RESUMEN
Objective There is a Few studies explored the association between vitamin intake and meta-bolic dysfunction-associated fatty liver disease(MAFLD),while the existing results were still contradictory.This study aimed to investigate the association between dietary vitamins and all-cause mortality as well as fibrosis risk in patients with MAFLD.Methods The data were extracted from the third National Health and Nutrition Examination Surveys 1988-1994.Dietary vitamins was assessed using a 24 h diet recall,including vitamin A,vitamin B6,vitamin B12,vitamin C,vitamin D,thiamin,riboflavin,folic acid and α-tocopherol.The non-alcoholic fatty liver disease fibrosis score(NFS)<-1.455 was considered as non-advanced fibrosis,while NFS≥-1.455 was considered as advanced fibrosis.Results A total of 3844 MAFLD participants were included in this study.The median time of follow-up was 310 months.1739 participants(45.3%)were deceased during the follow-up.The intake of thiamin,riboflavin,α-tocopherol,VB6,and VB12 were significantly higher in patients with NFS-determined non-advanced fibrosis(P<0.05).After adjusting,a significantly lower risk of fibrosis was found in patients with the highest quartile(>11.5 mg/d)of α-tocopherol intake compared to the lowest intake group(P = 0.031).Compared to the lowest quartile group,the risk of mortality was reduced by 0.34 folds in the group consuming the highest quartile amount(>130 mg/d)of VC(HRs:0.66,95%CI:0.51~0.85,P = 0.001).Conclusions More α-tocopherol intake reduced fibrosis grade in MAFLD patients.VC intake may reduce all-cause mortality in patients with MAFLD.
RESUMEN
Chronic hepatitis B virus (HBV) infection is the main cause of the disease burden of viral hepatitis worldwide, and meanwhile, due to changes in lifestyle and dietary habits, the incidence rate of metabolic associated fatty liver disease (MAFLD) is constantly increasing, making MAFLD the leading chronic liver disease around the world. Chronic HBV infection comorbid with MAFLD is becoming more and more common in clinical practice. Metabolic factors, rather than viral factors, are the main cause of chronic HBV infection comorbid with MAFLD. During disease progression, steatohepatitis and fibrosis, rather than steatosis, are the main influencing factors for the progression to liver cirrhosis and hepatocellular carcinoma. For patients with chronic HBV infection and MAFLD, integrated management of virus and metabolic factors is of great importance. This article reviews the tissues regarding the interaction, prognosis, and clinical management of chronic HBV infection and MAFLD.
RESUMEN
Chronic hepatitis B virus (HBV) infection is a worldwide public health issue and a leading cause of liver fibrosis, liver cirrhosis, liver failure, and primary liver cancer in China. The incidence rate of nonalcoholic fatty liver disease (NAFLD) is gradually increasing with the improvement in the living standards of people and the changes in dietary structure. Population-based studies have found that HBV infection can influence the development of NAFLD, but the mechanism remains unknown. Hepatic steatosis can also influence the expression of HBV serum pathogenic indicators, and its combination with NAFLD and other metabolic dysfunction diseases can increase the risk of liver fibrosis, liver cirrhosis, and liver cancer. Chronic HBV infection is closely associated with metabolic dysfunction, and more studies are needed in the future to better understand related mechanisms, so as to provide a theoretical foundation for clinical diagnosis and treatment.
RESUMEN
With the rapid growth of metabolic dysfunction (MD) worldwide, there is also a gradual increase in the number of patients with chronic hepatitis B virus (HBV) infection and MD. Comorbidity with metabolic disorders such as hyperglycemia, hypertension, and dyslipidemia may increase the risk of adverse liver outcomes and cardiovascular events in patients with chronic HBV infection and affect the response to anti-HBV therapy. The standardized management of patients with chronic HBV infection and MD has become a challenge at present, and further in-depth research on the interaction between MD and HBV and targeted management strategies will help to optimize the clinical management of patients with chronic HBV infection.
RESUMEN
BACKGROUND@#Metabolic Dysfunction-associated Steatotic Liver Disease (MASLD) has become a global epidemic, and air pollution has been identified as a potential risk factor. This study aims to investigate the non-linear relationship between ambient air pollution and MASLD prevalence.@*METHOD@#In this cross-sectional study, participants undergoing health checkups were assessed for three-year average air pollution exposure. MASLD diagnosis required hepatic steatosis with at least 1 out of 5 cardiometabolic criteria. A stepwise approach combining data visualization and regression modeling was used to determine the most appropriate link function between each of the six air pollutants and MASLD. A covariate-adjusted six-pollutant model was constructed accordingly.@*RESULTS@#A total of 131,592 participants were included, with 40.6% met the criteria of MASLD. "Threshold link function," "interaction link function," and "restricted cubic spline (RCS) link functions" best-fitted associations between MASLD and PM2.5, PM10/CO, and O3 /SO2/NO2, respectively. In the six-pollutant model, significant positive associations were observed when pollutant concentrations were over: 34.64 µg/m3 for PM2.5, 57.93 µg/m3 for PM10, 56 µg/m3 for O3, below 643.6 µg/m3 for CO, and within 33 and 48 µg/m3 for NO2. The six-pollutant model using these best-fitted link functions demonstrated superior model fitting compared to exposure-categorized model or linear link function model assuming proportionality of odds.@*CONCLUSION@#Non-linear associations were found between air pollutants and MASLD prevalence. PM2.5, PM10, O3, CO, and NO2 exhibited positive associations with MASLD in specific concentration ranges, highlighting the need to consider non-linear relationships in assessing the impact of air pollution on MASLD.
Asunto(s)
Humanos , Dióxido de Nitrógeno , Estudios Transversales , Contaminación del Aire/análisis , Contaminantes Atmosféricos/análisis , Material Particulado/análisis , Hepatopatías , Exposición a Riesgos Ambientales/análisisRESUMEN
ABSTRACT Background: Alcoholic liver disease (ALD) and metabolic-dysfunction associated steatotic liver disease (MASLD) are common, and gut microbiota (GM) is involved with both. Here we compared GM composition in animal models of MASLD and ALD to assess whether there are specific patterns for each disease. Methods: MASLD model- adult male Sprague Dawley rats, randomized into two groups: MASLD-control (n=10) fed a standard diet; MASLD-group (n=10) fed a high-fat-choline-deficient diet for 16 weeks. ALD model- adult male Wistar rats randomized: ALD-control (n=8) fed a standard diet and water+0.05% saccharin, ALD groups fed with sunflower seed and 10% ethanol+0.05% saccharin for 4 or 8 weeks (ALC4, n=8; ALC8, n=8). ALC4/8 on the last day received alcoholic binge (5g/kg of ethanol). Afterwards, animals were euthanized, and feces were collected for GM analysis. Results: Both experimental models induced typical histopathological features of the diseases. Alpha diversity was lower in MASLD compared with ALD (p<0.001), and structural pattern was different between them (P<0.001). Bacteroidetes (55.7%), Firmicutes (40.6%), and Proteobacteria (1.4%) were the most prevalent phyla in all samples, although differentially abundant among groups. ALC8 had a greater abundance of the phyla Cyanobacteria (5.3%) and Verrucomicrobiota (3.2%) in relation to the others. Differential abundance analysis identified Lactobacillaceae_unclassified, Lachnospiraceae_NK4A136_group, and Turicibacter associated with ALC4 and the Clostridia_UCG_014_ge and Gastranaerophilales_ge genera to ALC8. Conclusion: In this study, we demonstrated that the structural pattern of the GM differs significantly between MASLD and ALD models. Studies are needed to characterize the microbiota and metabolome in both clinical conditions to find new therapeutic strategies.
RESUMO Contexto: A doença hepática alcoólica (DHA) e a doença hepática esteatótica associada à disfunção metabólica (MASLD) são comuns, e a microbiota intestinal (MI) está envolvida em ambas. Aqui, comparamos a composição da MI em modelos animais de MASLD e DHA para avaliar se existem padrões específicos para cada doença. Métodos: Modelo de MASLD - ratos machos adultos da linhagem Sprague Dawley, randomizados em dois grupos: MASLD-controle (n=10) alimentados com uma dieta padrão; grupo MASLD (n=10) alimentados com uma dieta rica em gordura e deficiente em colina por 16 semanas. Modelo de DHA - ratos machos adultos da linhagem Wistar randomizados: DHA-controle (n=8) alimentados com uma dieta padrão e água+0,05% de sacarina; grupos DHA alimentados com semente de girassol e 10% de etanol+0,05% de sacarina por 4 ou 8 semanas (DHA4, n=8; DHA8, n=8). DHA 4/8 no último dia receberam binge alcoólico (5 g/kg de etanol). Posteriormente, os animais foram sacrificados, e as fezes foram coletadas para análise da MI. Resultados: Ambos os modelos experimentais induziram características histopatológicas típicas das doenças. A diversidade alfa foi menor na MASLD em comparação com a DHA (P<0,001), e o padrão estrutural foi diferente entre elas (P<0,001). Bacteroidetes (55,7%), Firmicutes (40,6%) e Proteobactérias (1,4%) foram os filos mais prevalentes em todas as amostras, embora com abundâncias diferenciadas entre os grupos. DHA8 teve uma maior abundância dos filos Cyanobacteria (5,3%) e Verrucomicrobiota (3,2%) em relação aos outros. A análise de abundância diferencial identificou Lactobacillaceae_unclassified, Lachnospiraceae_NK4A136 e Turicibacter associados ao grupo DHA4, e os gêneros Clostridia_UCG_014_ge e Gastranaerophilales_ge associados ao DHA8. Conclusão: Neste estudo, demonstramos que o padrão estrutural da MI difere significativamente entre os modelos de MASLD e DHA. Estudos são necessários para caracterizar a microbiota e os metabólitos ativos em ambas as condições clínicas, a fim de encontrar novas estratégias terapêuticas.
RESUMEN
ABSTRACT Background: This study aimed to assess the frequency and intensity of anxious and depressive symptoms in patients diagnosed with metabolic dysfunction-associated steatotic liver disease (MASLD). Methods: This is a descriptive and cross-sectional study, resulting from 106 patients from the Hepatology outpatient clinic at the Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC-FMUSP), São Paulo, Brazil without a history of alcohol abuse, verified by the alcohol use disorders identification test (AUDIT). These were assessed using the sociodemographic data sheet, Hospital Anxiety and Depression Scale (HADS), Hamilton Anxiety Rating Scale (HAM-A), and Hamilton Depression Scale (HAM-D). Results: A total of 69.8% were women and 30.2% were men, with a mean age of 61 years. The majority (71.7%) discovered MASLD through routine exams, presenting as comorbidities: Type 2 diabetes mellitus (59.4%), Dyslipidemia (49.1%), Arterial hypertension (68.9%), Obesity (61.3%) and Metabolic syndrome [MetS (63.2%)]. The HADS scale indicates 34% probability of anxiety and 33% depressive symptoms. The Hamilton's scales of intensity indicates 63.9% severe anxiety and 54.3% severe depression. There is also a relationship between anxiety, depression and the female gender, as well as between depression and MetS. Conclusion: The findings point to the presence of anxiety and depression in more than one third of MASLD patients, most with severe symptoms. The group is concentrated in the elderly, with many comorbidities, including MetS. There was a positive correlation between anxiety, depression and being female; also, being significant between MetS and depression.
RESUMO Contexto: Este estudo teve como objetivo avaliar a frequência e a intensidade dos sintomas ansiosos e depressivos em pacientes com diagnóstico de doença hepática esteatótica associada à disfunção metabólica [do inglês: Metabolic dysfunction-associated steatotic liver disease (MASLD)]. Métodos: Trata-se de um estudo descritivo e transversal, resultante do acompanhamento de 106 pacientes do Ambulatório de Doença Hepática Esteatótica Associada à Disfunção Metabólica (A2MG700) da Disciplina de Gastroenterologia Clínica do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC-FMUSP), São Paulo, Brasil, sem história de abuso de álcool, verificada pelo Alcohol Use Disorders Identification Test (AUDIT). Foram avaliados os dados sociodemográficos, Escala hospitalar de ansiedade e depressão [do inglês: Hospital Anxiety and Depression Scale (HADS)], Escala de avaliação de ansiedade de Hamilton [do inglês: Hamilton Anxiety Rating Scale (HAM-A)] e Escala de depressão de Hamilton [do inglês: Hamilton Depression Scale (HAM-D)]. Resultados: Um total 69,8% dos indivíduos eram do sexo feminino com idade média de 61 anos. A maioria dos indivíduos avaliados (71,7%) descobriu a doença por meio de exames de rotina e apresentavam diabetes mellitus tipo 2 (59,4%), dislipidemia (49,1%), hipertensão arterial (68,9%), obesidade (61,3%) e síndrome metabólica [SM (63,2%)]. A análise da escala HADS demonstrou probabilidade de ansiedade em 34% dos participantes e 33% de sintomas depressivos. A escala de intensidade de Hamilton demonstrou que 63,9% dos indivíduos apresentavam ansiedade severa e 54,3% depressão severa. Observamos também relação entre ansiedade, depressão e o sexo feminino, assim como, entre depressão e SM. Conclusão: Nossos achados demonstram a presença de ansiedade e depressão em mais de 1/3 dos indivíduos com MASLD avaliados e a maioria apresenta sintomas graves. O grupo era composto por pacientes idosos e com comorbidades, incluindo SM. Observamos correlação positiva entre ansiedade, depressão e sexo feminino, sendo significativa entre SM e depressão.
RESUMEN
OBJECTIVE Alzheimer's disease(AD)is a progressive neurological disease.Given the important role of gut microbiota composition in AD pathology,the observed perturbation in the microbiota composition and diversity may serve as the mechanisms underlying age-dependent APP/PS1/tau triple-transgenic mouse(3×Tg-AD)mice amyloid deposition and memory deficits.Here-in,we intended to investigate the gut microbiota and as-sessed its relationship with the triggering and develop-ment of cognitive impairment of AD.METHODS This study involves the comparative assessment of spatial learning,amyloid β-protein(Aβ)accumulation,and fecal microbiota alterations in 3×Tg-AD mice from three age groups:AD asymptomatic stage(3 m),presymptomatic stage(6 m),and the symptomatic stage of AD(9 m).RE-SULTS We demonstrate that spatial memory deficits,brain Aβ accumulation,and weight gain in 3×Tg-AD mice gradually appear after 6 months of age.However,the total gut bacterial counts underwent changes from 3 to 6 months of age and were further altered at 9 months of age.Importantly,changes in gut bacteria abundance of Desulfobacterota and Actinobacteriota phylain 6-month-old mice preceded apparent spatial memory deficits.CONCLUSION Changes in the gut microbial community are one of the mechanisms of early AD pathology.
RESUMEN
Metabolic associated fatty liver disease (MAFLD) is a common chronic liver disease around the world, affecting more than a quarter of the adult population worldwide. MAFLD is characterized by the co-occurrence of hepatic steatosis and metabolic disturbance. As a metabolic disorder, MAFLD shares a similar pathogenesis with cardiovascular disease (CVD), and both diseases are closely associated with the well-established cardiovascular risk factors such as obesity, type 2 diabetes, and atherogenic dyslipidemia. An increasing amount of evidence has shown that MAFLD is closely associated with CVD; however, as a new risk factor for CVD, MAFLD differs from traditional risk factors for CVD, which requires further investigation. In this context, this consensus statement used the Delphi method to achieve a consensus on the association between MAFLD and the risk of CVD through two rounds of surveys and discussed the association between MAFLD and CVD in terms of epidemiological and clinical characteristics, as well as a range of topics including pathophysiological mechanisms, surveillance, and management.
RESUMEN
Background: The terminology of nonalcoholic fatty liver disease (NAFLD) was changed to metabolic dysfunction ⁃ associated fatty liver disease (MAFLD) in 2020. NAFLD has been confirmed to be a risk factor for colorectal neoplasms, but the association between MAFLD and colorectal neoplasms is conflicting. Aims: To investigate the correlation of MAFLD with colorectal adenoma and early colorectal cancer. Methods: The clinical information of 701 patients who met the criteria and were admitted to Renmin Hospital of Wuhan University from January 2021 to August 2021 was collected retrospectively. Among them, 274 colorectal adenoma patients with low ⁃ grade intraepithelial neoplasia or without intraepithelial neoplasia were classified as adenoma group, 21 patients with high ⁃ grade intraepithelial neoplasia, intramucosal carcinoma, and submucosal carcinoma were classified as early cancer group, and 406 patients with normal colonoscopy or non⁃adenomatous polyps were served as control group. The general information and prevalence of MAFLD between these groups were compared. Furthermore, the correlation of MAFLD with colorectal adenoma and early colorectal cancer, and the gender difference of these correlations were analyzed by Logistic regression models. Subgroup analysis was performed based on the clinicopathological characteristics of colorectal adenoma. Results: When adjusting the confounding variables including gender, age, smoking, alcohol drinking, diabetes, hypertension, and serum creatinine, MAFLD was significantly associated with the prevalence of colorectal adenoma (OR=1.83, 95% CI: 1.04 ⁃ 3.22, P=0.037) and early colorectal cancer (OR=3.91, 95% CI: 1.14⁃13.42, P=0.031). When stratified as gender, the significant association remained in females (OR=4.04, 95% CI: 1.56 ⁃ 10.47, P=0.004), but not in males. In addition, no correlation was found between MAFLD and the location, size, number, and advanced histology of colorectal adenoma (all P>0.05). Conclusions: MAFLD is an independent risk factor for colorectal adenoma and early colorectal cancer. MAFLD is specifically associated with increased risk of colorectal adenoma in females but not in males.
RESUMEN
OBJECTIVE@#To explore the effect of leucine-rich α-2-glycoprotein (LRG1) derived from hepatocytes on activation of hepatic M1 Kupffer cells.@*METHODS@#A metabolic dysfunction-associated fatty liver disease (MAFLD) model was established in BALB/c mice by high-fat diet (HFD) feeding for 16 weeks. Oleic acid was used to induce steatosis in primary cultures of mouse hepatocytes. The mRNA and protein expressions of LRG1 in mouse liver tissues and hepatocytes were detected by real-time PCR and Western blotting. Primary hepatic macrophages were stimulated with the conditioned medium (CM) from steatotic hepatocyte along with LRG1 or transforming growth factor-β1 (TGF-β1), or both for 24 h, and the expression levels of inducible nitric oxide synthase (iNOS) was detected with Western botting, and the mRNA expressions of iNOS, chemokine ligand 1 (CXCL-1) and interleukin-1β (IL-1β) were measured by RT-PCR. The MAFLD mice were injected with LRG1 (n=6), TGF-β1 (n=6), or both (n=6) through the caudal vein, and the live tissues were collected for HE staining and immumohistochemical detection of F4/80 expression; the mRNA expressions of iNOS, CXCL-1 and IL-1β in liver tissues were detected using RT-PCR.@*RESULTS@#The mRNA and protein expression levels of LRG1 were significantly downregulated in the liver tissues of MAFLD mice and steatotic hepatocytes (P < 0.05). Treatment of the hepatic macrophages with CM from steatosis hepatocytes significantly enhanced the mRNA expression levels of iNOS, CXCL-1 and IL-1β, and these changes were significantly inhibited by the combined treatment with TGF-β1 and LRG1 (P < 0.05). In MAFLD mice, injections with either LRG1 or TGF-β1 alone reduced hepatic lipid deposition and intrahepatic macrophage infiltration, and these effects were significantly enhanced by their combined treatment, which also more strongly inhibited the mRNA expression levels of iNOS, CXCL-1 and IL-1β (P < 0.05).@*CONCLUSION@#LRG1 inhibits hepatic macrophage infiltration by enhancing TGF-β1 signaling to alleviate fatty liver inflammation in MAFLD mice.
Asunto(s)
Animales , Ratones , Factor de Crecimiento Transformador beta1 , Activación de Macrófagos , Transducción de Señal , Enfermedad del Hígado Graso no Alcohólico , Medios de Cultivo Condicionados , GlicoproteínasRESUMEN
ABSTRACT Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as Nonalcoholic fatty liver disease (NAFLD), is one of the most common hepatic diseases in individuals with overweight or obesity. In this context, a panel of experts from three medical societies was organized to develop an evidence-based guideline on the screening, diagnosis, treatment, and follow-up of MASLD. Material and methods: A MEDLINE search was performed to identify randomized clinical trials, meta-analyses, cohort studies, observational studies, and other relevant studies on NAFLD. In the absence of studies on a certain topic or when the quality of the study was not adequate, the opinion of experts was adopted. Classes of Recommendation and Levels of Evidence were determined using prespecified criteria. Results: Based on the literature review, 48 specific recommendations were elaborated, including 11 on screening and diagnosis, 9 on follow-up, 14 on nonpharmacologic treatment, and 14 on pharmacologic and surgical treatment. Conclusions: A literature search allowed the development of evidence-based guidelines on the screening, diagnosis, treatment, and follow-up of MASLD in individuals with overweight or obesity.
RESUMEN
ABSTRACT Background Insulin resistance (IR), assessed by different criteria, is an important factor in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). More recently with the characterization of this metabolic dysfunction-associated fatty liver disease (MAFLD), one of the proposed criteria for this diagnosis has been the determination of the homeostasis model assessment-insulin resistance (HOMA-IR). Objective: The purpose of this study was to evaluate the relationship of HOMA-IR>2.5 with clinical, metabolic, biochemical and histological data obtained in non-diabetic patients diagnosed with NAFLD by liver biopsy. Methods: Cross-sectional, retrospective study was carried out with data from 174 adult individuals of both genders with non-diabetics NAFLD, without obvious signs of portal hypertension. The body mass index (BMI) was classified according to the World Health Organization (1998), and the metabolic syndrome by the criteria of NCEP-ATP-III. Biochemical tests were evaluated using an automated method and insulinemia through immunofluorometric assay. Histological findings were classified according to Kleiner et al. (2005). Results: The mean age of the studied population was 53.6±11.2 years, with 60.3% being female. The average BMI was 30.3 kg/m2 and 75.9% of the patients had increased waist circumference. Among evaluated metabolic parameters, there was a higher prevalence of metabolic syndrome (MS) in patients with HOMA-IR>2.5, with no statistical difference in relation to BMI between studied groups. Values of liver enzymes and serum ferritin were significantly higher in patients with this marker of IR, who had a higher prevalence of non-alcoholic steatohepatitis (NASH) and advanced liver fibrosis. In the multivariate analysis, the clinical diagnosis of MS, hyperferritinemia and the presence of NASH in the liver biopsy were the factors independently associated with the presence of altered HOMA-IR. Conclusion: HOMA-IR values >2.5 identify patients with NAFLD with distinct clinical and metabolic characteristics and with a greater potential for disease progression, which validates this parameter in the identification of patients with MAFLD.
RESUMO Contexto A resistência à insulina (RI), avaliada por diferentes critérios, é um fator importante na patogênese da doença hepática gordurosa não alcoólica (DHGNA). Mas, recentemente, com a caracterização desta disfunção metabólica associada com a doença hepática gordurosa (DGH), um dos critérios propostos para este diagnóstico tem sido a determinação do modelo de avaliação da homeostase-resistência à insulina (HOMA-IR). Objetivo: O objetivo deste estudo foi avaliar a relação do HOMA-IR> 2,5 com dados clínicos, metabólicos, bioquímicos e histológicos obtidos em pacientes não diabéticos diagnosticados com DHGNA por biópsia hepática. Métodos Estudo transversal, retrospectivo, com dados de 174 indivíduos adultos de ambos os sexos com DHGNA não-diabética, sem sinais evidentes de hipertensão portal. O índice de massa corporal (IMC) foi classificado de acordo com a Organização Mundial da Saúde (1998) e a síndrome metabólica pelos critérios do NCEP-ATP-III. Os exames bioquímicos foram avaliados pelo método automatizado e a insulinemia por imunofluorometria. Os achados histológicos foram classificados de acordo com Kleiner et al. (2005). Resultados: A média de idade da população estudada foi de 53,6±11,2 anos, sendo 60,3% do sexo feminino. O IMC médio foi de 30,3 kg/m2 e 75,9% dos pacientes apresentaram circunferência da cintura aumentada. Entre os parâmetros metabólicos avaliados, houve maior prevalência de síndrome metabólica (SM) em pacientes com HOMA-IR >2,5, sem diferença estatística em relação ao IMC entre os grupos estudados. Os valores das enzimas hepáticas e da ferritina sérica foram significativamente maiores nos pacientes com este marcador de RI, que apresentaram maior prevalência de esteato-hepatite não alcoólica (EHNA) e fibrose hepática avançada. Na análise multivariada, o diagnóstico clínico de SM, hiperferritinemia e a presença de EHNA na biópsia hepática foram os fatores independentemente associados à presença de HOMA-IR alterado. Conclusão: Valores de HOMA-IR >2,5 identificam pacientes com DHGNA com características clínicas e metabólicas distintas e com maior potencial de progressão da doença, o que valida esse parâmetro na identificação de pacientes com DHG.
RESUMEN
Metabolic-dysfunction associated fatty liver disease (MAFLD) is a common concomitant disease of breast cancer. It is one of the main causes of liver damage during chemotherapy and also an important cause of liver damage during endocrine therapy or follow-up, which seriously affects the quality of life and prognosis of breast cancer patients. Nonalcoholic fatty liver disease was renamed as MAFLD, which changed the original "exclusive diagnosis" to "inclusive diagnosis" and the non-negligible role of metabolic factors in the occurrence and development of fatty liver disease was recognized, but the clinical attention is not enough at present. More attention should be paid to the diagnosis and treatment of MAFLD in breast cancer patients because the proportion and risk of metabolic disorders are higher than that in general people. In this article, we will focus on the clinical significance, prevention and treatment of the new definition of MAFLD in the comprehensive management of concomitant diseases of breast cancer, so as to further improve the quality of life and prognosis of breast cancer patients.
RESUMEN
ObjectiveTo explore the effect of Jiangtang Xiaozhi tablet (JTXZT) on metabolic dysfunction-associated fatty liver disease and to study the mechanism from the perspective of circadian clock-related genes such as circadian locomotor output cycles kaput (CLOCK), brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein 1 (BMAL1), reverse-eritroblastosis receptor (REV-ERB)α and β. MethodA total of 50 male SPF C57BL/6J mice were randomized into normal group (n=10) and modeling group (n=40). The normal group was fed with normal diet, and the modeling group with high-fat diet for 4 weeks. Then the model mice were randomly classified into model group, high-dose (12.5 g·kg-1) and low-dose (6.25 g·kg-1) Jiangtang Xiaozhi tablet groups, and orlistat group (70 mg·kg-1), with 10 mice in each group. The normal group and model group received equivalent volume of distilled water (8 weeks). Then, the body weight of mice was measured, and the content of serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) was determined with biochemical method. Serum content of free fatty acid (FFA) and leptin was detected by enzyme-linked immunosorbent assay (ELISA). Pathological changes of liver tissue and epididymal adipose tissue were observed based on hematoxylin-eosin (HE) staining. Liver fibrosis was examined based on Masson's trichrome staining, and changes of lipids based on oil red O staining. The expression of CLOCK, BMAL1, REV-ERBα, and REV-ERBβ was detected by Western blot and immunohistochemistry assay. ResultCompared with the normal group, the model group had high content of TG, TC, LDL-C, HDL-C, AST, ALT, FFA, and leptin (P<0.05, P<0.01), showed ballooning degeneration and focal microvesicular steatosis of liver cells, enlarged adipocytes, and inflammatory cell clusters and fibrous tissue hyperplasia, and displayed increased protein expression of sterol regulatory element binding protein (SREBP) 1 and peroxisome proliferators-activated receptor (PPAR)γ (P<0.01) and decreased protein expression of PPARα (P<0.05), CLOCK, BMAL1, REV-ERBα and β (P<0.05, P<0.01). Compared with the model group, JTXZT-H group down-regulated the content of TG, TC, LDL-C, HDL-C, AST, ALT, FFA, and leptin in mice (P<0.05, P<0.01), and the JTXZT groups demonstrated reduction in the degree and range of ballooning degeneration of liver tissue, alleviation of the compression of hepatic sinusoidal tissue, unobvious inflammatory cell infiltration and fibrous tissue proliferation, reduction in the expression of SREBP1 and PPARγ (P<0.05, P<0.01), and rise of the protein expression of PPARα (P<0.01), CLOCK, BMAL1, REV-ERBα, and REV-ERBβ (P<0.05, P<0.01). ConclusionJTXZT can significantly alleviate the metabolic dysfunction-associated fatty liver disease in mice caused by high-fat diet. The mechanism is the likelihood that it regulates downstream related lipid metabolism proteins (such as SREBP1, PPARγ, and PPARα).
RESUMEN
ObjectiveTo explore the effect of Jiangtang Xiaozhi tablet (JTXZT) on metabolic dysfunction-associated fatty liver disease and to study the mechanism from the perspective of circadian clock-related genes such as circadian locomotor output cycles kaput (CLOCK), brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein 1 (BMAL1), reverse-eritroblastosis receptor (REV-ERB)α and β. MethodA total of 50 male SPF C57BL/6J mice were randomized into normal group (n=10) and modeling group (n=40). The normal group was fed with normal diet, and the modeling group with high-fat diet for 4 weeks. Then the model mice were randomly classified into model group, high-dose (12.5 g·kg-1) and low-dose (6.25 g·kg-1) Jiangtang Xiaozhi tablet groups, and orlistat group (70 mg·kg-1), with 10 mice in each group. The normal group and model group received equivalent volume of distilled water (8 weeks). Then, the body weight of mice was measured, and the content of serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) was determined with biochemical method. Serum content of free fatty acid (FFA) and leptin was detected by enzyme-linked immunosorbent assay (ELISA). Pathological changes of liver tissue and epididymal adipose tissue were observed based on hematoxylin-eosin (HE) staining. Liver fibrosis was examined based on Masson's trichrome staining, and changes of lipids based on oil red O staining. The expression of CLOCK, BMAL1, REV-ERBα, and REV-ERBβ was detected by Western blot and immunohistochemistry assay. ResultCompared with the normal group, the model group had high content of TG, TC, LDL-C, HDL-C, AST, ALT, FFA, and leptin (P<0.05, P<0.01), showed ballooning degeneration and focal microvesicular steatosis of liver cells, enlarged adipocytes, and inflammatory cell clusters and fibrous tissue hyperplasia, and displayed increased protein expression of sterol regulatory element binding protein (SREBP) 1 and peroxisome proliferators-activated receptor (PPAR)γ (P<0.01) and decreased protein expression of PPARα (P<0.05), CLOCK, BMAL1, REV-ERBα and β (P<0.05, P<0.01). Compared with the model group, JTXZT-H group down-regulated the content of TG, TC, LDL-C, HDL-C, AST, ALT, FFA, and leptin in mice (P<0.05, P<0.01), and the JTXZT groups demonstrated reduction in the degree and range of ballooning degeneration of liver tissue, alleviation of the compression of hepatic sinusoidal tissue, unobvious inflammatory cell infiltration and fibrous tissue proliferation, reduction in the expression of SREBP1 and PPARγ (P<0.05, P<0.01), and rise of the protein expression of PPARα (P<0.01), CLOCK, BMAL1, REV-ERBα, and REV-ERBβ (P<0.05, P<0.01). ConclusionJTXZT can significantly alleviate the metabolic dysfunction-associated fatty liver disease in mice caused by high-fat diet. The mechanism is the likelihood that it regulates downstream related lipid metabolism proteins (such as SREBP1, PPARγ, and PPARα).
RESUMEN
The increasing incidence of metabolic diseases is in part due to the high fructose consumption, a carbohydrate vastly used in industry, with a potent lipogenic capacity. Thyroid hormones (TH) are essential for metabolism regulation and are associated with changes in body weight, energy expenditure, insulin sensitivity, and dyslipidemia. This study aimed to investigate the influence of fructose intake on thyroid function and thyroid-related genes. Male Wistar rats were divided into Control (CT, n=8) and Fructose (FT - 10% in drinking water, n=8) groups for three weeks. The FT group showed higher glycemia and serum triacylglycerol, indicating metabolic disturbances, and increased thyroid mass, accompanied by higher expression of Srebf1c and Lpl, suggesting increased lipid synthesis. The FT group also presented higher expression of Tpo and Dio1 in the thyroid, suggesting activation of the thyroid gland, but with no alterations in serum TH concentrations. Brown adipose tissue (BAT) of the FT group exhibited higher expression of Dio2, Thra, and Thrb, indicating increased T3 intra-tissue bioavailability and signaling. These responses were accompanied by increased BAT mass and higher expression of Adrb3, Pparg, Srebf1c, Fasn, Ppara, and Ucp1, suggesting increased BAT adrenergic sensitivity, lipid synthesis, oxidation, and thermogenesis. Therefore, short-term fructose consumption induced thyroid molecular alterations and increased BAT expression of thyroid hormone-related signaling genes that potentially contributed to higher BAT activity.
RESUMEN
Objective:To explore the diagnostic performance of ultrasound attenuation imaging (ATI) in grading the degree of hepatic steatosis in metabolic dysfunction-associated fatty liver disease (MAFLD).Methods:The liver gray-scale ultrasound and ATI examinations were performed on 212 subjects who were treated in Zhongshan Hospital Affiliated to Fudan University from August 2020 to March 2021. The attenuation coefficient(AC) values among different degrees of hepatic steatosis were analyzed and the diagnostic performance of ATI was evaluated. Relationships between AC values and clinical characteristics were assessed by Pearson′s correlation analysis.Results:The AC values for normal liver, mild, moderate and severe fatty liver were (0.56±0.05)dB·cm -1·MHz -1, (0.68±0.09)dB·cm -1·MHz -1, (0.82±0.09)dB·cm -1·MHz -1, (0.94±0.09)dB·cm -1·MHz -1, respectively. There were significant differences in AC values among different hepatic steatosis divisions( P<0.008). There was highly significant correlation between AC values and the degree of hepatic steatosis( r=0.860, P<0.01), moderate correlation between AC values and BMI( r=0.425, P<0.01), weak correlation between AC values and HDL-C( r=-0.237, P=0.029), no correlations between AC values and age, TC, TG, LDL-C ( r=0.083, 0.055, 0.133, -0.039, all P>0.05) .The areas under the receiver operating characteristics curve of ATI for mild fatty liver and above, moderate fatty liver and above, severe fatty liver and above were 0.958, 0.962, 0.918; the sensitivity were 90.1%, 95.8%, 94.9%, the specificity were 96.1%, 87.1%, 73.9%, and the cut-off values were 0.666 dB·cm -1·MHz -1, 0.719 dB·cm -1·MHz -1, 0.803 dB·cm -1·MHz -1, respectively. Conclusions:ATI is a reliable and convenient method for evaluating the degree of hepatic steatosis in MAFLD.
RESUMEN
Migraine is a common disabling primary headache disorder, and it imposes heavy burden on individual sufferer and the whole society, while its mechanism is not entirely clear. Recent year researches between migraine and mitochondria have made certain progresses on morphology, magnetic resonance imaging, biochemistry, pharmacology and genetics. Here, we systematically review their research progresses and hope to provide guidance for preventive medication of migraine.
RESUMEN
Polycystic ovary syndrome (PCOS)is the most common cause of anovulatory infertility in women of reproductive age, exerting significant impacts on glucose and lipid metabolism, cardiovascular and endometrial deseases, as well as breast, skin, bone, and psychology fields. As a complex, multi-system of endocrine and metabolic disease, PCOS would be recognized as a component of metabolic syndrome in an overall consideration. The clinical treatment of PCOS is expected to turn simply regulating menstruation and ovulation adjustment into the combination of insulin resistance improvement with antihyperandrogen and ovulation treatment comprehensively.