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Sex-influenced association of nonalcoholic fatty liver disease with coronary heart disease.

ABSTRACT: This study investigated whether nonalcoholic fatty liver disease (NAFLD) predicts prevalent coronary heart disease (CHD).Epidemiologic studies have used various definitions for NAFLD. Here, we considered both liver fat burden measured by CT (FL) and the non-specific measure of hepatic inflammation -alanine aminotransferase (ALT). The association of FL and ALT with CHD (self report of coronary bypass, myocardial infarction, or percutaneous transluminal coronary angioplasty) was investigated in 2756 European-American participants of the Family Heart Study.FL (p = 0.0084) and ALT (?40 U/L, p = 0.014) were each individually associated with prevalent CHD. However, when accounting for traditional metabolic risk factors in a multivariate model FL had no predictive value for CHD in either men or women; whereas ALT was a significant predictor of CHD in men, and the association strengthened among non-diabetic men. In non-diabetic women, neither FL nor ALT was associated with CHD.ALT (?40 U/L) was a predictor of prevalent CHD in men but not in women, while CT measured FL was not significant in either sex. The failure to account for traditional risk factors, heterogeneity by sex, and varying definitions of NAFLD may account for some of the conflicting evidence in the literature regarding the association between NAFLD and coronary disease.

SUBMITTER: Feitosa MF

PROVIDER: S-EPMC3602396 | biostudies-literature | 2013 Apr

REPOSITORIES: biostudies-literature

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Sex-influenced association of nonalcoholic fatty liver disease with coronary heart disease.

Feitosa Mary F MF Reiner Alexander P AP Wojczynski Mary K MK Graff Mariaelisa M North Kari E KE Carr Jeffrey J JJ Borecki Ingrid B IB

Atherosclerosis 20130125 2

<h4>Objective</h4>This study investigated whether nonalcoholic fatty liver disease (NAFLD) predicts prevalent coronary heart disease (CHD).<h4>Methods</h4>Epidemiologic studies have used various definitions for NAFLD. Here, we considered both liver fat burden measured by CT (FL) and the non-specific measure of hepatic inflammation -alanine aminotransferase (ALT). The association of FL and ALT with CHD (self report of coronary bypass, myocardial infarction, or percutaneous transluminal coronary a ...[more]

PMID: 23390892

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Project description:BACKGROUND:Previous study reported that patients who suffered coronary heart disease (CHD) complicated with non-alcoholic fatty liver disease (NAFLD) had worse cardiac function and clinical outcomes than patients with CHD only. Notably, the mechanism is still unclear. This study aimed to investigate the changes and roles of intestinal bacterial microbiota in CHD-NAFLD patients. METHODS AND RESULTS:People were recruited and divided into three groups, including CHD patients (without NAFLD), CHD-NAFLD patients and healthy controls (HCs). Each group contained 24 people. Fecal samples and clinical information were carefully collected. The Illumina sequencing of 16S rRNA was applied to profile the overall structure of the fecal bacterial microbiota and the characteristics of the bacterial microbiota based on the Operational Taxonomic Units. In clinical information, the CHD-NAFLD patients showed an increase in BMI, uric acid and triglyceride. There was a significant reduction in the abundance of Parabacteroides and Collinsella in overall CHD patients (including CHD-NAFLD and CHD patients). The intestinal bacterial microbiota in CHD-NAFLD patients showed an increase in the abundance of Copococcus and Veillonella, and a reduction in the abundance of Parabacteroides, Bacteroides fragilis, Ruminococcus gnavus, Bacteroides dorei, and Bifidobacterium longum subsp infantis. Among them, the abundance of Ruminococcus gnavus and Bacteroides dorei was significantly lower than that in CHD patients. Additionally, BMI positively correlated with the abundance of Copococcus and negatively correlated with the abundance of Bifidobacterium longum subsp infantis. The abundance of Veillonella positively correlated with AST. The abundance of Bacteroides dorei negatively correlated with ALT and AST. It indicates that the abundance of intestinal microbiota was related to the changes in clinical indexes. CONCLUSIONS:Changes of intestinal bacterial microbiota in CHD-NAFLD patients may be important factors affecting the degree of metabolic disorder, which may be one of the important reasons for the worse clinical outcome and disease progression in CHD-NAFLD patients than in CHD patients.

Project description:Background:Sex hormone-binding globulin (SHBG), a glycoprotein synthesized by hepatocytes, has been linked to insulin resistance and hepatic lipid metabolism and is suggested to be associated with nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate the association of SHBG with NAFLD in Chinese adults. Methods:We conducted a community-based, cross-sectional study in China involving 2912 participants aged 40-75 years old. All participants underwent detection for hepatic fat infiltration by ultrasound in addition to providing complete medical history and undergoing physical and blood biochemical examinations. The association of serum SHBG with the presence of NAFLD was reported by adjusted odds ratio after applying logistic regression models. To further explore the relationship between SHBG and NAFLD, mRNA expression of SHBG and hepatocyte nuclear factor 4-? (HNF4?), as well as intrahepatic triglycerides, were determined from the liver tissues of 32 subjects with different degrees of steatosis. Results:Serum SHBG levels in patients with NAFLD (median, 43.8 nmol/L; interquartile range, 33.4-56.8 nmol/L) were significantly lower than those in non-NAFLD subjects (median, 63.4 nmol/L; interquartile range, 47.6-83.1 nmol/L). Serum SHBG levels were inversely correlated with WHR, trunk fat percentage, glucose, HOMA-IR, TG, UA and DHEAS, and were positively correlated with HDL-C levels (all p?<? 0.001). Logistic regression analysis indicated that serum SHBG levels were negatively associated with the presence of NAFLD in all subjects, as well as the subgroups stratified by sex, BMI and HOMA-IR (all p?<? 0.05). In human liver tissues, SHBG and HNF4? mRNA expression decreased along with the elevated grade of hepatic steatosis. Both SHBG and HNF4? mRNA expression levels were negatively correlated with intrahepatic triglycerides. Conclusions:These results demonstrate that SHBG levels were negatively associated with the presence of NAFLD in middle-aged and elderly Chinese adults.

Project description:Coronary artery disease (CAD) is the principal cause of death in patients with nonalcoholic fatty liver disease (NAFLD). The aim of the present study was to investigate whether NAFLD is causally involved in the pathogenesis of CAD. For this, previously reported NAFLD susceptibility genes were clustered and tested for an association with CAD in the Coronary Artery Disease Genome-Wide Replication and Meta-Analysis plus the Coronary Artery Disease Genetics (CARDIoGRAMplusC4D) Consortium data set. The role of plasma lipids as a potential mediator was explored by using data from the Global Lipids Genetics Consortium. Statistical analyses revealed that the combination of 12 NAFLD genes was not associated with CAD in 60,801 CAD cases and 123,504 controls (odds ratio [OR] per NAFLD risk allele, 1.0; 95% confidence interval [CI], 0.99-1.00). In a subsequent sensitivity analysis, a positive relationship was observed after exclusion of gene variants that are implicated in NAFLD through impaired very low-density lipoprotein secretion (i.e., microsomal triglyceride transfer protein [MTTP], patatin-like phospholipase domain containing 3 [PNPLA3], phosphatidylethanolamine N-methyltransferase [PEMT], and transmembrane 6 superfamily member 2 [TM6SF2]) (OR, 1.01; 95% CI, 1.00-1.02). Clustering of the excluded genes showed a significant negative relationship with CAD (OR, 0.97; 95% CI, 0.96-0.99). A substantial proportion of the observed heterogeneity between the individual NAFLD genes in relation to CAD could be explained by plasma lipids, as reflected by a strong relationship between plasma lipids and CAD risk conferred by the NAFLD susceptibility genes (r = 0.76; P = 0.004 for low-density lipoprotein cholesterol). Conclusion: NAFLD susceptibility genes do not cause CAD per se. The relationship between these genes and CAD appears to depend to a large extent on plasma lipids. These observations strongly suggest taking plasma lipids into account when designing a new drug to target NAFLD.

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Sex-influenced association of nonalcoholic fatty liver disease with coronary heart disease.

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Sex-influenced association of nonalcoholic fatty liver disease with coronary heart disease.

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