جستجوی مقالات مرتبط با کلیدواژه « hepatic steatosis » در نشریات گروه « پزشکی »

Non-alcoholic fatty liver disease (NAFLD) incidence and prevalence are rapidly increasing globally. The combined effects of metformin and quercetin (Que) have yet to be investigated. However, both have demonstrated the potential to reduce triglyceride (TG) levels and treat NAFLD by promoting autophagy. The objective of the present study was to elucidate the mechanism of action and assess the role of autophagy in the lipid-lowering effects of Que, both individually and in combination with metformin, in a HepG2 cell model of hepatic steatosis. Triglyceride levels and lipogenic gene expression were reduced in HepG2 cells exposed to palmitic acid (PA) when treated with Que-metformin, as evidenced by triglyceride measurements and real-time PCR. The LDH release assay also showed that this combination induced autophagy to protect HepG2 cells from PA-induced cell death. According to the Western blot analysis outcomes, Que-metformin increased LC3-I and LC3-II protein levels while decreasing p62 expression to induce autophagy. In HepG2 cells, the co-administration of Que-metformin elevated cAMP, phosphorylated AMP-activated protein kinase (p-AMPK), and Beclin-1 levels. Additionally, the inhibition of SIRT1 reversed the autophagy induced by Que-metformin. The findings of this study demonstrated for the first time that Que-metformin reduced hepatosteatosis by stimulating autophagy through the cAMP/AMPK/SIRT1 signaling pathway and diminishing inflammatory cytokines.

The high-fat-low-carbohydrate diet is an efficient diet for reducing body weight, with increased satiety and diminishing energy consumption. This study aimed to determine the effects of a high-fat-low-carbohydrate diet on the metabolic function of the liver and pancreas in a mouse model.

This experimental research was conducted in 2021 on 60 albino mice that were divided into 6 groups (each group containing 10 mice). At the beginning of the experiment, 40 mice were fed a high-fat-high-carbohydrate diet for 12 weeks to enhance gaining weight;  then the 4 groups were fed a high-fat-low-carbohydrate diet, while the other two groups were considered as control groups. For sample collection, animals were sacrificed and blood samples were collected for biochemical analysis, tissue samples were taken for histopathological assay. Data were analyzed by SPSS 26 using the ANOVA.

The result of this study showed that mice fed a high-fat-low-carbohydrate diet had high levels of aspartate aminotransferase, alanine aminotransferase, and cholesterol in the blood serum. In addition, the level of triglycerides and blood glucose decreased in the same groups. Histopathological study showed severe fatty changes that led to edema and degeneration of hepatocytes in the periportal area due to degeneration of the microvasculature and the formation of bridging fibrosis between the central hepatic lobes and the peripheral area in the high-fat-low-carbohydrate diet group. The tissue sections of the pancreas did not show any signs of pathology.

Long-term administration of a high-fat-low-carbohydrate diet affects histologically and functionally in mice liver.

COVID 19 may affect organs other than lungs, including liver, leading to parenchymal changes. These changes are best assessed by unenhanced computed tomography (CT). We aim to investigate the effect of COVID 19 on liver parenchyma by measuring the attenuation in CT scan Hounsfield unit (HU).

A cohort of patients, who tested COVID 19 polymerase chain reaction positive, were enrolled and divided into two groups: fatty liver (FL) group (HU ≤ 40) and nonfatty liver (NFL) group (HU > 40) according to liver parenchyma attenuation measurements by high resolution noncontrast CT scan. The CT scan was performed on admission and on follow up (10–14 days later). Liver enzyme tests were submitted on admission and follow up.

Three hundred and two patients were enrolled. Liver HU increased significantly from 48.9 on admission to 53.4 on follow up CT scan (P<0.001) in all patients. This increase was more significant in the FL group (increased from 31.9 to 42.9 [P =0.018]) Liver enzymes were abnormal in 22.6% of the full cohort. However, there was no significant change in liver enzymes between the admission and follow up in both groups.

The use of unenhanced CT scan for assessment of liver parenchymal represents an objective and noninvasive method. The significant changes in parenchymal HU are not always accompanied by significant changes in liver enzymes. Increased HU values caused by COVID 19 may be due to either a decrease in the fat or an increase in the fibrosis in the liver.

Non-alcoholic fatty liver disease (NAFLD) is common in people with type 2 diabetes mellitus (T2DM). We aimed to explore predictive factors of NAFLD in T2DM and identify high risk subgroups.

This was a cross-sectional study including 100 individuals with T2DM and 100 without diabetes matched for age, sex, and body mass index (BMI). Hepatic steatosis grades (calculated by controlled attenuation parameters-CAP score-3), and liver fibrosis stages (F0-F4) were determined using transient elastography.

The frequency of NAFLD was comparable between the two study groups. However, CAP scores were significantly higher in individuals with diabetes (294.90 ± 53.12 vs. 269.78 ± 45.05 dB/m; P < 0.001). Fifty percent of individuals with diabetes had severe steatosis (S3), while this figure was 31.6% in those without diabetes (P < 0.05). Significant fibrosis (F2-F4) was more frequent in individuals with T2DM (13% vs. 4.1%, P = 0.02). Individuals with T2DM and advanced fibrosis had significantly higher BMI, waist circumference (WC), waist-hip ratio (WHR), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and CAP score compared to those without fibrosis (P < 0.05). In the regression analysis, a model including BMI, WHR, AST and female gender explained 50% of the variation in CAP score in patients with diabetes (all P < 0.05, adjusted R2 : 0.508). CAP scores were also the major determinant of liver fibrosis in this group (OR: 1.04; CI: 1.017–1.063; P = 0.001).

Individuals with diabetes are more likely to have severe fibrosis. Obesity (especially central obesity), the female gender, elevated liver enzymes, and higher degree of insulin resistance are associated with more advanced liver disease in individuals with T2DM.

Non-alcoholic fatty liver disease (NAFLD) is emerging as a major health problem worldwide. NAFLD is a continuum of disease ranging from mild liver steatosis to severe steatohepatitis, which will ultimately lead to end-stage liver disease with high morbidity and mortality rates. This disorder is considered as a silent liver disease. The metabolic syndrome and its components are accounted as the major risk factors for the progression of NAFLD to NASH and cirrhosis. Liver transplantation is considered as an appropriate treatment for the end-stage disease. For the last two decades, NASH has been the most common reason for liver transplantation, especially in the developed countries; however, the outcome of post-transplantation in these patients is of a great concern. The recurrent NASH and NAFLD seem to be the usual issues in LT. Steatosis appears in more than 80% of LTs; however, re-transplantation caused by steatohepatitis is rare. Recently, several risk factors of the recurrent NAFLD, including age, donor steatosis, metabolic syndrome, and immunosuppressant agents, have been introduced. Among the metabolic syndrome components, obesity seriously has negative effects on the outcomes of post-liver transplantation in patients. Unfortunately, there is no standard medicine to prevent or treat the recurrent NAFLD; however, it seems that weight loss and lifestyle modification play critical roles in controlling or inhibiting the recurrent NAFLD or NASH.