Sarcopenia and risk of nonalcoholic fatty liver disease: A meta-analysis.
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ABSTRACT:
SUBMITTER: Wijarnpreecha K
PROVIDER: S-EPMC5848318 | biostudies-literature | 2018 Jan-Feb
REPOSITORIES: biostudies-literature
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Project description:This sudy aims to investigate the association between insomnia or excessive daytime sleepiness (EDS) and risk of nonalcoholic fatty liver disease (NAFLD).We searched published studies indexed in MEDLINE and EMBASE database from inception to December 2015. Studies that reported odds ratios (ORs), risk ratios, hazard ratios or standardized incidence ratio with 95% confidence intervals (CI) comparing the risk of NAFLD among participants who had insomnia or EDS versus those without insomnia or EDS were included. Pooled ORs and 95% CI were calculated using a random-effect, generic inverse variance method of DerSimonian and Laird. Cochran's Q test and I2 statistic were used to determine the between-study heterogeneity.Our search strategy yielded 2117 potentially relevant articles (781 articles from MEDLINE and 1336 articles from EMBASE). After comprehensive review, seven studies (three cross-sectional studies and four case-control studies) were found to be eligible and were included in the meta-analysis. The risk of NAFLD in participants who had insomnia was significantly higher with the pooled OR of 1.13 (95% CI, 1.00-1.27). The statistical heterogeneity was moderate with an I2 of 62%. Elevated risk of NAFLD was also observed among participants with EDS even though the 95% CI was wider and did not reach statistical significance (pooled OR 2.21; 95% CI, 0.84-5.82). The statistical heterogeneity was moderate with an I2 of 62%.Our study demonstrated an increased risk of NAFLD among participants who had insomnia or EDS. Whether this association is causal needs further investigations.
| S-EPMC5664866 | biostudies-other
Project description:With the aging of the population, sarcopenia has become more common. Studies have shown a broad association between liver disease and sarcopenia. However, this link remains unclear. Our study explored the link between NAFLD and sarcopenia and predicting the pathogenesis. To begin, we investigated the causal relationship and genetic correlation between them using MR and LDSC. Second, each GWAS was annotated by MAGMA. The annotated genes were analyzed for pleiotropy using the PLACO approach. Finally, functional analysis was conducted on the identified pleiotropic genes. We observed a significant genetic correlation between NAFLD and sarcopenia. Subsequently, we conducted gene-level pleiotropy analysis using PLACO and identified a total of 153 genes with pleiotropic effects. Functional analysis revealed enrichment of these genes in various tissues, including pancreas, liver, heart, blood, brain, and muscle, with involvement in cellular regulation, intracellular function, and antigen response. Moreover, our MR analysis provided evidence of a causal relationship between NAFLD and sarcopenia. Our study has discovered the genetic and causal relationships between NAFLD and sarcopenia, providing further insights into their pathophysiological mechanisms. The identification of pleiotropic genes also offers potential targets for future drug therapies aimed at controlling or treating NAFLD and sarcopenia.
| S-EPMC10834579 | biostudies-literature
Project description:BackgroundThe association between nonalcoholic fatty liver disease (NAFLD) and sarcopenia has been suggested. We investigated the association between sarcopenia and NAFLD independent of visceral adiposity and searched for the clinical characteristics that affect this association.MethodsWe performed a retrospective study including of 5,989 subjects (mean age, 53.2 years; men, 57.3%) who underwent bioelectrical impedance analysis (BIA) and abdominal ultrasonography in 2012. The appendicular skeletal muscle mass (ASM) was assessed by BIA method. Sarcopenia was defined as ASM/weight (ASM%) <2 standard deviation of the mean for healthy young reference population. NAFLD was diagnosed by ultrasonography.ResultsThe prevalence of sarcopenia was 5.3%. The prevalence of NAFLD was significantly higher in subjects with sarcopenia than in those without (69.5% vs. 36.5%, P<0.001). After adjusting with age, sex, visceral fat area, hypertension, diabetes, total and low-density lipoprotein cholesterol, subjects with sarcopenia showed significantly high odds of NAFLD (odds ratio [OR], 1.37; 95% confidence interval [CI], 1.02-1.84; P=0.036). Subjects with sarcopenia have more likely severe grade of NAFLD compared to non-sarcopenic group (OR, 1.58; 95% CI, 1.25-2.00; P<0.001). There was significant interaction for effect modification in the association between sarcopenia and NAFLD by age (P of interaction for effect modification, 0.007).ConclusionSarcopenia was significantly associated with the presence and the severity of ultrasonography-graded NAFLD in our study population independent of visceral fatness and other metabolic confounder. Younger age showed greater magnitude of association between sarcopenia and NAFLD.
| S-EPMC6604841 | biostudies-literature
Project description:Liver fibrosis is the most important predictor of mortality in nonalcoholic fatty liver disease (NAFLD). Quantitative risk of mortality by fibrosis stage has not been systematically evaluated. We aimed to quantify the fibrosis stage-specific risk of all-cause and liver-related mortality in NAFLD. Through a systematic review and meta-analysis, we identified five adult NAFLD cohort studies reporting fibrosis stage-specific mortality (0-4). Using fibrosis stage 0 as a reference population, fibrosis stage-specific mortality rate ratios (MRRs) with 95% confidence intervals (CIs) for all-cause and liver-related mortality were estimated. The study is reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement. Included were 1,495 NAFLD patients with 17,452 patient years of follow-up. Compared to NAFLD patients with no fibrosis (stage 0), NAFLD patients with fibrosis were at an increased risk for all-cause mortality, and this risk increased with increases in the stage of fibrosis: stage 1, MRR = 1.58 (95% CI 1.19-2.11); stage 2, MRR = 2.52 (95% CI 1.85-3.42); stage 3, MRR = 3.48 (95% CI 2.51-4.83); and stage 4, MRR = 6.40 (95% CI 4.11-9.95). The results were more pronounced as the risk of liver-related mortality increased exponentially with each increase in the stage of fibrosis: stage 1, MRR = 1.41 (95% CI 0.17-11.95); stage 2, MRR = 9.57 (95% CI 1.67-54.93); stage 3, MRR = 16.69 (95% CI 2.92-95.36); and stage 4, MRR = 42.30 (95% CI 3.51-510.34). Limitations of the study include an inability to adjust for comorbid conditions or demographics known to impact fibrosis progression in NAFLD and the inclusion of patients with simple steatosis and nonalcoholic steatohepatitis without fibrosis in the reference comparison group.ConclusionThe risk of liver-related mortality increases exponentially with increase in fibrosis stage; these data have important implications in assessing the utility of each stage and benefits of regression of fibrosis from one stage to another. (Hepatology 2017;65:1557-1565).
| S-EPMC5397356 | biostudies-literature
Project description:Background and aimsAlcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) have become common chronic liver diseases. Recent evidence has shown the value of transient elastography (TE) in the context of ALD/NAFLD. The aim of this study is to investigate the accuracy of TE for diagnosing steatosis and fibrosis in ALD/NAFLD patients.MethodsWe retrieved relevant English studies from the databases of PubMed, Embase, the Web of Science, and the Cochrane Library through March 31st 2019. We included studies regarding the diagnosis or staging of steatosis or fibrosis by using controlled attenuation parameter (CAP) or liver stiffness measurement (LSM) measured by TE in patients with ALD or NAFLD. The reference standard of all included studies was liver biopsy. A random-effects model was applied. Statistical analyses were performed using STATA.ResultsA total of 62 articles were included and analyzed in our meta-analysis. In patients with ALD/NAFLD, the pooled results revealed that the sensitivity and specificity of CAP were 0.84, 0.83, and 0.78 and 0.83, 0.71, and 0.62 for steatosis grades ≥ S1, ≥S2, and =S3, respectively. The sensitivity and specificity of LSM for identifying fibrosis grades ≥ F1, ≥F2, ≥F3, and =F4 were 0.77, 0.77, 0.83, and 0.91 and 0.80, 0.82, 0.84, and 0.86, respectively.ConclusionIn patients with ALD/NAFLD, CAP was feasible for identifying and screening steatosis, and LSM was accurate for diagnosing fibrosis, especially severe fibrosis and cirrhosis.
| S-EPMC7840258 | biostudies-literature
Project description:BACKGROUND & AIMS:Previous studies examining the relationship between the C282Y and H63D HFE mutations and presence of nonalcoholic fatty liver disease (NAFLD) have yielded conflicting results. The goal of this study was to systematically evaluate and summarize data on the association between these two variants and the presence of NAFLD. METHODS:The authors searched EMBASE and PUBMED from August 1, 1996 to August 12, 2010. Two investigators independently conducted data abstraction. Ethnic specific weighted prevalence was calculated and pooled odds ratios were estimated using the random effects model. RESULTS:From 2542 references, the authors included 16 case-control studies and 14 case-only studies, or 2610 cases and 7298 controls. The majority of the studies came from Caucasian populations (2287 cases and 4275 controls). The weighted prevalence of HFE mutations in cases was comparable to controls. The meta-analysis was restricted to Caucasians only because of the small sample size of non Caucasian participants. The pooled odds ratio for the presence of any HFE genetic variant in cases was 1.03 (95%CI: 0.90, 1.17; I(2): 65.8%, 95%CI: 38.5, 81.0). The presence of other genotypes and secondary analyses yielded similar non significant findings. CONCLUSIONS:Our systematic review does not support an association between the HFE genetic variants and the presence of NAFLD.
| S-EPMC3611963 | biostudies-literature
Project description:Abstract The pathophysiology and risk factors of nonalcoholic fatty liver disease (NAFLD) among lean patients is poorly understood and therefore investigated. We performed a meta‐analysis of observational studies. Of 1175 articles found through searching from Medline/PubMed, Banglajol, and Google Scholar by two independent investigators, 22 were selected. Data from lean (n = 6768) and obese (n = 9253) patients with NAFLD were analyzed; lean (n = 43 398) and obese (n = 9619) subjects without NAFLD served as controls. Age, body mass index, waist circumference, systolic blood pressure, and diastolic blood pressure (DBP) had significantly higher estimates in lean NAFLD patients than in lean non‐NAFLD controls. Fasting blood sugar [MD(mean difference) 5.17 mg/dl, 95% CI(confidence interval) 4.14–6.16], HbA1c [MD 0.29%, 95% CI 0.11–0.48], and insulin resistance [HOMA‐IR] [MD 0.49 U, 95% CI 0.29–0.68]) were higher in lean NAFLD patients than in lean non‐NAFLD controls. All components of the lipid profile were raised significantly in the former group except high‐density lipoprotein. An increased uric acid (UA) level was found to be associated with the presence of NAFLD among lean. Cardio‐metabolic profiles of nonlean NAFLD patients significantly differs from the counter group. However, the magnitude of the difference of lipid and glycemic profile barely reached statistical significance when subjects were grouped according to lean and nonlean NAFLD. But DBP (slope: 0.19, P < 0.037), HOMA‐IR (slope: 0.58, P < 0.001), and UA (slope: 0.36, P = 0.022) were significantly higher if NAFLD was present compared to that of non‐NAFLD group. Lean and nonlean NAFLD patients are metabolically similar and share common risk factors. A meta‐analysis of 22 articles comprising data from lean (n = 6768) and obese (n = 9253) patients with nonalcoholic fatty liver disease (NAFLD), and lean (n = 43398) and obese (n = 9619) subjects without NAFLD (healthy) revealed that both lean and obese patients shared similar risk factors associated with NAFLD including age, body mass index, waist circumference, systolic blood pressure, diastolic blood pressure, HbA1c, insulin resistance (HOMA‐IR), total cholesterol, low‐density lipoprotein, high‐density lipoprotein, triglycerides, and uric acid.
| S-EPMC8593777 | biostudies-literature
Project description:Background and aimsSarcopenia has been demonstrated to be closely associated with nonalcoholic fatty liver disease (NAFLD). However, whether there are causal relationships between sarcopenia and NAFLD remains undetermined. Here, we aim to address the question using a two-sample bidirectional Mendelian randomization (MR) analysis approach.MethodsWe performed a two-sample bidirectional MR study using summary-level data from genome-wide association studies (GWAS) of the whole body lean mass (n = 38,292), appendicular (arms and legs) lean mass (n = 28,330), and NAFLD (1,483 biopsy-proven NAFLD cases and 17,781 controls). We first conducted MR analysis with five single nucleotide polymorphisms (SNPs) as genetic instruments for whole body lean mass and three SNPs as instruments for appendicular lean mass to estimate the causal effect of genetically predicted sarcopenia on the risk of NAFLD using the inverse-variance weighted (IVW) method. Then we performed reverse MR analysis with four SNPs as instruments to examine the causality of genetically predicted NAFLD with whole body lean mass and appendicular lean mass. Further sensitivity analysis was conducted to testify the reliability of the MR results.ResultsGenetic predisposition to decreased whole body lean mass was not associated with NAFLD [IVW-random effects, odds ratio (OR) = 1.054, 95%CI: 0.750-1.482, P = 0.761]. Similar results were observed using genetic instruments of appendicular lean mass (IVW-random effects, OR = 0.888, 95%CI: 0.386-2.042, P = 0.780). Reverse MR analysis revealed that genetically predicted NAFLD using four genetic instruments was not associated with whole body lean mass (IVW, β = -0.068, 95%CI: -0.179 to 0.043, P = 0.229) and appendicular lean mass (IVW, β = -0.020, 95%CI: -0.092 to 0.051, P = 0.574). MR analyses using other methods and sensitivity analysis showed consistent results.ConclusionThese results suggested no causal relationships between sarcopenia and NAFLD, indicating that sarcopenia may not be directly involved in the pathogenesis of NAFLD and vice versa.
| S-EPMC9682105 | biostudies-literature
Project description:(1) Background: Recently, adipokines, including visfatin, have been studied in nonalcoholic fatty liver disease (NAFLD). Several studies evaluated visfatin levels in NAFLD, the presence and severity of hepatic steatosis, liver fibrosis, lobar inflammation, nonalcoholic steatohepatitis (NASH), and gender differences. However, inconclusive results have been reported. Accordingly, we performed a systematic review and meta-analysis, aiming to address these gaps in evidence. (2) Methods: We performed a systematic electronic search on PubMed, EMBASE, and Cochrane Library using predefined keywords. Diagnosis of NAFLD by liver biopsy or imagistic investigations was accepted. Full articles satisfying our inclusion and exclusion criteria were included. NHLBI quality assessment tools were used to evaluate included studies. The principal summary outcome was the mean difference in visfatin levels. (3) Results: There were 21 studies involving 1923 individuals included in our qualitative assessment, while 14 studies were included in the quantitative assessment. No statistical significance was found assessing visfatin levels in NAFLD [3.361 (95% CI -0.175-6.897)], simple steatosis [7.523 (95% CI -16.221-31.267)], hepatic steatosis severity [-0.279 (95% CI -1.843-1.285)], liver fibrosis [4.133 (95% CI -3.176-11.443)], lobar inflammation [0.358 (95% CI -1.470-2.185)], NASH [-2.038 (95% CI -6.839-2.763)], and gender [(95% CI -0.554-0.556)]. (4) Conclusions: In conclusion, visfatin levels are not associated with NAFLD, presence or severity of hepatic steatosis, liver fibrosis, lobar inflammation, NASH, and gender. However, due to the limited methodological quality of the included studies, results should be interpreted with caution.
| S-EPMC8306785 | biostudies-literature
Project description:Nonalcoholic fatty liver (NAFL) is an emerging global epidemic which progresses to nonalcoholic steatohepatitis (NASH) and cirrhosis in a subset of subjects. Various reviews have focused on the etiology, epidemiology, pathogenesis and treatment of NAFLD. This review highlights specifically the triggers implicated in disease progression from NAFL to NASH. The integrating role of genes, dietary factors, innate immunity, cytokines and gut microbiome have been discussed.
| S-EPMC4491606 | biostudies-literature