Our objective was to evaluate the association between habitual daytime napping and the prevalence of metabolic syndrome.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a critical role in the cholesterol metabolism by negatively regulating the low-density lipoprotein receptor (LDLR). Lipid metabolic and ovarian disorders are the common clinical manifestation of polycystic ovary syndrome (PCOS). Here, we intended to elucidate the role of PCSK9 in the pathogenesis of PCOS conducted on a human population in case-control design and animal part in an interventional study.

This study examines the relationship between adherence to different dietary patterns and the presence of metabolic syndrome and its components among Korean adults. The sample consisted of 406 Korean adults aged 22 to 78 years recruited from hospitals. Metabolic syndrome was defined according to the criteria issued by the Adult Treatment Panel III, with the exception of central obesity, which was defined according to the Asian-Pacific criteria. Dietary information was obtained by means of a 24-hour recall and a 3-day food record, and factor analysis was used to define dietary patterns. Factor analysis identified 4 major dietary patterns, which explained 28.8% of the total variance, based on the percentage of total daily energy intake from each food group: Korean traditional, alcohol and meats, sweets and fast foods, and fruit and dairy. After controlling for all potential confounders, we found that the Korean traditional dietary pattern was not associated with individual components of the metabolic syndrome but was significantly associated with increased odds of having metabolic syndrome. The fruit and dairy pattern was significantly associated with decreased odds of impaired blood glucose, hypertriglyceridemia, and metabolic syndrome. Our findings suggest that the fruit and dairy pattern is associated with reduced risk of having metabolic syndrome.

Metabolic syndrome (MetS) is a cluster of metabolic abnormalities sharing potential common underlying mechanisms. Insulin-degrading enzyme (IDE) plays a primary role in insulin degradation and cellular insulin processing and therefore affects glucose and lipid metabolism. Genetic association studies have been focused on the relationship between the IDE gene and the development of MetS. To identify specific genetic risks for MetS associated with IDE gene, a case-control association study was performed on 563 Chinese elders in Shanghai, China. Cases were those with MetS (n = 241), and controls were those without MetS (n = 219). Five unrelated genetic markers (single nucleotide polymorphisms) at the IDE gene were used for association analyses. The single-locus association analysis revealed that the A/T allele of rs11187033 was associated with MetS (odds ratio = 0.698; 95% confidence interval, 0.526-0.928; P = .013). Patients with MetS had more haplotype G-T-Ts than controls (P = .008). None of the other 4 single nucleotide polymorphisms was significantly associated with MetS. This result suggests that the rs11187033 at IDE gene might contribute to MetS susceptibility in Chinese elders.

We examined whether a prevalent caveolin-1 gene (CAV1) variant, previously related to insulin resistance, is associated with metabolic syndrome (MetS).

Although inflammation has been shown to play an important role in metabolic syndrome (MetS), the association between inflammatory marker gene polymorphisms and the risk of MetS has not been fully elucidated. This study was initiated to investigate the association between functional variants of inflammatory marker genes and the risk of MetS in Taiwanese adults. The sample population comprised 615 unrelated subjects, of which 22% had MetS. The single nucleotide polymorphisms rs5491 on the intercellular adhesive molecule 1 (ICAM1) gene and rs3091244 on C-reactive protein (CRP) were genotyped. The ICAM1 rs5491 polymorphism was significantly associated with the level of soluble intercellular adhesive molecule 1 (P < .001). Both the ICAM1 rs5491 and the CRP rs3091244 were shown to have significant association with MetS after adjustment for age, sex, smoking, and body mass index, but not after adjustment for levels of the respective serum marker. Independent associations between the combined ICAM1-CRP (rs5491 and rs3091244) genotypes and MetS were found by multivariate analysis (P = .005). In subgroup analysis, association of combined genotypes with insulin resistance and MetS mainly occurred in subjects with central obesity. In conclusion, inflammatory marker gene polymorphisms play an important role in modulating the risk of insulin resistance and MetS for subjects with central obesity. These findings will contribute toward a better understanding of the mechanism of association between inflammatory markers and the risk of developing atherosclerotic disease.

Some observational studies have suggested that serum uric acid (SUA) levels are one of the determinants of the metabolic syndrome (MetS). However, previous studies reported combined results for men and women after adjusting for sex and few studies take body composition into consideration. Therefore, we performed this sex-specific longitudinal study to investigate how baseline SUA levels influence incident MetS, including body composition as an adjusting factor in a large number of subjects.

Metabolic syndrome (MetS) is characterized by a cluster of interconnected risk factors -hyperglycemia, dyslipidemia, hypertension and obesity- leading to an increased risk of cardiovascular events. Small extracellular vesicles (sEVs) can be considered as new biomarkers of different pathologies, and they are involved in intercellular communication. Here, we hypothesize that sEVs are implicated in MetS-associated endothelial dysfunction.

The aims of this study were to investigate the extent of concordance between metabolic syndrome (MS) and insulin resistance (IR), the features of discordance, and the magnitude of their independent association with cardiovascular disease (CVD) risk. After exclusion of individuals with diabetes and impaired fasting glucose, the population sample of 1534 men and women, representative of Turkish adults (mean age, 52.2 years), were evaluated cross-sectionally and at a mean 2 years' follow-up. Metabolic syndrome was identified by criteria of the Adult Treatment Panel III, except for male waist circumference (>94 cm). Insulin resistance was defined by the upper quartile in the sample (>2.245) of the homeostatic model assessment (HOMA) index. Clinical fatal and nonfatal CVD existed or developed in 165 subjects. Waist circumference proved to be by far the strongest significant determinant of HOMA in both sexes, followed by triglycerides. The cohort was categorized into 4 by the presence or absence of MS and IR. Each of the latter represented 34% and 25%, but together constituted 45% of the sample, thus disclosing concordance in a third of the conditions combined. The nonconcordant IR/NoMS group was less common than the MS/NoIR group and was distinct from the latter in having significantly lower waist girth, blood pressure, apolipoprotein B and triglyceride levels, and higher high-density lipoprotein cholesterol, glucose, and insulin levels and physical activity in both sexes. When adjusted for 5 important risk factors, although the excess risk in men with MS failed to attain significance, men with IR were associated with a significant 1.9-fold CVD risk. The IR/NoMS group had a 2.2-fold (95% confidence interval, 0.97-5.11) CVD likelihood compared with the large insulin-sensitive group, after adjustment for age, sex, log C-reactive protein, low-density lipoprotein cholesterol, smoking status, physical activity, and the 2 groups of MS with or without IR. Overlapping between MS and IR is limited in either sex, and MS/NoIR is more common than IR/NoMS. Overall, IR is more significantly associated with CVD risk than MS in men and in both sexes after adjustment for important confounders. Insulin resistance without MS tends to implicate in middle-aged and elderly Turkish men roughly a 2-fold CVD risk, corresponding to 50% excess risk per 1 SD in HOMA index, independent of MS and important covariates.

Muscle weakness is followed by insulin resistance which is associated with metabolic disorders leading to metabolic syndrome (MetS). Therefore, muscle strength decline may be associated with MetS. The aim of this study was to investigate the relationships between muscle strength and MetS and its separate components.

The objective of the study was to determine the most accurate metabolic syndrome (MS) definition among the definitions proposed by the International Diabetes Federation (IDF), the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III [ATPIII]), and the World Health Organization (WHO) and to evaluate the cutoff point of waist circumference using the IDF definition for optimally defining MS in the Chinese population. One thousand thirty-nine Chinese patients older than 30 years and diagnosed with type 2 diabetes mellitus were investigated by randomized cluster sampling in the Shanghai downtown, and 1008 patients were analyzed in this study. Body mass measurements, resting blood pressure, fasting blood measures, and carotid atherosclerotic measurements including common carotid artery intima-media thickness (IMT) and carotid plaque were investigated. The IDF definition was compared with the other 2 definitions, and the carotid atherosclerosis was evaluated among the patients according to these definitions. (1) The MS prevalence was 50.0%, 55.7%, and 70.0% under the IDF, ATPIII, and WHO definitions, respectively. (2) The percentage of all the participants categorized as either having or not having the MS was 69.9% (under the IDF and ATPIII definitions) and 70.2% (under the IDF and WHO definitions). (3) Common carotid artery IMT of patients with MS determined by the IDF definition was thicker than those determined by the WHO and ATPIII definitions, and the percentage of carotid plaque of patients with MS determined by the IDF definition was greater than those determined by the WHO and ATPIII definitions. (4) When the cutoff point of waist circumference in men determined by the IDF definition was modified from 90 to 85 cm, common carotid artery IMT of the emerging male patients with MS was thicker than that of the male patients with MS determined by the original IDF definition. In conclusion, the prevalence of MS was 50.0%, 55.7%, and 70.0% under the IDF, ATPIII, and WHO definitions, respectively. The preferable IDF definition served as a better predictor of cardiovascular disease risk in the Chinese patients diagnosed with type 2 diabetes mellitus compared with the ATPIII and WHO definitions. The modified cutoff point of waist circumference in men under the IDF definition specific for the Chinese population (from 90 to 85 cm) might be more suitable for predicting atherosclerosis.

To establish animal models with diet-induced metabolic disorders similar to human metabolic syndrome, 2 unhealthy dietary habits featuring a high fat content and a sucrose-containing beverage intake, alone or in combination, were tested on Wistar rats and C57BL/6J mice. The 2 dietary habits were, respectively, simulated by feeding a high-fat diet (regimen A) or additionally providing 30% sucrose (wt/vol) in the drinking water (regimen B). Using a 2 x 2 factorial design, 4 groups of animals were fed chow diet plus plain water (group C), high-fat diet (30% [wt/wt] fat) plus plain water (group A), chow diet plus sucrose in drinking water (group B), and high-fat diet plus sucrose in drinking water (group AB) for 26 weeks. In Wistar rats, regimen B caused a significant increase in visceral fat; serum levels of lipids, glucose, insulin, and uric acid; insulin resistance; and blood pressure, whereas regimen A only caused a significant increase in visceral fat and serum insulin levels (P < .05). In contrast, regimen A induced a full array of metabolic syndrome in C57BL/6J mice; but regimen B only caused slight obesity and hyperlipidemia. In both Wistar rats and C57BL/6J mice, there were no additive effects of the 2 regimens, indicated by significant interactions between regimens A and B on the metabolic indexes measured. These results show that, in terms of inducing metabolic syndrome, Wistar rats are more responsive to sucrose water regimen, whereas C57BL/6J mice are more responsive to the high-fat diet regimen.

Klinefelter syndrome (KS), in which subjects have additional copies of X chromosomes, is the most common male sex chromosome abnormality, with a prevalence of 1 in 660 and an incidence of about 1 in 500-700 newborns. Its sign and symptoms include infertility, generally low testosterone levels, and an increased prevalence of obesity and metabolic syndrome. Epicardial fat thickness (EFT) reflects visceral adiposity rather than general obesity.

Polycystic ovary syndrome (PCOS) is often associated with higher levels of LH, and arrested ovarian follicular growth. The direct impact of high LH on FSH mediated metabolic responses in PCOS patients is not clearly understood.

Polycystic ovary syndrome (PCOS) is the most common metabolic and endocrine disorder among reproductive-age women, and the leading cause of anovulatory infertility. 11β-hydroxysteroid dehydrogenases-1 (11β-HSD1) catalysing the conversion of inactive cortisone to active cortisol plays a crucial role in various metabolic diseases. However, whether 11β-HSD1 is associated with the pathogenesis of PCOS and whether 11β-HSD1 can be a treating target of PCOS remain unknown.

Reduced β-cell mass and impaired β-cell function are primary causes of all types of diabetes. However, the intrinsic molecular mechanism that regulates β-cell growth and function remains elusive. Here, we demonstrate that the small GTPase Rheb1 is a critical regulator of glucose-stimulated insulin secretion (GSIS) in β-cells. Rheb1 was highly expressed in mouse and human islets. In addition, β-cell-specific knockout of Rheb1 reduced the β-cell size and mass by suppressing β-cell proliferation and increasing β-cell apoptosis. However, tamoxifen-induced deletion of Rheb1 in β-cells had no significant effect on β-cell mass and size but significantly impaired GSIS. Rheb1 facilitates GSIS in human or mouse islets by upregulating GLUT1 or GLUT2 expression, respectively, in a mTORC1 signaling pathway-dependent manner. Our findings reveal a critical role of Rheb1 in regulating GSIS in β-cells and identified a new target for the therapeutic treatment of diabetes mellitus.

Fuel oxidation during exercise was studied in type 1 insulin-dependent (T1DM) patients mainly under quite constant insulin and glycemia; these protocols, however, likely do not reflect patients' usual metabolic conditions. The glucose oxidation rate (GLUox) in T1DM patients under usual life conditions was thus investigated during prolonged exercise (3-h) and its behavior was described mathematically.

High fructose consumption is associated with the development of fatty liver and dyslipidemia with poorly understood mechanisms. We used a matrix-assisted laser desorption/ionization-based proteomics approach to define the molecular events that link high fructose consumption to fatty liver in hamsters. Hamsters fed high-fructose diet for 8 weeks, as opposed to regular-chow-fed controls, developed hyperinsulinemia and hyperlipidemia. High-fructose-fed hamsters exhibited fat accumulation in liver. Hamsters were killed, and liver tissues were subjected to matrix-assisted laser desorption/ionization-based proteomics. This approach identified a number of proteins whose expression levels were altered by >2-fold in response to high fructose feeding. These proteins fall into 5 different categories including (1) functions in fatty acid metabolism such as fatty acid binding protein and carbamoyl-phosphate synthase; (2) proteins in cholesterol and triglyceride metabolism such as apolipoprotein A-1 and protein disulfide isomerase; (3) molecular chaperones such as GroEL, peroxiredoxin 2, and heat shock protein 70, whose functions are important for protein folding and antioxidation; (4) enzymes in fructose catabolism such as fructose-1,6-bisphosphatase and glycerol kinase; and (5) proteins with housekeeping functions such as albumin. These data provide insight into the molecular basis linking fructose-induced metabolic shift to the development of metabolic syndrome characterized by hepatic steatosis and dyslipidemia.

The pleiotropic proinflammatory cytokine, interleukin 18, plays a role in innate immunity and, based on mouse models, influences obesity. We investigated variation within the IL18 gene and its effect on markers of the metabolic syndrome. A tagging single nucleotide polymorphism set of 5 SNPs for the gene encoding interleukin 18 was selected and genotype was determined in 3 separate studies. In 2775 healthy middle-aged men, 6 common haplotypes were seen, but none was associated with body mass index (BMI). In 439 patients who underwent coronary artery bypass graft surgery, Hap2 (frequency, 22%) was present at a lower frequency than in healthy subjects and was associated with higher mean BMI compared with Hap1 (P = .011). In 483 men with type 2 diabetes mellitus, Hap2 was again associated with a higher haplotypic mean BMI (P = .002). Those homozygous for Hap2 had a BMI of 31.2 (1.3) kg/m(2), mean (SE), compared with 28.3 (1.0) kg/m(2) in those not carrying a copy of Hap2. No single SNP could fully explain the effects seen. Therefore, variation within IL18, previously shown to be associated with lower IL18 levels, is influencing measures of obesity both in men with type 2 diabetes mellitus and those with advanced coronary heart disease.