BackgroundThe triglyceride glucose (TyG) index has been suggested as a simple surrogate marker of insulin resistance. However, there are limited data regarding the association between the TyG index and arterial stiffness in adults. Therefore, we evaluated the relationship between the TyG index and arterial stiffness as measured based on brachial ankle pulse wave velocity (baPWV) in Korean adults.MethodsA total of 3587 subjects were enrolled in this study. Anthropometric and cardiovascular risk factors were measured. The TyG index was calculated as ln[fasting triglycerides(mg/dl) × fasting glucose(mg/dl)/2], and the insulin resistance index of homeostasis model assessment (HOMA-IR) was estimated. Arterial stiffness was determined by measuring baPWV.ResultsThe subjects were stratified into four groups based on the TyG index. There were significant differences in cardiovascular parameters among the groups; the mean baPWV increased significantly with increasing TyG index. According to the logistic regression analysis after adjusting for multiple risk factors, the odds ratio (95% CI) for increased baPWV (> 75th percentile) for the highest and lowest quartiles of the TyG index was 2.92 (1.92–4.44) in men and 1.84 (1.15–2.96) in women, and the odds ratio for increased baPWV for the highest and lowest quartiles of the HOMA-IR was 1.80 (1.17–2.78) in men and 1.46 (1.06–2.47) in women, respectively.ConclusionThe TyG index is more independently associated with increased arterial stiffness than HOMA-IR in Korean adults.

Statins were associated with slower progression of overall coronary atherosclerosis volume, with increased plaque calcification and reduction of high-risk plaque features. Statins did not affect the progression of percentage of stenosis severity of coronary artery lesions but induced phenotypic plaque transformation. (Progression of AtheRosclerotic PlAque DetermIned by Computed TomoGraphic Angiography Imaging [PARADIGM]; NCT02803411).

To investigate the triglyceride-glucose (TyG) index association with coronary artery calcification (CAC) progression in adult Koreans. RESEARCH DESIGN AND METHODS Various cardiovascular risk factors and anthropometric profiles were assessed in 1,175 subjects who previously had a CAC evaluation at least twice by multidetector computed tomography in a health care center. The TyG index was determined using ln(fasting triglycerides [mg/dL] 3 fasting glucose [mg/dL]/2). The CAC progression was defined as either incident CAC in a CAC-free population at baseline or an increase of ‡2.5 units between the square roots of the baseline and follow-up coronary artery calcium scores (CACSs) of subjects with detectable CAC at baseline. RESULTS CAC progression was seen in 312 subjects (27%) during 4.2 years follow-up. On the basis of the TyG index, subjects were stratified into three groups. Follow-up CACS and incidence of CAC progression were markedly elevated with rising TyG index tertile. Logistic regression analysis adjusted for various risk factors revealed an odds ratio for CAC progression of 1.82 (95% CI 1.20-2.77; P £ 0.01) when the highest and lowest TyG index tertiles were compared. CONCLUSIONS The TyG index is an independent predictor of CAC progression. Understanding the progression of cardiovascular disease (CVD) is important because the disease can lead to severe morbidity and mortality. An important risk factor for CVD is coronary artery calcification (CAC), and cardiovascular risk is commonly assessed by coronary artery calcium score (CACS), as determined by computed tomography (CT) (1-4). Insulin resistance (IR) is one of the major factors that leads to CVD, and several earlier studies have shown a relationship between IR and CAC (5,6). A reliable surrogate marker of IR was recently suggested to be the triglyceride-glucose (TyG) index, which is calculated using fasting triglyceride (TG) and fasting glucose measurements (7-9). Several previous studies indicated that the TyG index is associated with CAC and CVD (10-14); however, the results were inconsistent. In addition, although CAC progression is a powerful predictor of mortality compared with baseline CACS and traditional cardiovascular risk factors (15), no previous study has investigated the relationship between TyG index and CAC progression in adults. Therefore, we

In this study of the Saccharomyces cerevisiae G protein-coupled receptor Ste2p, we present data indicating that the first extracellular loop (EL1) of the ␣-factor receptor has tertiary structure that limits solvent accessibility and that its conformation changes in a ligand-dependent manner. The substituted cysteine accessibility method was used to probe the solvent exposure of single cysteine residues engineered to replace residues Tyr 101 through Gln 135 of EL1 in the presence and absence of the tridecapeptide ␣-factor and a receptor antagonist. Surprisingly, many residues, especially those at the N-terminal region, were not solvent-accessible, including residues of the binding-competent yet signal transduction-deficient mutants L102C, N105C, S108C, Y111C, and T114C. In striking contrast, two N-terminal residues, Y101C and Y106C, were readily solvent-accessible, but upon incubation with ␣-factor labeling was reduced, suggesting a pheromone-dependent conformational change limiting solvent accessibility had occurred. Labeling in the presence of the antagonist, which binds Ste2p but does not initiate signal transduction, did not significantly alter reactivity with the Y101C and Y106C receptors, suggesting that the ␣-factor-dependent decrease in solvent accessibility was not because of steric hindrance that prevented the labeling reagent access to these residues. Based on these and previous observations, we propose a model in which the N terminus of EL1 is structured such that parts of the loop are buried in a solventinaccessible environment interacting with the extracellular part of the transmembrane domain bundle. This study highlights the essential role of an extracellular loop in activation of a G protein-coupled receptor upon ligand binding. G protein-coupled receptors (GPCRs)3 are ubiquitous in eukaryotes and have been found in a diversity of organisms ranging from yeast to humans. In most eukaryotes, GPCRs comprise 1-2% of the total genes in the genome (1) and participate in virtually all aspects of cellular physiology, including hormonal responses, neuronal transmission, and mediation of taste, smell, and vision (2). Modulation of GPCR function is a major pharmaceutical target, currently accounting for Ͼ30% of all drugs prescribed (3-5). Thus a thorough understanding of the nature of the receptor-ligand interaction and subsequent signal transduction is essential for the development of more effective and safer therapeutic agents.The structural hallmarks of this diverse collection of receptors are seven membrane-spanning domains linked by extracellular and intracellular loops, oriented such that the N terminus is external to the cell and the C terminus is internal. Although the structure-function relationships in the membrane-spanning domains and the intracellular loop regions have been well examined in many GPCRs (6 -11), few studies have focused on the importance of the extracellular loop structures and their role in receptor activation. In those studies where the extracellular domains were studied in deta...