ABSTRACT
A elastografia hepática (EH) avalia as consequências sistêmicas da insuficiência cardíaca (IC). Este método pode auxiliar na avaliação prognóstica dos portadores de IC. A IC pode afetar de forma secundária a função de vários órgãos e sistemas, notadamente o hepático, mediante congestão venosa. O objetivo deste artigo é mostrar, através de uma revisão narrativa, a importância da EH na avaliação complementar da IC. As consequências hepáticas na doença cardíaca, por vezes, se mostram silenciosas, sem grandes alterações no exame físico e/ou em exames laboratoriais. Nesse contexto, a EH demonstrou ser um método não invasivo recomendável para a mensuração do dano hepático causado pela IC. (AU)
Liver elastography (LE) assesses the systemic consequences of heart failure (HF). This method may help in the prognostic assessment of patients with HF. HF can secondarily affect the function of various organs and systems, especially the liver, through venous congestion. The purpose of this article is to provide a narrative review of the importance of LE in the complementary evaluation of HF. The hepatic consequences of cardiac disease are sometimes silent, without significant changes in physical examination and/or laboratory tests. In this context, LE has emerged as a recommended non-invasive method to measure liver damage caused by HF. (AU)
Subject(s)
Humans , Male , Female , Aged , Aged, 80 and over , Fatty Liver/complications , Heart Failure/mortality , Heart Failure/diagnostic imaging , Liver Cirrhosis/complications , Bilirubin/physiology , Magnetic Resonance Spectroscopy/methods , Elasticity Imaging Techniques/methods , gamma-Glutamyltransferase/physiologyABSTRACT
Purpose: Tamoxifen, a widely used drug for breast cancer treatment, is associated with adverse effects on the liver, including the development of fatty liver. This study aimed to investigate the potential protective effect of caffeine against tamoxifen-induced fatty liver in Wistar rats. Methods: Rats were divided into normal control, tamoxifen + saline, and tamoxifen + caffeine. Plasma samples were assessed for biochemical markers related to oxidative stress, inflammation, liver function, and cell damage. Additionally, liver histopathology was examined to quantify the extent of fatty infiltration. Results: In the tamoxifen + saline group, elevated levels of plasma malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), alanine aminotransferase (ALT), cytokeratin 18, and soluble ST2 were observed compared to the normal control group, indicating increased oxidative stress, inflammation, and liver injury (p < 0.01). Moreover, histopathological examination revealed a significant increase in fatty infiltration (p < 0.001). However, in the tamoxifen + caffeine group, these markers were markedly reduced (p < 0.05, p < 0.01), and fatty infiltration was significantly mitigated (p < 0.001). Conclusions: The findings suggest that caffeine administration attenuates tamoxifen-induced fatty liver in rats by ameliorating oxidative stress, inflammation, liver injury, and cell damage. Histopathological evidence further supports the protective role of caffeine. This study highlights the potential of caffeine as a therapeutic intervention to counter tamoxifen-induced hepatic complications, contributing to the optimization of breast cancer treatment strategies.
Subject(s)
Tamoxifen , Caffeine , Rats, Wistar , Fatty LiverABSTRACT
La enfermedad de hígado graso no alcohólico (EHGNA) abarca desde una acumulación simple de lípidos neutros, triacilglicéridos (TAG) y colesterol en más del 5% de los hepatocitos, hasta una forma más avanzada llamada esteatohepatitis no alcohólica (EHNA), la que incluye inflamación lobular, balonamiento hepático y, en algunos casos, se asocia con fibrosis hepática. La creciente prevalencia de la EHGNA asociada a la dieta, especialmente aquellas ricas en grasas y carbohidratos, como la fructosa, ha orientado el enfoque de esta investigación. Nuestro objetivo fue analizar cómo la suplementación de fructosa, junto a una dieta alta en grasas, contribuye a la progresión desde EHGNA a EHNA, evaluando su efecto en marcadores lipogénicos y fibróticos. Ratones macho de la cepa C57BL/6 (n=9) fueron alimentados con dieta alta en grasa (DAG) (n=5) o dieta alta en grasa más fructosa (DAG+F) (n=4) durante 17 semanas. Se evaluaron parámetros generales (peso corporal, de tejido adiposo y hepático), niveles de glicemia e insulinemia, HOMA, histología hepática y adiposa; niveles de expresión de marcadores inflamatorios (TNF-α e IL-1b), lipogénicos (SREBP-1c, FAS) y fibrogénicos (TGF-ß, α-SMA). La suplementación con fructosa no generó diferencias respecto al peso corporal, peso del hígado o del tejido adiposo, ni sobre la glicemia basal y el HOMA-IR en comparación con la DAG, pero incrementó los niveles de insulina. Además, indujo esteatosis macrovesicular, junto con un incremento en el balonamiento celular, inflamación lobulillar y fibrosis. Concluimos que la suplementación de fructosa junto con la DAG indujo un estado pre-fibrótico, caracterizado por el incremento de α-SMA y de marcadores lipogénicos.
Non-alcoholic fatty liver disease (NAFLD) ranges from a simple accumulation of neutral lipids, triacylglycerides (TAG) and cholesterol in more than 5% of hepatocytes, to a more advanced form called non-alcoholic steatohepatitis (NASH), which includes lobular inflammation, hepatic ballooning and, in some cases, is associated with hepatic fibrosis. The increasing prevalence of NASH associated with diet, especially those rich in fats and carbohydrates, such as fructose, has guided the focus of this research. Our aim was to analyze how fructose supplementation, together with a high-fat diet, contributes to the progression from NAFLD to NASH, evaluating its effect on lipogenic and fibrotic markers. Male C57BL/6 strain mice (n=9) were fed high-fat diet (HFD) (n=5) or high-fat diet plus fructose (HFD+F) (n=4) for 17 weeks. General parameters (body, adipose and liver tissue weight), glycemia and insulinemia levels, HOMA, liver and adipose histology; expression levels of inflammatory (TNF-α and IL-1b), lipogenic (SREBP-1c, FAS) and fibrogenic (TGF-ß, α-SMA) markers were evaluated. Fructose supplementation did not generate differences with respect to body weight, liver or adipose tissue weight, nor on basal glycemia and HOMA-IR compared to DAG, but increased insulin levels. In addition, it induced macrovesicular steatosis, along with increased cell ballooning, lobular inflammation and fibrosis. We conclude that fructose supplementation together with DAG induced a pre-fibrotic state, characterized by increased α-SMA and lipogenic markers.
Subject(s)
Animals , Mice , Fatty Liver/chemically induced , Diet, High-Fat/adverse effects , Fructose/adverse effects , Body Weight , Insulin Resistance , Carbohydrates , Dietary Supplements , Sterol Regulatory Element Binding Protein 1 , Lipogenesis/drug effects , Mice, Inbred C57BLABSTRACT
La alteración de la microbiota intestinal es uno de los factores claves que afecta el inicio y la progresión de esteatosis hepática, al aumentar la permeabilidad intestinal e inducir un aumento circulante de la endotoxina lipopolisacárido (LPS). El LPS puede llegar al hígado a través de la vena porta, donde desencadena procesos inflamatorios y pro-oxidantes. Por otro lado, alimentos ricos en aceites esenciales podrían tener la capacidad de contrarrestar los efectos deletéreos del LPS a nivel hepático. El objetivo de este estudio fue evaluar el efecto del aceite de rosa mosqueta (ARM) en la prevención de procesos inflamatorios y oxidantes en hepatocitos humanos HepG2 tratados con LPS. Células HepG2 fueron expuestas a diferentes dosis de ARM (1,5, 3, 4,5, 6 y 7,5 µg/mL) por 24 horas y luego estimuladas con LPS (100 ng/mL) por 4 horas. Se evaluaron los niveles de expresión de citoquinas proinflamatorias (TNF-α, IL-6, IL-1ß, CCL2) y de la proteína antioxidante hemo oxigenasa 1 (HO-1), además de los niveles de activación de NF-κB. El tratamiento con 6 µg/mL de ARM resultó en un incremento en la viabilidad celular. El pretratamiento con ARM (1,5 - 4,5 µg/mL) fue efectivo para disminuir la expresión (TNF-α, IL-6 y CCL2) y secreción (TNF-α) de citoquinas proinflamatorias. Sin embargo, dosis altas de ARM incrementaron la activación de NF- κB y disminuyeron la expresión de HO-1 en células tratadas con LPS. Estos resultados sugieren un efecto antinflamatorio y un posible rol en el proceso antioxidante para dosis bajas de ARM en hepatocitos humanos frente al daño con LPS.
Rosa mosqueta (Rosa Rubiginosa) oil decreases inflammatory markers in human liver HepG2 cells treated with lipopolysaccharide. Gut microbiota alteration is one of the key factors affecting the onset and progression of hepatic steatosis by enhancing intestinal permeability and inducing an increase in circulating endotoxin lipopolysaccharide (LPS). LPS reaches the liver through the portal vein, where triggers inflammatory and pro-oxidant processes. On the other hand, essential oils-rich foods may have the capacity to abolish the deleterious effects of LPS in the liver. The objective of this study was to evaluate the effect of rosa mosqueta oil (ARM) in the prevention of inflammatory and oxidative processes in human hepatic cells HepG2 treated with LPS. HepG2 cells were exposed to different doses of ARM (1.5, 3, 4.5, 6 y 7.5 µg/mL) for 24 hours and then stimulated with LPS (100 ng/mL) for 4 hours. NF-κB activation, proinflammatory cytokines expression level (TNF-α, IL-6, IL-1ß, CCL2), and the antioxidant protein expression of hem oxygenase 1 (HO-1) were evaluated. Treatment with 6 µg/mL increased cellular viability. ARM pretreatment was effective in decreasing the expression (TNF-α, IL-6 y CCL2) and secretion (TNF-α) of proinflammatory cytokines. On the other hand, high doses of ARM increased NF-κB activation and decreased HO-1 expression in cells treated with LPS. These results may suggest an anti-inflammatory effect and a possible role in the antioxidant process in the case of the lower doses of ARM in human hepatic cells treated with LPS.
Subject(s)
Humans , Plant Oils/administration & dosage , Lipopolysaccharides/antagonists & inhibitors , Hep G2 Cells/drug effects , Cell Survival , Cytokines , Oxidative Stress/drug effects , Rosa , Fatty Liver , Inflammation/prevention & control , Anti-Inflammatory Agents , AntioxidantsABSTRACT
Introdução: Uma alta prevalência de doença hepática esteatótica metabólica (MASLD) tem sido descrita na psoríase. A influência da presença de fatores metabólicos, dos polimorfismos dos genes PNPLA3 e TM6SF2 e da dose acumulada de metotrexate (MTX) na progressão da doença esteatótica necessita melhor avaliação. O risco cardiovascular também é aumentado na MASLD e a presença de ateroesclerose subclínica pode representar um marcador do processo inflamatório que une os componentes da hipótese do eixo hepato-dérmico na psoríase. Objetivos: Avaliar o impacto dos polimorfismos dos genes PNPLA3 e TM6SF2, dos parâmetros metabólicos e da dose cumulativa de MTX na esteatose e fibrose hepática avançada em pacientes com psoríase. Avaliar a associação de esteatose e fibrose hepática avançada com ateroesclerose subclínica nestes pacientes. Métodos: Estudo transversal com inclusão prospectiva de pacientes ambulatoriais com psoríase, submetidos a análise clínica e laboratorial, elastografia hepática transitória (TE) com controlled atenuated parameter (CAP) com o equipamento FibroScan® (Echosens,Fr). Todos os pacientes realizaram a genotipagem para os polimorfismos PNPLA3/TM6SF2. A medida da velocidade de onda de pulso carótido-femoral (VOP-cf) foi adotada como medida de rigidez aórtica (rAO). A esteatose foi definida por CAP ≥275 dB/m, fibrose hepática avançada como rigidez hepática ≥10 kPa, aumento da rAo como VOP-cf ≥10m/s. Dose cumulativa significativa de metotrexato foi definida por ≥1500 mg (MTX1500). A análise de regressão logística avaliou as variáveis independentes relacionadas à esteatose e fibrose hepática avançada e ao aumento da rigidez aórtica; valor de p<0,05 foi considerado significativo. Resultados: Foram incluídos 199 pacientes (idade 54,6 ±12,6 anos, 57,3% mulheres). A prevalência de síndrome metabólica (SM), esteatose e fibrose hepática avançada foi de 55,8%, 54,8% e 9%, respectivamente. As frequências dos genótipos PNPLA3 e TM6SF2 foram CC 42,3%/CG 49,5%/GG 8,2% e CC 88,7%/ CT 11,3%/TT 0%. SM (OR3,01 IC95% 1,51- 5,98; p=0,002) e índice de massa corporal (OR1,17 IC95% 1,08-1,26; p<0,01) foram independentemente associados à esteatose. Diabetes Mellitus tipo 2 (DM2) (OR10,76 IC95% 2,42-47,87; p=0,002) e a presença de pelo menos um alelo PNPLA3 G (OR5,66 IC95% 1,08-29,52; p=0,039) foram associados à fibrose hepática avançada, mas não o polimorfismo TM6SF2 ou dose cumulativa de MTX. Para a análise das variáveis relacionadas com o aumento da rAo, um sub-grupo com 80 pacientes (idade 56,2±11,5 anos, 57,5% mulheres, IMC 28,6±5,3kg/m2), com prevalências de SM, DM2, dislipidemia, hipertensão arterial sistêmica, esteatose e fibrose hepática avançada de 57,5%, 40,0%, 67,5%, 70,0%, 50,0% e 16,3%, respectivamente, foi avaliado. Com relação ao tratamento da psoríase, 45% receberam dose de MTX≥1500 mg e 33,8%, tratamento imunobiológico. Neste grupo, a prevalência deVOP-cf≥10m/s foi de 21,2%. Na análise de regressão logística, a idade foi independentemente relacionada com o aumento da rAo (OR: 1,21; IC95%:1,06-1,38; p=0,003), mas não a esteatose ou fibrose hepática avançada. MTX1500 foi um fator protetor cardiovascular (OR: 0,18; IC95%: 0,038-0,87; p=0,033), mas não a terapia imunobiológica. Conclusões: Em indivíduos com psoríase, SM e DM2 conferem maiores chances de esteatose e fibrose avançada, respectivamente. O alelo PNPLA3 G, mas não o polimorfismo TM6SF2, impacta em risco 5 vezes maior de fibrose hepática avançada. O aumento da rAo é associado à idade, mas não à esteatose ou fibrose avançada. Um efeito cardiovascular protetor do MTX foi encontrado em uma população psoríase com alta prevalência de SM e seus componentes.(AU)
Introduction: A high prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) has been described in psoriasis. The influence of the presence of metabolic factors, PNPLA3 and TM6SF2 gene polymorphisms and the cumulative dose of methotrexate (MTX) on the progression of steatotic disease requires further evaluation. Cardiovascular risk is also increased in MASLD and the presence of subclinical atherosclerosis may represent a marker of the inflammatory process that joins the components of the hepato-dermal axis hypothesis in psoriasis. Objectives: To evaluate the impact of PNPLA3 and TM6SF2 gene polymorphisms, metabolic parameters and cumulative MTX dose on steatosis and advanced liver fibrosis in patients with psoriasis. To evaluate the association of steatosis and advanced fibrosis with subclinical atherosclerosis. Methods: Cross-sectional study with prospective inclusion of outpatients with psoriasis, submitted to clinical and laboratory analysis, transient elastography (TE) with controlled attenuated parameter (CAP), with FibroScan® (Echosens,Fr). All patients underwent genotyping for PNPLA3/TM6SF2 polymorphisms. The measurement of carotid-femoral pulse wave velocity (PWV-cf) was adopted as a measure of aortic stiffness (AoS). Steatosis was defined by CAP ≥275 dB/m, advanced liver fibrosis as liver stiffness ≥10 kPa, increased AoS as PWV-cf ≥10m/s. Significant cumulative dose of methotrexate was defined as ≥1500 mg (MTX1500). Logistic regression analysis evaluated the independent variables related to to steatosis and advanced liver fibrosis and increased AoS; p value <0.05 was considered significant. Results: 199 patients were included (age 54.6 ±12.6 years, 57.3% feminine). The prevalence of metabolic syndrome (MetS), steatosis and advanced liver fibrosis was 55.8%, 54.8% and 9%, respectively. The frequencies of the PNPLA3 and TM6SF2 genotypes were CC 42.3%/CG 49.5%/GG 8.2% and CC 88.7%/CT 11.3%/TT 0%. MetS (OR3.01 95% CI 1.51-5.98; p=0.002) and body mass index (OR1.17 95% CI 1.08-1.26; p<0.01) were independently associated with steatosis. Type 2 Diabetes Mellitus (DM2) (OR10.76 95% CI 2.42-47.87; p=0.002) and the presence of at least one PNPLA3 G allele (OR5.66 95% CI 1.08-29.52; p =0.039) were associated with advanced liver fibrosis, but not the TM6SF2 polymorphism or cumulative dose of MTX. To analyze the variables related to increased AoS, a sub-group with 80 patients (age 56.2±11.5 years, 57.5% feminine, BMI 28.6±5.3kg/m2), with prevalences of MetS, DM2, dyslipidemia, systemic arterial hypertension, steatosis and advanced liver fibrosis of 57.5%, 40.0%, 67.5%, 70.0%, 50.0% and 16.3%, respectively, was evaluated. Regarding psoriasis treatment, in this group, 45% received a dose of MTX≥1500 mg and 33.8%, immunobiological treatment. The prevalence of PWVcf≥10m/s was 21.2%. In the logistic regression analysis, age was independently related to increased AoS (OR: 1.21; 95% CI: 1.06-1.38; p=0.003), but not steatosis or advanced liver fibrosis. MTX1500 was a cardiovascular protective factor (OR: 0.18; 95% CI: 0.038-0.87; p=0.033), but not immunobiological therapy. Conclusions: In individuals with psoriasis, MetS and DM2 confer a greater risk for steatosis and advanced fibrosis, respectively. The PNPLA3 G allele, but not the TM6SF2 polymorphism, impacts a 5-fold increased risk of advanced liver fibrosis. Increased AoS is associated with age, but not with steatosis or advanced fibrosis. A protective cardiovascular effect of MTX was found in a psoriasis population with a high prevalence of MetS and its components.(AU)
Subject(s)
Humans , Polymorphism, Genetic , Psoriasis , Methotrexate , Metabolic Syndrome , Fatty Liver , Fatty Liver/genetics , Liver Cirrhosis , Liver Cirrhosis/geneticsABSTRACT
Se presenta el caso clínico de una gestante de 20 años de edad, quien acudió al Cuerpo de Guardia del bloque materno del Hospital General Docente Dr. Juan Bruno Zayas Alfonso de Santiago de Cuba por presentar decaimiento, náuseas y malestar general. Durante la exploración física se encontró piel sudorosa y fría, taquicardia e ictericia. Se realizaron diversos exámenes complementarios y se constató alteración hepática, así como cifras bajas de glucemia. Se diagnosticó hígado graso agudo del embarazo. Luego de varios días de hospitalizada con una evolución desfavorable, hasta llegar al estado crítico, la paciente falleció por síndrome de disfunción multiorgánica.
The case report of a 20 years pregnant woman is presented, who went to the maternal block emergency room of Dr. Juan Bruno Zayas Alfonso Teaching General Hospital in Santiago de Cuba due to run-down, nausea and diffuse discomfort. During the physical exploration sweaty and cold skin, tachycardia and jaundice were found. Diverse complementary exams were carried out and a hepatic disorder was verified, as well as low figures of glycemia. Acute fatty liver of pregnancy was diagnosed. After several days hospitalized with an unfavorable clinical course until getting to the critical state, the patient died due to multiple organ dysfunction syndrome.
Subject(s)
Pregnancy, High-Risk , Fatty Liver , Liver Diseases , Pregnancy , Fetal Death , Maternal Death , Multiple Organ FailureABSTRACT
Fundamento: El hígado graso no alcohólico es la enfermedad hepática por depósito de grasa en ausencia de un consumo significativo de alcohol. La mayoría de los pacientes tienen un nexo epidemiológico común asociado a factores de riesgo metabólico. Objetivo: Describir características clínico epidemiológicas de pacientes con enfermedad por hígado graso no alcohólico. Metodología: Se realizó un estudio descriptivo de una serie de casos en la consulta de Gastroenterología del Hospital General Provincial "Camilo Cienfuegos" de Sancti Spíritus, durante el período 6 de mayo de 2019 al 6 de mayo de 2020. Se consideró un total de 1167 pacientes pertenecientes a la provincia Sancti Spíritus; a 346 pacientes se le diagnosticó esteatosis hepática por ultrasonido; la muestra se conformó por 114 pacientes que cumplieron con los criterios de inclusión. Resultados: La mayoría de los pacientes con la enfermedad eran sintomáticos, hombres y tenían comorbilidad como la hipertensión arterial y obesidad, el índice de masa corporal y el índice de cintura abdominal/cadera estaban elevados en el sexo femenino, las alteraciones en la química sanguínea fueron colesterol y triacilglicéridos. Conclusiones: Predominó en el sexo masculino y la comorbilidad con la HTA y la obesidad, y la dislipidemia, además los hábitos alimenticios inadecuados y el sedentarismo; las medidas antropométricas resultaron elevadas en el sexo femenino.
Background: Nonalcoholic fatty liver disease is a resulting from fat accumulation in the absence of significant alcohol consumption. Most patients have a common epidemiologic link associated with metabolic risk factors. Objective: To describe the clinical and epidemiologic characteristics of patients with nonalcoholic fatty liver disease. Methodology: A descriptive study of a series of cases was carried out in the Gastroenterology consultation of the "Camilo Cienfuegos" Provincial General Hospital of Sancti Spíritus, during the period from May 6, 2019 through May 6, 2020. A total of 1167 patients belonging to the province of Sancti Spiritus were included in the study; 346 patients were diagnosed with hepatic steatosis by means of ultrasound; the sample consisted of 114 patients who fulfilled the inclusion criteria. Results: Most patients with the disease were symptomatic, men, and had comorbidities including hypertension and obesity, the body mass index and the waist-to-hip ratio of the abdomen were increased in women., the blood chemistry changes were cholesterol and triacylglycerides. Conclusions: It predominated in the male sex and comorbidity with HBP and obesity and dyslipidemia, in addition to inadequate dietary habits and sedentary lifestyle; in women, the anthropometric measurements were high.
Subject(s)
Risk Factors , Fatty Liver , Non-alcoholic Fatty Liver DiseaseABSTRACT
OBJECTIVE@#To analyze the clinical features of overweight and obese rheumatoid arthritis (RA)patients, and the relationship between body mass index (BMI) and disease characteristics.@*METHODS@#The demographic data, extra-articular manifestations, comorbidities, and disease activity of RA patients admitted to the Rheumatology and Immunology Department of Peking University Third Hospital from January 2015 to December 2020 were collected, and the above characteristics of overweight and obese RA patients were retrospectively analyzed. According to the WHO, BMI≥30 kg/m2 referred to obese individuals, 25≤BMI < 30 kg/m2 referred to overweight individuals, 18.5≤BMI < 25 kg/m2 referred to normal individuals, BMI < 18.5 kg/m2 referred to reduced body mass individuals. t test was used for the quantitative data in accordance with normal distribution. Wilcoxon rank sum test was used for the quantitative data of non-normal distribution. The qualitative data were analyzed by chi square test. But while 1≤theoretical frequency < 5, Chi square test of corrected four grid table was used. And Fisher exact probability method was used when theoretical frequency < 1. Analyzing whether overweight or obesity was associated with comorbidities using Logistic regression adjusted confounding factors.@*RESULTS@#A total of 481 RA patients were included in this study, with an average BMI value of (23.28±3.75) kg/m2.Of the patients, 31 cases (6.5%) were with BMI < 18.5 kg/m2, 309 cases (64.2%) with 18.5≤ BMI < 25 kg/m2, amounting to 340 cases (70.7%). There were 119 overweight individuals (25≤ BMI < 30 kg/m2, 24.7%) and 22 obese individuals (BMI≥30 kg/m2, 4.6%), totaling 141 (29.3%).The proportion of the overweight and obese RA patients suffering from hypertension (57.4% vs. 39.1%, P < 0.001), diabetes (25.5% vs. 15.0%, P=0.006), hyperlipidemia (22.7% vs. 10.9%, P=0.001), fatty liver (28.4% vs. 7.4%, P < 0.001), osteoarthritis (39.0% vs. 29.4%, P=0.040) was significantly higher, and the proportion of the patients with osteoporosis(59.6% vs. 70.9%, P=0.016) and anemia (36.2% vs. 55.6%, P < 0.001) was significantly lower. However, there was no difference between the two groups in coronary heart disease (5.7% vs. 7.6%, P=0.442), cerebrovascular disease (6.4% vs. 8.8%, P=0.372) and peripheral atherosclerosis (9.2% vs. 7.6%, P=0.565).The median C-reactive protein (CRP, 1.52 mg/dL vs. 2.35 mg/dL, P=0.008), median erythrocyte sedimentation rate (ESR, 34.0 mm/h vs. 50.0 mm/h, P=0.003), pain visual simulation score (VAS) (3.66±3.08 vs. 4.40±2.85, P=0.011), and 28 joint disease activity scores (DAS-28, 5.05±1.60 vs. 5.45±1.52, P=0.010) in the overweight and obese RA group were all lower than those in the normal and reduced weight groups. Multivariate regression analysis showed that overweight and obesity was an independent risk factor for hypertension, diabetes, hyperlipidemia and fatty liver, and had protective effects on osteoporosis and anemia.@*CONCLUSION@#In RA patients, RA disease activity is lower in overweight and obesity patients. Overweight and obesity is associated with hypertension, diabetes and hyperlipidemia, but not with cardiovascular and cerebrovascular diseases.
Subject(s)
Humans , Body Mass Index , Overweight/epidemiology , Retrospective Studies , Arthritis, Rheumatoid/epidemiology , Obesity/epidemiology , Diabetes Mellitus , Hypertension/complications , Fatty Liver/complications , Hyperlipidemias/complications , Osteoporosis/complications , AnemiaABSTRACT
Objective: To investigate the clinical characteristics and maternal and fetal prognosis of pregnant women with acute fatty liver of pregnancy (AFLP). Methods: The clinical data of 86 AFLP pregnant women admitted to the Third Affiliated Hospital of Guangzhou Medical University from September 2017 to August 2022 were collected, and their general data, clinical characteristics, laboratory tests and maternal and fetal outcomes were retrospectively analyzed. Results: (1) General information: the age of the 86 pregnant women with AFLP was (30.8±5.4) years, and the body mass index was (21.0±2.5) kg/m2. There were 50 primiparas (58.1%, 50/86) and 36 multiparas (41.9%, 36/86). There were 64 singleton pregnancies (74.4%, 64/86) and 22 twin pregnancies (25.6%, 22/86). (2) Clinical characteristics: the main complaints of AFLP pregnant women were gastrointestinal symptoms, including epigastric pain (68.6%, 59/86), nausea (47.7%, 41/86), anorexia (46.5%, 40/86), vomiting (39.5%, 34/86). The main non-gastrointestinal symptoms were jaundice of skin and/or scleral (54.7%, 47/86), edema (38.4%, 33/86), fatigue (19.8%, 17/86), bleeding tendency (16.3%, 14/86), polydipsia or polyuria (14.0%, 12/86), skin itching (8.1%, 7/86), and 17.4% (15/86) AFLP pregnant women had no obvious symptoms. (3) Laboratory tests: the incidence of liver and kidney dysfunction and abnormal coagulation function in AFLP pregnant women was high, and the levels of blood ammonia, lactate dehydrogenase and lactic acid were increased, and the levels of hemoglobin, platelet and albumin decreased. However, only 24 cases (27.9%, 24/86) of AFLP pregnant women showed fatty liver by imageology examination. (4) Pregnancy outcomes: ① AFLP pregnant women had a high incidence of pregnancy complications, mainly including renal insufficiency (95.3%, 82/86), preterm birth (46.5%, 40/86), hypertensive disorders in pregnancy (30.2%, 26/86), gestational diabetes mellitus (36.0%, 31/86), fetal distress (24.4%, 21/86), pulmonary infection (23.3%, 20/86), disseminated intravascular coagulation (16.3%, 14/86), multiple organ dysfunction syndrome (16.3%, 14/86), hepatic encephalopathy (9.3%, 8/86), and intrauterine fetal death (2.3%, 2/86). ② Treatment and outcome of AFLP pregnant women: the intensive care unit transfer rate of AFLP pregnant women was 66.3% (57/86). 82 cases were improved and discharged after treatment, 2 cases were transferred to other hospitals for follow-up treatment, and 2 cases (2.3%, 2/86) died. ③ Neonatal outcomes: except for 2 cases of intrauterine death, a total of 106 neonates were delivered, including 39 cases (36.8%, 39/106) of neonatal asphyxia, 63 cases (59.4%, 63/106) of neonatal intensive care unit admission, and 3 cases (2.8%, 3/106) of neonatal death. Conclusions: AFLP is a severe obstetric complication, which is harmful to mother and fetus. In the process of clinical diagnosis and treatment, attention should be paid to the clinical manifestations and laboratory tests of pregnant women, early diagnosis and active treatment, so as to improve maternal and fetal outcomes.
Subject(s)
Pregnancy , Infant, Newborn , Female , Humans , Adult , Retrospective Studies , Premature Birth/epidemiology , Pregnancy Complications/diagnosis , Fatty Liver/diagnosis , Fetal Death , StillbirthABSTRACT
In light of the liver injury risk associated with the oral administration of Xianlin Gubao oral preparation, this study compared the differences in liver injury induced by two different extraction processes in rats and explored the correlation between hepatotoxicity and extraction process from the perspective of the differences in the content of the relevant components. Thirty male Sprague-Dawley(SD) rats were randomly divided into a normal group, tablet extract groups of different doses, and capsule extract groups of different doses, with 6 rats in each group. Each group received continuous oral administration for 4 weeks. The assessment of liver injury caused by different extracts was conducted by examining rat body weight, liver function blood biochemical indicators, liver coefficient, and liver pathological changes. In addition, a high-performance liquid chromatography(HPLC) method was established to simultaneously determine the content of icariin, baohuoside I, and bakuchiol in the extracts to compare the differences in the content of these three components under the two extraction processes. The results showed that both extracts caused liver injury in rats. Compared with the normal group, the tablet extract groups, at the studied dose, led to slow growth in body weight, a significant increase in triglyceride levels(P<0.05), a significant decrease in liver-to-brain ratio(P<0.05), and the appearance of hepatic steatosis. The capsule extract groups, at the studied dose, resulted in slow growth in body weight, a significant increase in aspartate aminotransferase levels(P<0.05), a significant decrease in body weight, liver weight, and liver-to-brain ratio(P<0.05), and the presence of hepatic steatosis and inflammatory cell infiltration. In comparison, the capsule extraction process had a higher risk of liver injury. Furthermore, based on the completion of the liquid chromatography method, the content of icariin and baohuoside Ⅰ in the capsule extract groups was 0.83 and 0.81 times that in the tablet extract groups, respectively, while the bakuchiol content in the capsule extract group was 29.80 times that in the tablet extract groups, suggesting that the higher risk of liver injury associated with the capsule extraction process may be due to its higher bakuchiol content. In summary, the differences in rat liver injury caused by the two extracts are closely related to the extraction process. This should be taken into consideration in the formulation production and clinical application.
Subject(s)
Rats , Male , Animals , Rats, Sprague-Dawley , Liver/pathology , Chemical and Drug Induced Liver Injury/pathology , Fatty Liver , Tablets , Body Weight , Plant Extracts , PhenolsABSTRACT
Metabolic associated fatty liver disease (MAFLD) has become a prevalent chronic liver disease worldwide because of lifestyle and dietary changes. Gut microbiota and its metabolites have been shown to play a critical role in the pathogenesis of MAFLD. Understanding of the function of gut microbiota and its metabolites in MAFLD may help to elucidate pathological mechanisms, identify diagnostic markers, and develop drugs or probiotics for the treatment of MAFLD. Here we review the pathogenesis of MAFLD by gut microbiota and its metabolites and discuss the feasibility of treating MAFLD from the perspective of gut microbes.
Subject(s)
Humans , Gastrointestinal Microbiome , Fatty Liver/microbiologyABSTRACT
Objective: To summarize the genotypes and clinical characteristics of homozygous family hypobetalipoproteinemia (Ho-FHBL) caused by apolipoprotein B (APOB) gene variations. Methods: The clinical, laboratory, genetic, and liver histology data of a boy with Ho-FHBL managed in the hepatology ward of the Children's Hospital of Fudan University in May 2021 were retrospectively analyzed. The literature was searched from China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform, China VIP database, China Biology Medicine disc and PubMed database (up to May 2022) with "familial hypobetalipoproteinemia" or "hypobetalipoproteinemias" or "hypo beta lipoproteinemia" or "hypolipoproteinemias" as the search terms. All relevant literatures were reviewed to summarize the clinical and genetic features of Ho-FHBL caused by APOB gene variations. Results: The male patient was admitted to the hospital due to abnormal liver function tests for 8 months at the age of 4 years and 6 months. Blood biochemistry showed transaminitis and abnormally low serum levels of lipids. Liver biopsy revealed fatty liver with inflammation and early cirrhosis (Brunt score was F3G2S4). Whole exome sequencing revealed two novel variants of APOB gene (c.3745C>T, p.Q1249 * from the father and c.4589_4592delinsAGGTAGGAGGTTTAACTCCTCCTACCT, p.T1530Kfs * 12 from the mother). He was diagnosed as Ho-FHBL caused by APOB gene compound heterozygous variations. Literature search retrieved 36 English literatures and 0 Chinese literature. A total of 55 (23 males and 32 females) Ho-FHBL cases, including this one, were caused by 54 APOB gene pathogenic variants (23 frameshift, 15 nonsense, 7 missense, 8 splice and 1 gross deletions). The age of the last follow-up was between 1 month and 75 years. Among them, 28 cases had lipid malabsorption, 19 cases had early dysplasia, 12 cases had no symptoms. Twenty-one patients had symptoms related to fat soluble vitamin deficiency, including 14 cases of acanthocytosis, 10 cases of neurological symptoms, and 6 cases of ocular lesions. Thirty-four patients had liver involvement, including 25 cases of elevated transaminase, 21 cases of fatty liver, 15 cases of hepatomegaly, 9 cases of liver fibrosis, 3 cases of liver cirrhosis, 1 case of hepatic hemangioma and 1 case of liver neoplastic nodule. Conclusions: The variants of APOB gene in Ho-FHBL are mainly frameshift and nonsense variations. Patients may have lipid malabsorption and (or) early dysplasia, or symptom-free. Liver involvement is common.
Subject(s)
Child , Female , Humans , Male , Child, Preschool , Infant , Abetalipoproteinemia/diagnosis , Retrospective Studies , Hypobetalipoproteinemias/diagnosis , Fatty Liver/genetics , Apolipoproteins B/genetics , LipidsABSTRACT
Alcoholic liver disease(ALD), with its increasing morbidity and mortality, has seriously and extensively affected the health of people worldwide. Methyl ferulic acid(MFA) has been proven to significantly inhibit alcohol-induced lipid production in L02 cells through the AMP-activated protein kinase(AMPK) pathway, but its in-depth mechanism remains unclear. This study aimed to further clarify the mechanism of MFA in improving lipid accumulation in L02 cells through the microRNA-378b(miR-378b)-mediated calcium/calmodulin-dependent protein kinase kinase 2(CaMKK2)-AMPK signaling pathway based on existing researches. L02 cells were induced by 100 mmol·L~(-1) ethanol for 48 h to establish the model of ALD in vitro, and 100, 50, and 25 μmol·L~(-1) concentration of MFA was treated. MiR-378b plasmids(containing the overexpression plasmid-miR-378b mimics, silence plasmid-miR-378b inhibitor, and their respective negative control-miR-378b NCs) were transfected into L02 cells by electroporation to up-regulate or down-regulate the levels of miR-378b in L02 cells. The levels of total cholesterol(TC) and triglyceride(TG) in cells were detected by commercial diagnostic kits and automatic biochemical analyzers. The expression levels of miR-378b in L02 cells were detected by real-time quantitative polymerase chain reaction(qRT-PCR). CaMKK2 mRNA levels were detected by PCR, and protein expressions of related factors involved in lipid synthesis, decomposition, and transport in lipid metabolism were detected by Western blot. The results displayed that ethanol significantly increased TG and TC levels in L02 cells, while MFA decreased TG and TC levels. Ethanol up-regulated the miR-378b level, while MFA effectively inhibited the miR-378b level. The overexpression of miR-378b led to lipid accumulation in ethanol-induced L02 cells, while the silence of miR-378b improved the lipid deposition induced by ethanol. MFA activated the CaMKK2-AMPK signaling pathway by lowering miR-378b, thus improving lipid synthesis, decomposition, and transport, which improved lipid deposition in L02 cells. This study shows that MFA improves lipid deposition in L02 cells by regulating the CaMKK2-AMPK pathway through miR-378b.
Subject(s)
Humans , Ethanol/toxicity , AMP-Activated Protein Kinases/metabolism , Fatty Liver , Triglycerides , MicroRNAs/genetics , Calcium-Calmodulin-Dependent Protein Kinase Kinase/geneticsABSTRACT
In recent years, reports of adverse reactions related to traditional Chinese medicine(TCM) have been on the rise, especially some traditionally considered "non-toxic" TCM(such as Dictamni Cortex). This has aroused the concern of scholars. This study aims to explore the metabolomic mechanism underlying the difference in liver injury induced by dictamnine between males and females through the experiment on 4-week-old mice. The results showed that the serum biochemical indexes of liver function and organ coefficients were significantly increased by dictamnine(P<0.05), and hepatic alveolar steatosis was mainly observed in female mice. However, no histopathological changes were observed in the male mice. Furthermore, a total of 48 differential metabolites(such as tryptophan, corticosterone, and indole) related to the difference in liver injury between males and females were screened out by untargeted metabolomics and multivariate statistical analysis. According to the receiver operating characteristic(ROC) curve, 14 metabolites were highly correlated with the difference. Finally, pathway enrichment analysis indicated that disorders of metabolic pathways, such as tryptophan metabolism, steroid hormone biosynthesis, and ferroptosis(linoleic acid metabolism and arachidonic acid metabolism), may be the potential mechanism of the difference. Liver injury induced by dictamnine is significantly different between males and females, which may be caused by the disorders of tryptophan metabolism, steroid hormone biosynthesis, and ferroptosis pathways.
Subject(s)
Female , Male , Animals , Mice , Tryptophan , Metabolomics , Fatty Liver , Steroids , HormonesABSTRACT
Context and objectives As the global epidemic of obesity and metabolic syndrome progresses, the coexistence of fatty liver disease in patients with chronic viral hepatitis B (VHB) becomes significant. The objective of this work was to determine the frequency of hepatic steatosis assessed by Fibroscan/CAP (Controlled Attenuation Parameter) in patients with chronic VHB in Côte d'Ivoire. Methods. The study included 83 patients with chronic VHB. These were black patients who had performed a Fibroscan/CAP during the recruitment period and were willing to participate in the study. Patients with significant alcohol consumption, a secondary cause of hepatic steatosis, another liver disease regardless of the etiology associated with VHB were not included. Results. The frequency of hepatic steatosis in chronic HBV carriers assessed by CAP in our study population was 48.19 %, including 24.10 % of severe steatosis. Obesity was statistically correlated with the presence of steatosis in our patients. Patients who had steatosis on ultrasound were 5 times more likely to have steatosis on CAP. Significant fibrosis was insignificantly associated with steatosis. Conclusion. The frequency of fatty liver disease detected by fibroscan/CAP is high in patients with chronic VHB.
Contexte et objectifs Avec la progression de l'épidémie mondiale d'obésité et du syndrome métabolique, la coexistence d'une stéatose hépatique chez les patients porteurs d'une hépatite virale B chronique devient non négligeable. L'objectif de ce travail était de déterminer la fréquence de la stéatose hépatique chez les patients porteurs d'une hépatite virale B (HVB) chronique. Méthodes. Il s'agissait d'une série des cas de HVB de race noire, ayant réalisé un Fibroscan/CAP pendant la période du recrutement et consentants à participer à l'étude. Les patients ayant une consommation d'alcool significative, une cause secondaire de stéatose hépatique, une autre hépatopathie quelle que soit l'étiologie associée à l'hépatite B n'ont pas été inclus. Résultats. Quatre-vingt-trois patients porteurs d'une HVB ont été inclus. La fréquence de la stéatose hépatique chez les porteurs du VHB chronique était de 48,19 % dont 24,10 % de stéatose sévère. L'obésité était statistiquement corrélée à la présence d'une stéatose chez nos patients. Les patients qui avaient une stéatose à l'échographie étaient 5 fois plus à risque d'avoir une stéatose au CAP. La fibrose significative était associée de façon non significative à la stéatose. Conclusion : Près de la moitié des patients porteurs d'une hépatite virale B chronique présente une stéatose hépatique.
Subject(s)
Humans , Male , Female , Fatty LiverABSTRACT
Consuming a high-fat diet causes a harmful accumulation of fat in the liver, which may not reverse even after switching to a healthier diet. Different reports dealt with the role of purslane as an extract against high-fat diet; meanwhile, it was necessary to study the potential role of fresh purslane as a hypolipidemic agent. This study is supposed to investigate further the potential mechanism in the hypolipidemic effect of fresh purslane, by measuring cholesterol 7a-hydroxylase (CYP7A1) and low-density lipoprotein receptor (Ldlr). Rats were divided into two main groups: the first one is the normal control group (n=7 rats) and the second group (n=28 rats) received a high fat diet for 28 weeks to induce obesity. Then the high fat diet group was divided into equal four subgroups. As, the positive control group still fed on a high fat diet only. Meanwhile, the other three groups were received high-fat diet supplemented with a different percent of fresh purslane (25, 50 and 75%) respectively. At the end of the experiment, rats were sacrificed and samples were collected for molecular, biochemical, and histological studies. Current study reported that, supplementation of fresh purslane especially at a concentration of 75% play an important role against harmful effects of high-fat diet at both cellular and organ level, by increasing CYP7A1 as well as Ldlr mRNA expression. Also, there were an improvement on the tested liver functions, thyroid hormones, and lipid profile. Fresh purslane plays the potential role as a hypolipidemic agent via modulation of both Ldlr and Cyp7A, which will point to use fresh purslane against harmful effects of obesity.
O consumo de uma dieta rica em gordura causa um acúmulo prejudicial de gordura no fígado, que pode não reverter mesmo após a mudança para uma dieta mais saudável. Diferentes relatórios trataram do papel da beldroega como um extrato contra uma dieta rica em gordura; entretanto, foi necessário estudar o papel potencial da beldroega fresca como agente hipolipemiante. Este estudo pretende investigar mais profundamente o mecanismo potencial no efeito hipolipidêmico da beldroega fresca, medindo o colesterol 7a-hidroxilase (CYP7A1) e o receptor de lipoproteína de baixa densidade (Ldlr). Os ratos foram divididos em dois grupos principais: o primeiro é o grupo controle normal (n = 7 ratos) e o segundo grupo (n = 28 ratos) recebeu dieta rica em gorduras por 28 semanas para induzir a obesidade. Em seguida, o grupo de dieta rica em gordura foi dividido em quatro subgrupos iguais. Como, o grupo de controle positivo ainda se alimentava apenas com dieta rica em gordura. Enquanto isso, os outros três grupos receberam dieta rica em gordura suplementada com diferentes porcentagens de beldroegas frescas (25%, 50% e 75%), respectivamente. Ao final do experimento, os ratos foram sacrificados e amostras coletadas para estudos moleculares, bioquímica e histológicos. O estudo atual relatou que a suplementação de beldroegas frescas, especialmente a uma concentração de 75%, desempenha papel importante contra os efeitos prejudiciais da dieta rica em gordura em nível celular e orgânico, aumentando a expressão de CYP7A1 e Ldlr mRNA. Além disso, houve melhora nas funções hepáticas testadas, nos hormônios tireoidianos e no perfil lipídico. Beldroegas frescas desempenham papel potencial como agente hipolipemiante por meio da modulação de Ldlr e Cyp7A, o que apontará para o uso de beldroegas frescas contra os efeitos nocivos da obesidade.
Subject(s)
Animals , Rats , Diet, High-Fat , Fatty Liver/drug therapy , Fatty Liver/veterinary , Obesity/drug therapy , Portulaca , Mice, ObeseABSTRACT
Introdução: A esteatose hepática está presente em 25% da população geral. O termo "metabolic-dysfunction associated fatty liver disease" (MAFLD) foi recomendado por especialistas para destacar a contribuição dos fatores de risco cardiometabólicos na progressão da esteatose hepática. Desde a introdução da terapia antirretroviral, pessoas vivendo com HIV/AIDS (PVHA) vêm apresentando maiores taxas de morbi-mortalidade por doenças crônicas. Porém, o papel da infecção pelo HIV na MAFLD ainda é desconhecido. Objetivo: O objetivo primário deste estudo é avaliar a associação da infecção pelo vírus HIV na presença de MAFLD em PVHA e controles pareados. Os objetivos secundários são descrever a prevalência e fatores associados com a presença de MAFLD em pacientes infectados e não infectados pelo vírus HIV. Metodologia: Fatty Liver Index (FLI) foi utilizado para o diagnóstico de esteatose hepática. MAFLD foi definida pela presença de esteatose hepática associada com sobrepeso/obesidade [índice de massa corporal (IMC) ≥ 25 Kg/m2 ], diabetes ou disfunção metabólica conforme recomendação de painel de especialistas. Comparamos pessoas vivendo com HIV do INI/FIOCRUZ (coorte INI-ELSA-HIV, n=649) com indivíduos nãoinfectados pelo HIV do estudo ELSA-Brasil (n=15105). Utilizamos ponderação por escores de propensão para balancear os dados entre os grupos e uma técnica não-paramétrica, chamada "generalized boosted regression modeling" (GBM) para construção do modelo melhor adaptado. O equilíbrio entre os grupos comparados foi testado pelos métodos usuais. Resultados: 15087 indivíduos não HIV foram incluídos, dentre os quais 36% foram caracterizados como MAFLD, ao passo que 649 indivíduos HIV foram incluídos, sendo 33% caracterizados como MAFLD. Fatores metabólicos foram associados ao desenvolvimento de MAFLD em ambas as coortesA razão de chances de um paciente com HIV ter MAFLD comparado a um paciente não HIV foi de 1.30 (IC 0.97-1.74, p-valor 0.076). Conclusão: A doença hepática gordurosa metabólica foi altamente prevalente em duas coortes de indivíduos com e sem HIV. Infecção pelo HIV mostrou uma tendência para aumento do risco de MAFLD, no entanto estudos prospectivos serão necessários para confirmar esta relação
Background: Nonalcoholic fatty liver disease (NAFLD) is a significant public health issue affecting up to 25% of the general population. It is characterized by hepatic steatosis without significant alcohol consumption or other causes of chronic liver disease. The association between metabolic dysregulation and NAFLD has led to the adoption of the new MAFLD terminology. Meanwhile, HIV infection continues to be a major global health concern, with increasing mortality from liver diseases among people living with HIV (PLWH). Fatty liver disease is highly prevalent in PLWH, but its association with HIV infection remains unclear. Methods: This retrospective study analyzed data from two large cohorts: the ELSA-Brasil study (uninfected individuals) and the INI-ELSA-HIV study (PLWH). The Fatty Liver Index (FLI) was used to diagnose hepatic steatosis, and MAFLD was defined based on hepatic steatosis and the presence of metabolic risk factors. Propensity score matching was applied to balance the samples, and logistic regression was used to assess the association between HIV infection and MAFLD. Results: A total of 15087 uninfected individuals and 649 PLWH were included in the analysis. The prevalence of MAFLD was found to be 36% in uninfected individuals and 33% in PLWH. Both populations showed similar risk factors associated with MAFLD, including type-2 diabetes, dyslipidemia, hypertension, and higher BMI. After propensity score matching, HIV infection showed a trend towards association with MAFLD (OR=1.30, 95% CI 0.97-1.74, p=0.076). Conclusion: This study highlights the high prevalence of MAFLD in non-HIV individuals and PLWH, with similar risk factors contributing to its development. HIV infection showed a trend towards being associated with MAFLD, but further prospective studies are needed to confirm this relationshipUnderstanding the risk factors for MAFLD in PLWH is essential for tailoring preventive and therapeutic interventions to mitigate liver-related complications in this population
Subject(s)
Acquired Immunodeficiency Syndrome , HIV , Diabetes Mellitus , Fatty Liver , Non-alcoholic Fatty Liver Disease , ObesityABSTRACT
Purpose: To explore the effect and potential mechanism of dihydroartemisinin (DHA) on metabolism-related fatty liver disease. Methods: A metabolic associated fatty liver disease (MAFLD) mice model was induced with continuous supplies of high-fat diet. DHA was intraperitoneally injected into mice. The weight of mice was monitored. The concentrations of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) in serum were detected by an automatic biochemical analyzer. The liver tissues were stained by hematoxylin and eosin and oil red O. The level of inflammation, oxidative stress, and autophagy was assessed by reverse transcription polymerase chain reaction, biochemical examination, Western blot and transmission electron microscope assays. Results: DHA treatment reduced theMAFLD-enhanced the level of weight gain, the concentrations of TC, TG, LDL and malonaldehyde, while increasedthe MAFLD-decreased the concentrations of HDL and superoxide dismutase. DHA ameliorated the MAFLD-aggravated pathological changes and the number of lipid droplets. Low dose of DHA declined the MAFLD-induced the enhancement of the expression of inflammatory factor. DHA treatment increased the MAFLD-enhanced the level of autophagy related protein, while decreased the MAFLD-reduced the protein level of p62. The increased level of autophagy was confirmed by transmission electron microscope. Conclusions: DHA can improve liver steatosis in MAFLD mice by inhibiting inflammation and oxidative stress and promoting autophagy.
Subject(s)
Animals , Mice , Autophagy/drug effects , Oxidative Stress/drug effects , Fatty Liver/therapy , InflammationABSTRACT
La interrupción de la simbiosis que existe entre el cuerpo humano y su microbioma puede resultar en una disbiosis, un desequilibrio en la interacción huésped-microbiota, que puede asociarse al desarrollo de diversas enfermedades como el síndrome de intestino irritable, hígado graso no alco-hólico, enfermedad hepática alcohólica y cirrosis, entre otras. En ciertas condiciones patológicas y por múltiples factores de riesgo, la capacidad de autorregulación del intestino se puede alterar, contribuyendo al incremento de la permeabilidad con inflamación intestinal crónica. El diagnóstico y el tratamiento, así como la relación entre la permeabilidad intestinal, la disbiosis y las patologías gastrointestinales y hepatobiliares, todavía no tienen estudios clínicos validados o con el soporte científico adecuado, por lo que se realiza una revisión de la literatura con la finalidad de aportar conceptos que puedan orientar con respecto a la importancia del estudio del microbioma humano en estas enfermedades.
Disruption of the symbiosis that exists between the human body and its microbiome can result in dys-biosis, an imbalance in the host-microbiota interaction, which may be associated with the develop-ment of various diseases such as irritable bowel syndrome, non-alcoholic fatty liver disease, alcoholic liver disease and cirrhosis, among others. In certain pathological conditions and due to multiple risk factors, the self-regulating capacity of the intestine may be lost, contributing to increased permeability with chronic intestinal inflammation. Its diagnosis and treatment as well as the relationship between intestinal permeability, dysbiosis and gastrointestinal and hepatobiliary pathologies have not been validated in clinical studies or have adequate scientific support, so a review of the literature is carried out in order to provide concepts that can guide with respect to the importance of the study of the human microbiome in these diseases