Comparison of the triglyceride glucose index and blood leukocyte indices as predictors of metabolic syndrome in healthy Chinese population.

Triglyceride glucose (TyG) index and inflammatory markers are reported to have a positive association with metabolic syndrome (MetS). However, no previous study has assessed the value of TyG index and inflammatory markers as predictors of metabolic syndrome in the same study. This study looks at the comparison of the triglyceride index and blood leukocyte indices as predictors of metabolic syndrome in the Chinese population. The study cohort involved 1542 Chinese population without metabolic syndrome. The subjects underwent comprehensive routine health examination in 2011 and returned for a follow-up examination in 2016. Metabolic syndrome was defined according to Chinese Diabetes Society criteria, using body mass index for the replacement of waist circumference. TyG index, total leukocytes, neutrophils, lymphocytes, and neutrophil-to-lymphocyte ratio (NLR) were measured. Adjust d logistic models were used to assess the relationship between TyG index, blood leukocyte indices, and incident MetS. Receiver operating characteristic (ROC) curves were performed to determine the predictive value of TyG index and blood leukocyte indices for MetS. Results from multivariate logistic regression analysis showed that, in the adjusted model, the subjects with the highest quartile of TyG index and neutrophils had a 3.894- and 1.663-fold increased incidence of MetS (P < 0.0001 and P = 0.027), respectively. No significant association was observed between total leukocytes, lymphocytes, NLR with incident MetS. ROC analysis showed that the AUC of TyG index and neutrophils were 0.674 and 0.568 for incident MetS, respectively. TyG index rather than blood leukocyte indices may have the strongest predictive value in MetS development over a 5-year period.

Direct Bilirubin Levels and Risk of Metabolic Syndrome in Healthy Chinese Men.

BACKGROUND: Serum bilirubin is a potent endogenous antioxidant with anti-inflammatory properties. Several cross-sectional studies have reported that bilirubin was negatively associated with metabolic syndrome. However, in recent longitudinal studies, the relations between bilirubin and metabolic syndrome are inconsistent. Moreover, previous studies mainly focused on serum total bilirubin which is the sum of direct bilirubin and indirect bilirubin. For these reasons, the longitudinal effect of bilirubin subtypes on incident metabolic syndrome was evaluated in Chinese men. METHODS: The study cohort involved 1339 Chinese men without metabolic syndrome. Metabolic syndrome was defined by the American Heart Association/National Heart, Lung and Blood Institute (AHA/NHLBI) criteria, using BMI for the replacement of waist circumference. RESULTS: There are 117 incident metabolic syndrome cases (8.7%) during 5 years of follow-up among 1339 metabolic syndrome-free participants at baseline. After adjusting for age, drinking, smoking, physical activity, TG, and LDL-C, the odd ratios (ORs) and 95% confidence intervals (CIs) for MetS incidence in the second, third, and fourth quartiles versus the first quartile of DBil concentration were 1.00 (0.61-1.63), 0.57 (0.32-1.02), and 0.51 (0.28-0.92) (Ptrend = 0.031), respectively. CONCLUSIONS: Our findings support the negative association between direct bilirubin and incident metabolic syndrome in healthy Chinese men over 5-year period.

Association of Microalbuminuria with Metabolic Syndrome among Aged Population.

Background. The impact of the various components of metabolic syndrome (MetS) on chronic kidney disease has been conflicting. We aim to investigate the association between MetS and microalbuminuria and identify the major contributing components of MetS that result in microalbuminuria in the Chinese aged population. Methods. A total of 674 adults aged 55-98 years (males: 266; mean age: 66.5 ± 7.5 years) were studied. MetS was defined by the 2004 Chinese Diabetes Society criteria and microalbuminuria by urine albumin-creatinine ratio (UACR) ≥3 mg/mmoL. Results. The prevalence of microalbuminuria was gradually increased with increasing number of MetS components (P < 0.05). In multivariate regression, after adjusting for age and sex, MetS was the strongest correlate of microalbuminuria (OR = 1.781, 95% CI = 1.226-2.587; P < 0.05) followed by the fasting plasma glucose (FPG) (OR = 1.217, 95% CI = 1.044-1.092; P < 0.05), systolic blood pressure (SBP) (OR = 1.011, 95% CI = 1.107-1.338; P < 0.05), and high-density lipoprotein cholesterol (HDL-C) (OR = 0.576, 95% CI = 0.348-0.953; P < 0.05). Conclusions. MetS is independently associated with microalbuminuria in the Chinese aged population. Elevated FPG is the most predominant component of metabolic syndrome associated with microalbuminuria followed by elevated SBP and reduced HDL-C.

Downregulation of protein kinase Cα was involved in selenite-induced apoptosis of NB4 cells.

We revealed in our previous research that sodium selenite induced obvious apoptosis of human leukemia NB4 cells, with reactive oxygen species (ROS), mitochondrial apoptosis pathway, and endoplasmic reticulum stress (ER stress) involved. In the present study, we revealed protein kinase Ca (PKCalpha) was dramatically downregulated in selenite-induced apoptosis, which was mediated by ROS. Besides, we confirmed PKCalpha played an antiapoptotic role through its effects on ERK1/2 and Akt, while its downregulation was attributed to caspase-3 and PP2Ac under the regulation of ROS. In summary, we speculated that in apoptosis of NB4 cells induced by selenite, PKCalpha functioned to counteract apoptosis, thus its downregulation seemed a mechanism aggravating apoptosis.

[Mitochondrial transmembrane potential loss caused by reactive oxygen species plays a major role in sodium selenite-induced apoptosis in NB4 cells].

OBJECTIVE: To investigate the role of reactive oxygen species (ROS) and ROS-caused mitochondrial transmembrane potential loss in sodium selenite-induced apoptosis in NB4 cells. METHODS: ROS production was measured by ROS-specific probe DCFH-DA. Sodium selenite mitochondrial transmembrane potential loss was evaluated by flow cytometry with Rh123 staining. Protein levels of cytochrome C, Bid, Bcl-xl, and Bax were measured by Western blot using protein-specific antibodies. NB4 cells were pre-incubated by MnTmPy or BSO before selenite treatment to further confirm the effects of ROS on NB4 cells. RESULTS: 20 micromol/L sodium selenite induced ROS production and mitochondrial transmembrane potential loss in NB4 cells time-dependently. Cytochrome C accumulated in cytoplasm after selenite treatment. Sodium selenite also downregulated Bcl-xl and activated Bax and Bid at protein level. Pretreatment with antioxidant MnTmPy almost fully abrogated the proapoptotic effect of sodium selenite prevented the cleavage of Bid protein and in turn the mitochondrail transmembrane potential loss. On the contrary, pretreatment with BSO intensified the mitochondrail transmembrane potential loss induced by sodium selenite. CONCLUSIONS: Sodium selenite may induce apoptosis by inducing ROS production in NB4 cells, which leads to the downregulation of Bcl-xl, upregulation of Bax, and cleavage and activation of Bid. Bax and tBid then agregate on mitochondrial membrane, which in turn causes a decrease of mitochondrial transmembrane potential and release of cytochrome C into cytoplasm.