Relationship of visceral adipose tissue with surrogate insulin resistance and liver markers in individuals with metabolic syndrome chronic complications

Abstract

Background: Visceral adipose tissue (VAT) has a hazardous influence on systemic inflammation, insulin resistance and an adverse metabolic profile, which increases the risk of developing non-alcoholic fatty liver disease (NAFLD) and chronic complications of diabetes. In our study we aimed to evaluate the association of VAT and the triglyceride glucose (TyG) as a proxy of insulin resistance surrogated with metabolic and liver risk factors among subjects diagnosed with metabolic syndrome (MetS). Methods: A cross-sectional study was performed including 326 participants with MetS (55–75 years) from the PREDIMED-Plus study. Liver-status markers, VAT and TyG were assessed. Participants were stratified by tertiles according to VAT ( n = 254) and TyG ( n = 326). A receiver operating characteristic curve was used to analyse the efficiency of TyG for VAT. Results: Subjects with greater visceral fat depots showed worse lipid profile, higher homeostatic model assessment for insulin resistance (HOMA-IR), TyG, alanine transaminase (ALT), fibroblast growth factor-21 (FGF-21), fatty liver index (FLI) and hepatic steatosis index (HSI) compared with participants in the first tertile. The multi-adjusted linear-regression analyses indicated that individuals in the third tertile of TyG (>9.1−10.7) had a positive association with HOMA-IR [ β = 3.07 (95% confidence interval (CI) 2.28−3.86; p trend < 0.001)], ALT [ β = 7.43 (95% CI 2.23−12.63; p trend = 0.005)], gamma glutamyl transferase (GGT) [ β = 14.12 (95% CI 3.64−24.61; p trend = 0.008)], FGF-21 [ β = 190.69 (95% CI 93.13−288.25; p trend < 0.001)], FLI [ β = 18.65 (95% CI 14.97−22.23; p trend < 0.001)] and HSI [ β = 3.46 (95% CI, 2.23−4.68; p trend < 0.001)] versus participants from the first tertile. Interestingly, the TyG showed the largest area under the receiver operating curve (AUC) for women (AUC = 0.713; 95% CI 0.62−0.79) compared with men (AUC = 0.570; 95% CI 0.48−0.66). Conclusions: A disrupted VAT enlargement and impairment of TyG are strongly associated with liver status and cardiometabolic risk factors linked with NAFLD in individuals diagnosed with MetS. Moreover, the TyG could be used as a suitable and reliable marker estimator of VAT.

Application of a Novel Prediction Model for Predicting 2-Year Risk of Non-Alcoholic Fatty Liver Disease in the Non-Obese Population with Normal Blood Lipid Levels: A Large Prospective Cohort Study from China

“…Higher bilirubin levels are negatively associated with insulin levels, insulin resistance and diabetes. 51 , 52 Elevated bilirubin levels are also associated with lowering the risk of cardiovascular disease, including coronary heart disease, stroke, and peripheral vascular disease. 53 , 54 A number of cohort studies have found that DBIL levels are significantly associated with a reduction in the risk of NAFLD, and provide a protective biomarker for NAFLD.…”

Construction of a Personalized Insulin Resistance Risk Assessment Tool in Xinjiang Kazakhs Based on Lipid- and Obesity-Related Indices

“…Second, the TyG index is closely related to cytokines such as adiponectin and C-reactive proteins, 39 which play a crucial role in IR progression. Third, visceral fat accumulation, characterized by intense lipolytic activity, seems to be the reason for IR, 40 and the TyG index is a good marker of visceral fat accumulation.…”

Triglyceride-glucose index and common carotid artery intima-media thickness in patients with ischemic stroke

“…In addition, IR has been reported to be associated with chronic inflammation, which could be induced by various proinflammatory cytokines and oxidative stress biomarkers [ 41 ]. Second, the TyG index has also been considered as a suitable and reliable marker of systemic inflammation [ 42 – 44 ]. Furthermore, higher plasma TG levels were thought to promote endothelial dysfunction, plaque rupture and arterial inflammation [ 45 ], while elevated FPG levels could induce oxidative stress, alter protein kinase signaling, and trigger certain miRNA and epigenetic modifications [ 46 ], which were regarded as another possible pathogenesis in the atherosclerosis process.…”