atrium, which is the major etiology of post-sinusoidal portal hypertension; by comparison, SOS is characterized as the obstruction at the level of hepatic sinusoids and terminal venulae, which is a cause of sinusoidal portal hypertension. Both of them can cause hepatic congestion with life-threatening complications, especially acute liver failure and chronic portal hypertension, and share some similar features in terms of imaging and clinical presentations, but they have heterogeneous risk factors, management strategy, and prognosis. Herein, this paper reviews the current evidence and then summarizes the difference between primary BCS and SOS in terms of risk factors, clinical features, diagnosis, and treatment.


Assuntos
Síndrome de Budd-Chiari , Hepatopatia Veno-Oclusiva , Hipertensão Portal , Complicações na Gravidez , Feminino , Humanos , Síndrome de Budd-Chiari/diagnóstico , Síndrome de Budd-Chiari/etiologia , Síndrome de Budd-Chiari/terapia , Hepatopatia Veno-Oclusiva/complicações , Veias Hepáticas , Hipertensão Portal/complicações
15.
Hepatol Int ; 18(1): 168-178, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38127259

RESUMO

BACKGROUND: The classification and nomenclature of non-alcoholic fatty liver disease (NAFLD) has been the subject of ongoing debate in the medical community. Through the introduction of metabolic dysfunction-associated fatty liver disease (MAFLD) and the later release of metabolic dysfunction-associated steatotic liver disease (MASLD), the limitations associated with NAFLD are intended to be addressed. Both terminologies incorporate the metabolic component of the disease by providing diagnostic criteria that relies on the presence of underlying metabolic risk factors. MATERIALS AND METHODS: An epidemiologic cross-sectional study of individuals who had undergone abdominal ultrasound and vibration-controlled transient elastography (VCTE) as part of a routine check was performed. We evaluated clinical, anthropometric, and biochemical variables to determine the metabolic profile of each subject. RESULTS: The study included a total of 500 participants, 56.8% (n = 284) males and 43.2% (n = 216) females, with a mean age of 49 ± 10 years. 59.4% (n = 297) were diagnosed with MAFLD and MASLD, 10.2% (n = 51) were diagnosed only with MASLD and 30.4% (n = 152) were not diagnosed with either MAFLD or MASLD. The differences in prevalence were mainly based on the detection of individuals with a BMI < 25 kg/m2, where MASLD captures the largest number (p < 0.001). CONCLUSIONS: Although MASLD has a higher capture of lean patients compared to MAFLD, patients with MAFLD and MASLD have a worse metabolic profile than those with only MASLD. Our results provide evidence that MAFLD better identifies patients likely to have a higher risk of liver fibrosis and of disease progression.


Assuntos
Doenças Metabólicas , Hepatopatia Gordurosa não Alcoólica , Feminino , Masculino , Humanos , Adulto , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica/diagnóstico por imagem , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Estudos Transversais , Fatores de Risco , Medição de Risco
16.
Biochem Pharmacol ; 218: 115871, 2023 12.
Artigo em Inglês | MEDLINE | ID: mdl-37866803

RESUMO

Adiponectin replacement therapy holds the potential to benefit numerous human diseases, and ongoing research applies particular interest in how adiponectin acts against Metabolic-associated Fatty Liver Disease (MAFLD) and Nonalcoholic Steatohepatitis (NASH). However, the pharmacological limitations of the intact protein have prompted a focus on alternative options, specifically peptidic and small molecule agonists targeting the adiponectin receptor. AdipoRon is an extensively researched non-peptidic drug candidate in adiponectin replacement therapy. In turn, ADP355 is an adiponectin-based active short peptide. They have garnered significant attention due to their potential as substitutes for adiponectin. Researchers have studied AdipoRon's and ADP355's efficacy and therapeutic applications in various disease conditions. However, the effects of AdipoRon and ADP355 against NAFLD and NASH models advanced more, and no systematic review explored this area before. This systematic review was conceived to address the deficiency mentioned above and consider the lack of clinical evidence. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were utilized. To assess the risk of bias in systematic review, The Joanna Briggs Institute (JBI) Critical Appraisal Checklist was employed. Results from pre-clinical evidence show that AdipoRon and ADP355 represent promising effects in NAFLD and NASH-related models, including reducing hepatic steatosis, modulating inflammation, improving insulin sensitivity, enhancing mitochondrial function, and protecting against liver fibrosis. While AdipoRon and ADP355 exhibit promise in pre-clinical studies and experimental models, additional clinical trials are necessary to assess their effectiveness, safety, and potential translational therapeutic potential uses in NAFLD and NASH human cases.


Assuntos
Hepatopatia Gordurosa não Alcoólica , Humanos , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Hepatopatia Gordurosa não Alcoólica/metabolismo , Receptores de Adiponectina/metabolismo , Adiponectina
17.
Antibiotics (Basel) ; 12(10)2023 Sep 22.
Artigo em Inglês | MEDLINE | ID: mdl-37887176

RESUMO

Impairments in liver function lead to different complications. As chronic liver disease progresses (CLD), hypoalbuminemia and alterations in bile acid compositions lead to changes in gut microbiota and, therefore, in the host-microbiome interaction, leading to a proinflammatory state. Alterations in gut microbiota composition and permeability, known as gut dysbiosis, have important implications in CLD; alterations in the gut-liver axis are a consequence of liver disease, but also a cause of CLD. Furthermore, gut dysbiosis plays an important role in the progression of liver cirrhosis and decompensation, particularly with complications such as hepatic encephalopathy and spontaneous bacterial peritonitis. In relation to this, antibiotics play an important role in treating CLD. While certain antibiotics have specific indications, others have been subjected to continued study to determine whether or not they have a modulatory effect on gut microbiota. In contrast, the rational use of antibiotics is important, not only because of their disrupting effects on gut microbiota, but also in the context of multidrug-resistant organisms. The aim of this review is to illustrate the role of gut microbiota alterations in CLD, the use and impact of antibiotics in liver cirrhosis, and their harmful and beneficial effects.

18.
Adv Ther ; 2023 Oct 06.
Artigo em Inglês | MEDLINE | ID: mdl-37801231

RESUMO

INTRODUCTION: Bowel wall thickening is commonly observed in liver cirrhosis, but few studies have explored its impact on the long-term outcomes of patients with cirrhosis. METHODS: Overall, 118 patients with decompensated cirrhosis were retrospectively enrolled, in whom maximum wall thickness of small bowel, ascending colon, transverse colon, descending colon, sigmoid colon, and rectum could be measured in computed tomography (CT) images. X-tile software was employed to determine the best cut-off values of each segment of bowel wall thickness for predicting the risk of further decompensation and death. Cumulative rates of further decompensation and death were calculated by Nelson-Aalen cumulative risk curve analyses. Predictors of further decompensation and death were evaluated by competing risk analyses. Sub-distribution hazard ratios (sHRs) were calculated. RESULTS: Cumulative rates of further decompensation were significantly higher in patients with wall thickness of ascending colon ≥ 11.7 mm (P = 0.014), transverse colon ≥ 3.2 mm (P = 0.043), descending colon ≥ 9.8 mm (P = 0.035), and rectum ≥ 7.2 mm (P = 0.045), but not those with wall thickness of small bowel ≥ 8.5 mm (P = 0.312) or sigmoid colon ≥ 7.1 mm (P = 0.237). Wall thickness of ascending colon ≥ 11.7 mm (sHR = 1.70, P = 0.030), transverse colon ≥ 3.2 mm (sHR = 2.15, P = 0.038), descending colon ≥ 9.8 mm (sHR = 1.43, P = 0.046), and rectum ≥ 7.2 mm (sHR = 2.38, P = 0.045) were independent predictors of further decompensation, but not wall thickness of small bowel ≥ 8.5 mm (sHR = 1.19, P = 0.490) or sigmoid colon ≥ 7.1 mm (sHR = 0.63, P = 0.076). Small bowel, ascending colon, transverse colon, descending colon, sigmoid colon, and rectum wall thickness were not significantly associated with death. CONCLUSIONS: Colorectal wall thickening, but not small bowel wall, may be considered for the prediction of further decompensation in cirrhosis.

19.
Genes (Basel) ; 14(10)2023 10 13.
Artigo em Inglês | MEDLINE | ID: mdl-37895284

RESUMO

Gallstone disease and metabolic dysfunction-associated fatty liver disease (MAFLD) share numerous common risk factors and progression determinants in that they both manifest as organ-specific consequences of metabolic dysfunction. Nevertheless, the precise molecular mechanisms underlying fibrosis development in cholecystectomized MAFLD patients remain inadequately defined. This study aimed to investigate the involvement of farnesoid X receptor 1 (FXR1) and fibroblast growth factor receptor 4 (FGFR4) in the progression of fibrosis in cholecystectomized MAFLD patients. A meticulously characterized cohort of 12 patients diagnosed with MAFLD, who had undergone liver biopsies during programmed cholecystectomies, participated in this study. All enrolled patients underwent a follow-up regimen at 1, 3, and 6 months post-cholecystectomy, during which metabolic biochemical markers were assessed, along with elastography, which served as indirect indicators of fibrosis. Additionally, the hepatic expression levels of FGFR4 and FXR1 were quantified using quantitative polymerase chain reaction (qPCR). Our findings revealed a robust correlation between hepatic FGFR4 expression and various histological features, including the steatosis degree (r = 0.779, p = 0.023), ballooning degeneration (r = 0.764, p = 0.027), interphase inflammation (r = 0.756, p = 0.030), and steatosis activity score (SAS) (r = 0.779, p = 0.023). Conversely, hepatic FXR1 expression did not exhibit any significant correlations with these histological features. In conclusion, our study highlights a substantial correlation between FGFR4 expression and histological liver damage, emphasizing its potential role in lipid and glucose metabolism. These findings suggest that FGFR4 may play a crucial role in the progression of fibrosis in cholecystectomized MAFLD patients. Further research is warranted to elucidate the exact mechanisms through which FGFR4 influences metabolic dysfunction and fibrosis in this patient population.


Assuntos
Hepatopatia Gordurosa não Alcoólica , Humanos , Estudos de Coortes , Fatores de Risco , Biópsia , Fibrose , Proteínas de Ligação a RNA
20.
World J Gastroenterol ; 29(25): 3999-4008, 2023 Jul 07.
Artigo em Inglês | MEDLINE | ID: mdl-37476582

RESUMO

The relationship between metabolic derangements and fatty liver development are undeniable, since more than 75% of patients with type 2 diabetes mellitus present with fatty liver. There is also significant epidemiological association between insulin resistance (IR) and metabolic (dysfunction)-associated fatty liver disease (MAFLD). For little more than 2 years, the nomenclature of fatty liver of non-alcoholic origin has been intended to change to MAFLD by multiple groups. While a myriad of reasons for which MAFLD is thought to be of metabolic origin could be exposed, the bottom line relies on the role of IR as an initiator and perpetuator of this disease. There is a reciprocal role in MAFLD development and IR as well as serum glucose concentrations, where increased circulating glucose and insulin result in increased de novo lipogenesis by sterol regulatory element-binding protein-1c induced lipogenic enzyme stimulation; therefore, increased endogenous production of triglycerides. The same effect is achieved through impaired suppression of adipose tissue (AT) lipolysis in insulin-resistant states, increasing fatty acid influx into the liver. The complementary reciprocal situation occurs when liver steatosis alters hepatokine secretion, modifying fatty acid metabolism as well as IR in a variety of tissues, including skeletal muscle, AT, and the liver. The aim of this review is to discuss the importance of IR and AT interactions in metabolic altered states as perhaps the most important factor in MAFLD pathogenesis.


Assuntos
Diabetes Mellitus Tipo 2 , Resistência à Insulina , Hepatopatia Gordurosa não Alcoólica , Humanos , Resistência à Insulina/fisiologia , Diabetes Mellitus Tipo 2/metabolismo , Obesidade/complicações , Hepatopatia Gordurosa não Alcoólica/metabolismo , Fígado/patologia , Tecido Adiposo/metabolismo , Glucose/metabolismo , Ácidos Graxos/metabolismo , Insulina/metabolismo
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