جستجوی مقالات مرتبط با کلیدواژه « NAFLD » در نشریات گروه « پزشکی »

Liver diseases, including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), pose significant global public health challenges. This study investigates the therapeutic effects of quercetin (QC), Capparis spinosa (CS), a QC and CS combination, and Saroglitazar (SARO) on NASH in a Wistar rat model.

NASH was induced by a 42-day high-fat diet regimen in male Wistar rats. Post-induction, rats were divided into five groups receiving SARO, QC, CS, and CS+QC combination. We monitored changes in liver and body weights and evaluated the expression of genes associated with fatty acid biosynthesis (e.g., ACC and FAS), β-oxidation (e.g., CPT1, PPAR α), inflammation (e.g., TNF-α and IL-6), and fibrosis (e.g., TGF-β and COL1A), as well as protein expression levels of p-Smad2/3 and p-Smad3.

Treatment with QC+CS significantly decreased liver weight, body mass gain, and liver triglyceride (TG) compared to other treatments. The QC and CS combined therapy also resulted in a greater normalization of hepatic enzymatic activities, including decreases in ALT and AST levels, coupled with improvements in lipid profile indicated by decreased LDL-C and increased HDL-C concentrations, as compared to SARO and QC alone. Furthermore, this combined treatment significantly down-regulated the expression of TGF-β, TNF-α, IL-6 genes, and Smad2/3 and Smad3 protein levels. 

Our study demonstrates that an interactive effect between QC and CS can effectively reduce liver fibrosis and steatosis by inhibiting the TGF-β/Smad3 signaling pathway in a diet-induced model of nonalcoholic steatohepatitis and fibrosis in rats.

Non-alcoholic fatty liver disease (NAFLD) is a chronic steatohepatitis disorder. If left untreated, it can progress to hepatocellular carcinoma. Several studies have shown that saroglitazar, a PPARα/γ dual agonist, and curcumin (the principal constituent of turmeric) may be effective in the treatment of NAFLD. This research aimed to study the pharmacological mechanism of these compounds in rats with NAFLD.

NAFLD was induced in male Wistar rats (aged 6–8 weeks) by feeding them a high-fat diet (HFD) for 6 weeks. Subsequently, the rats were divided into four groups, with Group 1 continuing on HFD, while groups 2, 3, and 4 received HFD supplemented with saroglitazar, curcumin, and both saroglitazar and curcumin, respectively. We evaluated the expression of Nrf2, ERK1/2, NOX1,2,4, antioxidant enzymes, PPARα, γ, and genes regulating lipid metabolism in the liver. Histopathology of liver tissue was also examined. Furthermore, we analyzed serum levels of lipid profiles and hepatic enzymes.

Rats with NAFLD that received treatment involving saroglitazar and curcumin showed a significant decrease in the expression of ERK1/2, SREBP1, PPARγ, pro-inflammatory cytokines, NOXs, and ROS levels. Additionally, the levels of Nrf2, PPARα, and antioxidant enzymes showed a significant increase. The serum levels of lipid profiles and hepatic enzymes also decreased significantly after drug treatment.

Our results confirm that both saroglitazar and curcumin ameliorate NAFLD by regulating the Nrf2 and ERK1/2 signaling pathways. These findings suggest that curcumin could serve as a suitable substitute for saroglitazar, although they appear to have a synergistic effect.

Metabolic dysfunction-associated fatty liver disease (MAFLD) is a rising global public health concern. It has been demonstrated that its prevalence and characteristics vary by region and racial/ethnicity. We aimed to investigate the prevalence of MAFLD and its characteristics among Turkmen and non-Turkmen ethnic groups in a multiethnic population region of Iran.

In this cross-sectional study, we analyzed baseline data for 1614 participants, aged above 50 years, from the PolyIran-Liver trial who were randomly selected from Gonabad city and determined the prevalence of MAFLD and its demographic and metabolic disorders for both the Turkmen and non-Turkmen ethnic groups. Multivariate binary logistic regressions were applied to identify MAFLD-associated factors for men and women separately for the Turkmen and non-Turkmen populations.

The mean (SD) age of the participants was 59.1(6.7) years. Of the participants, 51.5% (n = 831) were men, and 52.9% (n = 854) were Turkmen. The prevalence of MAFLD among the overall study population was 39.8% (n = 614). It was more common among women (45.8% vs. 34.1% in men, P < 0.001), non-Turkmens (43.9% vs. 36.1% in Turkmens, P < 0.001), and at age 50-64 (41.5% vs.36.1% in age ≥ 65 P = 0.004). The fully adjusted multivariate analysis in sex strata exhibited an independent negative association between Turkmen ethnicity only among men but not among women. The increased waist circumference (WC) was the most common metabolic disorder, observed in more than 95.5% of patients with MAFLD (P < 0.001). Multivariate analysis in sex/ethnic strata with adjustment for potential confounders revealed an independent association of MAFLD with increased WC, insulin resistance, impaired fasting glucose/diabetes type 2, and high alanine aminotransferase (ALT) among women in both ethnic groups while with elevated triglyceride (TG) only among Turkmen and high body mass index (BMI) only among non-Turkmen women. Increased WC had the strongest independent association with MAFLD among women and the highest odds ratio (OR) with MAFLD in Turkmen women (OR: 6.10; 95% CI 1.56-23.86 vs. 4.80 in non-Turkmen women). Among men, MAFLD was independently associated with insulin resistance, high BMI, and high ALT in both ethnic groups and elevated TG only in non-Turkmen men (all P < 0.001). Insulin resistance had the strongest independent OR with MAFLD among men with similar size in both ethnic groups (4.68 [95% CI 2.56-8.55]) in non-Turkmen men and 4.37 (95% CI 2.27-8.42 in Turkmen men).

This study revealed the high prevalence of MAFLD with a sex and ethnic disparity in the middle-aged population of Gonabad city. Further research is needed to understand the factors contributing to the higher prevalence of MAFLD in this region, particularly in women. Furthermore, considering the diverse ethnic population of Iran, it is suggested that future investigations on the sex and ethnic aspects of MAFLD in the Iranian population be conducted to provide targeted prevention strategies better suited for the Iranian population.

Non-alcoholic fatty liver disease (NAFLD) is regarded as a global health issue with increasing prevalence worldwide. Polyphenols play a pivotal role in alleviating inflammatory and oxidative stress pathways associated with the pathogenesis of NAFLD, however the literature are still scarce.

This systematic review and meta-analysis was designed to investigate the association between dietary polyphenols and the risk of NAFLD with a meta-analysis approach. All observational studies in the online databases of PubMed, Scopus, Web of Science, Embase and Google Scholar up to June 2021 were searched, determining appropriate keywords, to identify relevant articles. Data were summarized using risk ratios (RRs) with 95% confidence intervals (CIs).

Of the total number of 4144 articles identified in the first phase of the literature search, 6 studies covering 21 arms on polyphenol intake and NAFLD risk containing 9436 participants in the case groups and 19996 participants in the control groups were included in study. The summary effect size (ES) for the risk of NAFLD, comparing the highest with lowest intakes of polyphenol, was 0.80 (95% CI: 0.77-0.83, P<0.0001, I2 = 0.0%;), indicating a significant inverse association.

Our results proved that higher dietary intake of polyphenols can reduce the risk of NAFLD. However, due to small number of determined studies, these findings require further investigations to confirm recommendations for intensifying polyphenol intake in the general population.

Non-alcoholic fatty liver disease (NAFLD) is among the most common liver diseases. In recent years, the prevalence of fatty liver disease has been mostly attributed to obesity, an unhealthy lifestyle, and poor eating habits, which, in addition to Western countries, have also been reported in Iran. This study aimed to evaluate the effect of lifestyle modification (physical activity and diet) on the recovery of NAFLD in health insurance staff in Tabriz, Iran.

This randomized controlled clinical trial was conducted on 42 male and female NAFLD patients aged 20 to 55. The participants were randomly divided into intervention (diet along with aerobic exercise) (n=21) and control (without diet and exercise) (n=21) groups. The level of disease recovery was evaluated by measuring the level of liver enzymes (AST and ALT), liver ultrasound (to determine the degree of fatty liver), and body mass index (BMI) before and after three months of intervention. Paired and independent t-test, Mann-Whitney U test, and Wilcoxon test were performed using SPSS version 22 software. The clinical significance of the study was estimated using an epidemiological tool known as the number needed to treat (NNT).

No significant difference was observed between the two groups in anthropometric and biochemical parameters, as well as fatty liver grade. However, the decrease in BMI index in the intervention group was insignificant compared to the control group. The degree of liver recovery in the intervention and control groups was calculated to be 69.9% and 33.3%, respectively. Also, the decrease in fatty liver grade in the intervention group was significant compared to the control group (P = 0.028). There was a statistically significant reduction in the severity of fatty liver disease in the intervention group at the end of the research (NNT = 3.5), meaning that for every 3.5 patients with NAFLD treated with diet and exercise for 3 months, one patient showed improvement.

This study showed that lifestyle modifications, such as physical activity and dietary habits, significantly affected fatty liver in NAFLD patients.

Considering the impact of serum testosterone levels on metabolic diseases, this study aims to investigate testosterone levels in patients with non-alcoholic fatty liver disease (NAFLD).

A prospective cohort study was performed between two groups: Group A, 58 patients with NAFLD, and Group B, 59 patients without NAFLD. Fatty liver was diagnosed based on Abdominal ultrasound using the Hamaguchi score. Blood specimens were obtained from all patients between 8 and 10 AM and analyzed for testosterone, aspartate aminotransferase, alanine transaminase, serum lipid profile, ferritin, and fasting blood sugar levels.

The mean weight and body mass index were significantly higher in the study group (Group A) (P-value = 0.0001). The mean aspartate aminotransferase and alanine transaminase were 37.7 and 56.6 in Group A, respectively, and were significantly higher than the control group (Group B) (P-value = 0.0001). Fasting blood sugar, lipid profile, and serum ferritin differed between the two groups. The mean serum testosterone level was 3.38 ± 0.72 in Group A and 4.79 ± 0.88 ng/dL in Group B (P-value = 0.0001). The testosterone level negatively correlated with age and hepatic steatosis grade (P-value = 0.0001). However, it has a weak and positive correlation with BMI (P-value = 0.454).

This study revealed that the patients with NAFLD had a significantly lower level of testosterone compared to the other individuals. This study highlights the role of NAFLD as a potential cause of hypogonadism in men.

In addition to oxidative stress, the apoptosis of liver cells plays a main role in non-alcoholic steatohepatitis pathogenesis. Nevertheless, the main mechanisms of the response of liver cell apoptosis in non-alcoholic steatohepatitis (NASH) models caused by a high-fat diet, as well as the effects of exercise with and without calorie restriction on these mechanisms, have not been assessed to date.

The present study aimed to investigate the effects of two exercise protocols with and without calorie restriction on apoptosis and liver damage in rats with non-alcoholic fatty liver disease (NAFLD).

Sixty-four male Wistar rats were subjected to a high-fat diet for eight weeks and were divided randomly into eight groups: Control, calorie restriction (CR), aerobic exercise (AE), and aerobic exercise + calorie restriction (AC) for eight and twelve weeks. Also, two groups of rats that had normal and free access to food werenamedsham groups. The training groups exercised on the treadmill for five sessions a week for eight and twelve weeks. Two-way ANOVA was utilized for data analysis at a significance level of 0.05.

According to the findings, in both 8- and 12-week protocols, the expression of Bax proteins in the exercise and exercise + calorie restriction groups showed a significant decrease compared to the control group (P < 0.05). Also, Bcl-2 protein expression significantly increased in the exerciseandexercise+calorie restriction groups than the controlgroup(P< 0.05). The training groups showed no significant difference between the 8- and 12-week protocols.

It was revealed that exercise with and without caloric restriction and independent of the protocol duration can improve the apoptosis of hepatocytes in NAFLD.

 Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are 2 common liver diseases that currently lack effective treatment options.

 This study aimed to investigate the effect of lipopolysaccharide (LPS)-stimulated adipose-derived stem cells (ADSCs) on NAFLD treatment in an animal model.

 Male Wistar rats were fed a high-fat diet (HFD) to induce NAFLD for 7 weeks. The rats were then categorized into 3 groups: Mesenchymal stem cell (MSC), MSC + LPS, and fenofibrate (FENO) groups. Liver and body weight were measured, and the expression of genes involved in fatty acid biosynthesis, β-oxidation, and inflammatory responses was assessed.

 Lipopolysaccharide-stimulated ADSCs were more effective in regulating liver and body weight gain and reducing liver triglyceride (TG) levels compared to the other groups. Treatment with LPS-stimulated ADSCs effectively corrected liver enzymes, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and lipid factors, including low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) values, better than treatment with both FENO and MSCs. ADSCs + LPS treatment significantly decreased transforming growth factor β (TGF-β) and genes associated with inflammatory responses. Additionally, there was a significant reduction in reactive oxygen species (ROS) levels in the rats treated with ADSCs + LPS.

 Lipopolysaccharide-stimulated ADSCs showed potential in alleviating NAFLD by reducing inflammatory genes and ROS levels in HFD rats, demonstrating better results than treatment with ADSCs and FENO groups alone.

Nonalcoholic fatty liver disease (NAFLD) is a common obesity‑related disease. In this study, we aimed to investigate the effects of pioglitazone on NAFLD in morbid obese patients.

This is a randomized controlled trial study that was performed in 2020–2021 on 44 patients who had grade 3 NAFLD. At the beginning of the study, we collected the following data: age, gender, body mass index (BMI), fasting blood glucose (FBS), lipid profile, aspartate aminotransferase, alanine aminotransferase (ALT), and the total size and volume of the liver and the left lobe of the liver. Patients in the control group were given a special diet. For patients in the treatment group, pioglitazone 15 mg tablets were administered twice daily for 4 months.

At the beginning of the study, all patients in both groups had grade 3 of NAFLD. After the treatments, 50% of the pioglitazone group had grade 1 NAFLD, and 50% of other patients had grade 2 that showed significant improvements in patients (P < 0.001). We also found significant improvements in the following items in the intervention group: liver size (P < 0.001), size of the left liver lobe (P < 0.001), FBS (P = 0.036), ALT (P = 0.011), and BMI (P < 0.001). No significant improvements were found in the control group (P > 0.05).

The use of pioglitazone for 4 months resulted in improvements in fatty liver stage, liver size, BMI, FBS, and lipid profile. These data show the effectiveness of pioglitazone in NAFLD.

 This study aimed to investigate the combined effects of resveratrol (RES) and saroglitazar (SARO) on a high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) in a rat model.

 In this animal study, rats were treated with RES, SARO, or a combination of both. Male rats were fed with an HFD to induce nonalcoholic steatohepatitis (NASH) and then divided into 4 groups: RES treatment, SARO treatment, combined RES and SARO treatment, and no treatment. Various parameters were measured, including body and liver weight, liver enzymes, gene expression of inflammatory markers and reactive oxygen species (ROS), protein expression levels of transforming growth factor-beta (TGF-β) and p-Smad3, and liver histology.

 The combination of RES and SARO significantly reduced blood and hepatic lipids, attenuated weight gain, and decreased inflammatory cytokine production in a NAFLD study. The combination diminished hepatic lipid accumulation, oxidative stress, and TGF-β1 expression, suggesting antifibrotic effects. Histological evaluations showed antisteatotic and antifibrotic outcomes of the combined treatment. Improved glycemic index, blood lipids, and reduced NASH indicators (i.e., aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) were observed after 6 weeks. The treatment also decreased ROS and NOX family expression, lessening oxidative stress. The inhibition of the TGF-β-Smad3 pathway in HFD-induced rats resulted in reduced NASH (P < 0.05).

 The results indicated that the group receiving the combination of RES and SARO showed a more efficient reduction in fibrosis and steatosis in the NASH model induced by an HFD than the groups receiving RES or SARO alone.

Non-alcoholic fatty liver disease (NAFLD) is a hepatic manifestation of clinical metabolic syndrome. Insulin resistance is an important factor in the pathogenesis of NAFLD. Ghrelin, widely distributed in peripheral tissues and the central nervous system, plays a vital role in regulating food intake, energy balance, and substance metabolism. In this study, the effect of intracerebroventricular (ICV) injection of ghrelin receptor antagonist on NAFLD was explored.

A rat model of NAFLD was established by feeding a high-fat diet, and a selective ghrelin receptor antagonist [D-Lys-3]-GHRP-6 was injected via ventricular intubation implantation. The serum total cholesterol (TC), triglycerides (TGs), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and hepatic TGs were measured using the colorimetric method. Fasting plasma glucose (FPG) and fasting plasma insulin (FPI) were determined to calculate homeostatic model assessment insulin resistance (HOMA-IR). Hematoxylin-eosin (HE) and Oil Red O staining were conducted to observe the pathological changes and lipid accumulation in the liver. Hosphatidylinositide3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway protein expressions were measured using western blot analysis.

ICV injection of [D-Lys-3]-GHRP-6 significantly reduced serum lipids, transaminase, and HOMA-IR, improved liver injury, and inhibited lipid accumulation in the liver of NAFLD rats. Moreover, ICV injection of [D-Lys-3]-GHRP-6 significantly up-regulated the phosphorylation levels of PI3K/Akt/mTOR signaling protein expressions in the hypothalamus, indicating a significant improvement in hypothalamic insulin resistance.

Blockade of central ghrelin receptor can treat NAFLD possibly via the hypothalamic PI3K/Akt/mTOR signaling pathway to improve insulin resistance.

Nonalcoholic fatty liver disease (NAFLD) refers to fat accumulation in hepatic cells due to alcohol consumption, hepatitis, and drugs. The prevalence of this disease has been reported at 20-50% in western and 12 - 13% in Latin countries. Patients who suffer from obesity, diabetes, and insulin resistance may be affected more than others. This disease is symptomless, and its paraclinical diagnosis is achievable by increasing the hepatic enzymes. Ultrasonography and fibroscan are some of the common diagnostic methods for this disease. The first treatment for this disease is weight loss and physical activities. Vitamin E can improve histopathological changes in terms of medications. While pioglitazone is an effective blood sugar-lowering drug, metformin has no role in treating diabetes or prediabetes.

Nonalcoholic fatty liver disease (NAFLD) is the most common type of chronic liver disease worldwide. Left untreated, it can be a risk factor for developing cirrhosis or hepatocellular carcinoma (HCC). Although experts have made many efforts to find the underlying mechanisms of NAFLD, they remain a mystery.

This study aimed to distinguish common gene signatures and pathways in the human liver during NAFLD progression through systems biology.

In this study, the researchers selected three microarray datasets, GSE48452, GSE63067, and GSE89632, from the NCBI GEO database to explore differentially expressed genes (DEGs) among healthy controls, simple steatosis, and nonalcoholic steatohepatitis (NASH) patients. Furthermore, protein-protein interaction (PPI) networks and pathway enrichment analyses were used to detect common genes and biological pathways in different stages of NAFLD.

The current study included 45 healthy participants, 36 simple steatosis patients, and 46 NASH patients. Common genes for NAFLD progression were Chi3L1, ICAM1, MT1A, MT1H, ABCB11, ACOT1, CYP2C9, HSP90B1, and CPB2, which are involved in inflammation and oxidative stress pathways.

The present study investigated the shared vital genes and pathways between different stages of NAFLD, which may facilitate understanding NAFLD mechanisms and identifying potential therapeutic targets in this disease.

NAFLD is one of the most common liver diseases in the world. HOMA-IR as an indicator of insulin resistance is commonly used in clinical trials in NAFLD patients. The aim of this study was to evaluate the application of HOMA-IR index in the diagnosis of NAFLD.

This study was performed on 54 patients with NAFLD and 54 non-NAFLD patients that referred to Razi Hospital in Rasht during 2019-2020. FibroScan was used to diagnose NAFLD in the patient group and ultrasound was used to rule it out in the control group. Metabolic and hepatic parameters were measured for each patient. Data were entered into SPSS 22 software and the necessary analyses were performed.

The mean age of the subjects in the study was 44.01±13.12 years and ranged from 18 to 75 years. 72.2% of people affected by NAFLD were men (p <0.001) .The optimal cut-off point for HOMA-IR in NAFLD was 1.65 with a sensitivity of 89.7% and a specificity of 76.9% in men and 1.90 with a sensitivity of 86.7% and a specificity of 82.9% in women. Overall, the optimal cut-off point for HOMA-IR in NAFLD was 1.75 with a sensitivity of 87.0% and a specificity of 81.5%. In addition, the results showed that there was no significant relationship between steatosis and hepatic fibrosis with HOMA-IR index.

The results showed that HOMA-IR can be used as a reliable criterion for early detection of NAFLD.

Visfatin is known as one of the adipokines associated with the development of inflammation, but its role in the pathogenesis of nonalcoholic fatty liver is less known so far. We aimed to investigate the association between visfatin gene polymorphism rs4730153 and insulin resistance and non-alcoholic fatty liver disease (NAFLD).

This case-control study was performed on 80 patients with NAFLD as well as 80 healthy participants as controls referred to Amir Al-Momenin and Bouali hospitals in Tehran. Genotyping was performed using PCR-RFLP method. Plasma concentrations of visfatin and insulin were measured using ELISA kit. The fasting blood glucose, TC, TG, LDL-C, HDL-C, ALT, AST, SBP, DBP, and BMI levels were measured using the standard methods. Statistical analysis was also performed using SPSS software.

A significant difference was found in Visfatin level in the patients with NAFLD compared to this level in healthy individuals. The levels of HDL-C and LDL-C in healthy individuals and triglyceride in patients for GG, AG, and AA genotypes carriers also were significantly different. There was a significant relationship between rs4730153 polymorphism and insulin resistance; however, no association was found between this polymorphism and NAFLD. Notably, Visfatin showed a significant association with age (all individuals), body mass index (healthy individuals), insulin, and HOMA (in patients).

Visfatin levels reduced in patients with NAFLD. Moreover, rs4730153 polymorphism was indicated to be associated with both lipid metabolism and insulin resistance, but no association was found between this polymorphism and nonalcoholic fatty liver disease.

Probiotics were first proposed by Metchnikoff as contributing factors to health. These living microorganisms, which mainly belong to the microflora bacteria of the gastrointestinal tract, can have beneficial effects on human health if consumed in moderation. The most studied probiotics are lactic acid bacteria, which include Lactobacillus and Bifidobacteria. The present study is an overview of some studies conducted on the effects of using probiotics and their possible patterns in the prevention or reduction of certain human diseases and disorders. The available data suggest that probiotics can play a role in improving constipation and liver enzymes level and functions, and have significant effects on rooting and improving the symptoms of Helicobacter pylori. It was concluded that probiotics have positive effects in metabolic syndrome treatment, preventing gestational diabetes, and improving oral health. Since many probiotics are microorganisms familiar to the gastrointestinal tract, if consumed in moderation, there are no side effects for the host. Using them as complementary therapies for some diseases related to the gastrointestinal tract microflora bacteria can be an effective and low-cost approach to alleviating the annoying symptoms of such diseases.

Inflammation has a significant impact on the development and progression of fatty liver diseases.In this study, we aimed to investigate the relation between serum levels of nuclear factor kappa B (NFkB) and Forkhead box protein P3 (FOXP3)with fibrosis severity among patients with non-alcoholic fatty liver disease(NAFLD).

In a prospective study, the patients suspicios of havingfatty liver were enrolled. The exclusion criteria lack of viral hepatitis, autoimmune hepatitis, Wilson’s or other known liver diseases,history of liver or biliary surgery,bariatric surgery, and medications that influence liver metabolism. The participantsunderwent liver fibroscan.According to liver fibrosis, the patients weredivided into two groups; 1)fibrosis less than 7.2 KP,2)advanced NAFLD, fibrosis ≥7.3 KP. A10 cc fasting blood sample was taken from each patient for laboratory assessments.The variables between the two groups were compared using Chi-square or Fisher’s exact test.The independence of cytokines was assessed by a logistic regression test.

Totally 90 patients were enrolled.The mean age was 42.21 ± 11 years. Of them, 50 and 47 participants were allocated to groups 1 and 2, respectively. In the univariate analysis, we revealed asignificant difference between age, body mass index (BMI), fasting blood glucose, liver enzymes , total cholesterol, andtriglyceride levels. Also, there was a significant difference betweenthe levels of NFKB and FOXP3 in group one compared with group two of the participants,as FOXP3(9.17 ± 10.0 vs. 18.63 ± 12.9; p < 0.001) and NFKB (1.70 ± 1.70; p < 0.01). After excluding the confounding factors, we observed a significant association between fibrosis level and cytokine levels in logistic regression.

Serum levels of NFKB and FOXP3 increased by advancing liver fibrosis in patients with NAFLD.This is an independent association. The identification of intermediary regulatory factors would be necessary

Recent data have suggested that nonalcoholic fatty liver disease (NAFLD) can occur in normal-weight subjects. This study examined the association of body fat percentage (BF%) with NAFLD and its risk factors in normal-weight individuals.

The present study aimed to explain the association of body fat with NAFLD and its cardiometabolic risk factors.

A total of 59 subjects with body mass index (BMI) within the range of 18.5 - 24.9 kg/m2 were selected from referrals to two major university polyclinics in Shiraz, Iran, from April to June 2019. Fatty liver grade, anthropometric characteristics, body composition, and cardiometabolic risk factors were measured in this study.

Waist circumference (P = 0.012), fat mass (P < 0.001), triglycerides (TG) (P = 0.027), very-low-density lipoprotein (VLDL) (P = 0.007), and TG/high-density lipoprotein cholesterol (HDL-C) ratio (P = 0.003) increased; however, skeletal muscle mass decreased (P < 0.001) across the tertiles of BF%. The average of fatty liver grade was similar in the first and second tertiles; nevertheless, the fatty liver grade of participants in the third tertile was significantly higher (1.3 ± 0.9 vs. 0.4 ± 0.7; P = 0.005). In ordinal regression analysis, BF% (1.13; 95% CI: 1.04 - 1.22; P = 0.003), BMI (1.95; 95% CI: 1.02 - 3.74; P = 0.045), VLDL (1.77; 95% CI: 1.00 - 3.12; P = 0.049), and TG/HDL-C ratio (2.21; 95% CI: 1.26 - 3.86; P = 0.006) had positive associations with NAFLD; nonetheless, HDL-C (0.33; 95% CI: 0.16 - 0.67; P = 0.002) and dietary cholesterol (0.97; 95% CI: 0.95 - 0.997; P = 0.028) had inverse associations with NAFLD after the adjustments for age, gender, BMI, and physical activity.

The results of this study suggested that within normal weight ranges, NAFLD occurs more frequently in individuals with higher BF%. In addition, BF% can be used as an important marker in NAFLD screening.