ライフサイエンスコーパス: MetS

1 MetS diagnosis was established in accordance with the Na

2 MetS increases the risk of BE compared to control groups

3 MetS is associated with significant alterations in heart

4 MetS offspring risk for paternal smoking increased dosew

5 MetS patients are strongly exposed to polypharmacy; howe

6 MetS severity seems highly heritable among whites and bl

7 MetS severity was inversely associated with the CI1-20 (

8 MetS subjects have significantly lower complexity index

9 MetS was defined by the Joint Interim Statement criteria

10 MetS was diagnosed using the criteria defined in the Adu

11 MetS-lEVs significantly promoted migration and prolifera

12 MetS-lEVs, but not non-MetS-lEVs, increased Rap1-depende

13 MetS-VLDL induced downregulation of Cx40 and Cx43 at tra

14 d 50-85) with (N = 61) and without (N = 103) MetS.

15 A total of 164 subjects with >/=2 MetS risk factors were randomly allocated to 1 of 3 inte

16 In 14 studies with a sample size of 108,416, MetS significantly increased the risk of BE (OR = 1.354;

17 with diabetes (HR, 1.30; 95% CI, 1.19-1.43), MetS (HR, 1.30; 95% CI, 1.20-1.41), and neither conditio

18 Z, percentage body fat at age 16/17 y, and a MetS score at age 16/17 y.

19 After WM, all groups had a MetS prevalence of 80-90% [healthy American diet (HAD) c

20 o Adult Treatment Panel III criteria absent (MetS-)] or with extended criteria with inflammation and

21 In whole-brain analyses, MetS was negatively associated with cortical thickness i

22 to univariate logistic regression analysis, MetS was significantly associated with RE and remained a

23 as significant for continent (P < 0.001) and MetS diagnostic criteria (P = 0.043), but was not signif

24 triglycerides, high blood pressure (BP), and MetS were more likely to have OAG compared with those wi

25 ose without high triglycerides, high BP, and MetS after adjusting for potential confounders.

26 the severity of periodontitis (exposure) and MetS (outcome).

27 per gastrointestinal endoscopic findings and MetS was defined according to the Taiwanese criteria.

28 erved for other plant-based diet indices and MetS.

29 e their relationship with dietary intake and MetS.

30 obtained optimal SPISE cutpoints for IR and MetS diagnosis.

31 inflammatory effects in patients with MS and MetS and should be further explored.

32 nonalcoholic fatty liver disease (NAFLD) and MetS.

33 association between severe periodontitis and MetS after adjustment for sex, age, household density, a

34 Diagnosis of periodontitis and MetS was performed according to various criteria.

35 ential association between periodontitis and MetS, as well as the influence of risk variables on this

36 ckness; 2) the relationship between PTSD and MetS; and 3) whether PTSD was associated with cortical t

37 d to evaluate the correlation between RE and MetS and its components.

38 were separated from normal (Normal-VLDL) and MetS (MetS-VLDL) individuals.

39 In vivo, in the supracoronary aortic banding+MetS animals, reducing IL-6, either by anti-IL-6 antibod

40 onditions, only supracoronary aortic banding+MetS rats developed precapillary PH, as measured by both

41 PH in supracoronary aortic banding+MetS was associated with macrophage accumulation and inc

42 his, we evaluated 1) the association between MetS and neural integrity, indexed by cortical thickness

43 An important risk association between MetS and periodontitis was reported, being that individu

44 The association between MetS and periodontitis was tested in structural equation

45 To determine the association between MetS components and DII Logistic regression was used (P

46 f genetic and phenotypic correlation between MetS severity and the individual components of MetS amon

47 ducted to determine the relationship between MetS and BE.

48 atistically significant relationship between MetS and DII.

49 imed to investigate the relationship between MetS and pro-inflammatory diet by using the food inflamm

50 ation effect of childhood insulin on the BMI-MetS and BMI-hyperglycemia associations was estimated at

51 results of this study, patients affected by MetS showed a greater prevalence of peri-implant disease

52 These results highlight that Rap1 carried by MetS-lEVs may be a novel determinant of diagnostic value

53 These data demonstrate that Rap1 carried by MetS-lEVs participates in the enhanced SMC proliferation

54 preclinical model of group 2 PH by combining MetS with LHD.

55 In conclusion, MetS-VLDL modulates gap junctions and delays both atrial

56 er MetS severity as assessed by a continuous MetS score is heritable and whether this varies by race.

57 This continuous MetS severity Z score may provide a more useful means of

58 food consumption had more likely to develop MetS, this relationship was not statistically significan

59 50 obese patients with MS who also developed MetS.

60 using CAC scores among those with diabetes, MetS, or neither condition.

61 ng, and betel chewing, on the risks of early MetS in human offspring.

62 The PCOS women with high ZAG had fewer MetS, IGT and polycystic ovaries as compared with the lo

63 Furthermore, among the five MetS components, elevated blood pressure (adjusted OR(ga

64 sensitivity (90%) and specificity (74%) for MetS diagnosis.

65 not associated with number of components for MetS in obese subjects (P = 0.14).

66 reased with increasing number components for MetS in total population and in non-obese subjects (P <

67 In males, the optimal cutoff for MetS diagnosis was 5.0 (sensitivity: 97%; specificity: 8

68 Inflammation is an important risk factor for MetS.

69 Causal factors for MetS are not well defined or yet unidentified.

70 while one latent variable was identified for MetS.

71 nt of functional ingredients from lentil for MetS management.

72 p between BMP-9 and conventional markers for MetS and insulin resistance (IR).

73 er of pharmacological compounds required for MetS treatment can be reduced by the application of mult

74 studies should examine whether treatment for MetS reduces the risk of BE.

75 -inflammatory effects of treatments used for MetS, such as metformin hydrochloride and pioglitazone h

76 ere performed to define latent variables for MetS and periodontitis.

77 ults using observed and latent variables for MetS and periodontitis.

78 GTPase, Rap1 was overexpressed in lEVs from MetS patients compared with those from non-MetS subjects

79 ompletely prevented the effects of lEVs from MetS patients.

80 vesicles released from plasma membrane, from MetS patients were shown to induce endothelial dysfuncti

81 Of the 2419 normal weight adults, 377 had MetS.

82 d was associated with reduced odds of having MetS (OR: 0.795[0.082]; P = 0.026).

83 nset dietary intervention and risk of having MetS between 15 and 20 years of age.

84 associated with higher likelihood of having MetS.

85 However, MetS or its components exhibited no significant associat

86 as the index that most accurately identified MetS status in men (AUC = 0.853) and women (AUC = 0.817)

87 es were larger for Adult Treatment Panel-III MetS among black compared with white cohort members (JHS

88 te heritability of Adult Treatment Panel-III MetS and a sex- and race-specific MetS severity Z score

89 ility estimate for Adult Treatment Panel-III MetS of 0.24 (95% CI, 0.11-0.36) and for the MetS severi

90 In MetS only, these relationships were absent but education

91 ed atrial conduction is a mechanism of AF in MetS.

92 fibrillation and ventricular arrhythmias in MetS.

93 S criterion, the prevalence of components in MetS was 57.75% for abdominal obesity, 44.05% for elevat

94 tage increase in PCB serum concentrations in MetS+ compared with MetS- subjects (median: 58% compared

95 ell adaptation, identity, and dysfunction in MetS.

96 d hyperglycaemia to cognitive dysfunction in MetS/T2DM and AD.

97 Among the numerous pathways dysregulated in MetS, inflammation plays also a critical role in both PH

98 A total of 183 patients were enrolled: in MetS subjects, peri-implantitis was detected in 36.9% (n

99 t tissues that elevated glucose, as found in MetS/T2DM, and oligomeric beta-amyloid (Abeta) peptide,

100 BMI --> insulin was significantly greater in MetS than in non-MetS groups (0.510 vs 0.190, p < 0.001)

101 WMH volume was greater in MetS, but verbal recall performance was not impaired.

102 fected by dairy fat quantity but is lower in MetS adults, potentially because of greater inflammation

103 ing BMP-9 levels were significantly lower in MetS patients compared to those of the healthy controls.

104 phisms and FA status on metabolic markers in MetS.

105 electrocardiography (ECG)-based measures in MetS subjects.

106 481 ng/g lipid weight; P = 0.01) but not in MetS+ compared with MetS- subjects.

107 e clustering of cardiometabolic variables in MetS alters their individual relationships with cognitio

108 Incident MetS and T2DM were identified in adulthood (mean age = 3

109 years, 2,583 participants developed incident MetS.

110 I had 50% higher risk of developing incident MetS, adjusting for demographic characteristics and life

111 ently predicted early occurrence of incident MetS in offspring, corroborating previously reported tra

112 Then we induced MetS by a combination of high-fat diet and olanzapine tr

113 1082639 and TGFBR2 rs3773651 SNPs influenced MetS.

114 ental factors and these genes in influencing MetS and its individual components.

115 idual relationships with cognition; instead, MetS is characterised by a greater reliance on cognitive

116 P = 0.005) and an adjusted 0.03 units lower MetS score (95% CI: -0.05, -0.01; P = 0.01) at age 16/17

117 eparated from normal (Normal-VLDL) and MetS (MetS-VLDL) individuals.

118 IGF-1 in a rodent model of multigenerational MetS.

119 m MetS patients compared with those from non-MetS subjects.

120 as significantly greater in MetS than in non-MetS groups (0.510 vs 0.190, p < 0.001), and greater in

121 In non-MetS, higher HbA1c, SBP, and number of MetS components w

122 In non-MetS, strategies to control HbA1c and SBP should be prio

123 MetS-lEVs, but not non-MetS-lEVs, increased Rap1-dependent endothelial cell per

124 oups according to the presence or absence of MetS, defined using IDF criteria.

125 Our data showed a nominal association of MetS with the APOA5 rs662799, BUD13 rs11216129, BUD13 rs

126 results showed a significant association of MetS with the two single nucleotide polymorphisms (SNPs)

127 The association of MetS with these SNPs remained significant after performi

128 R: 0.614(95%CI 0.457-0.823)] lower chance of MetS (p = 0.001) and the subjects with a serum copper >1

129 1.423 (95% CI: 1.09-1.857) higher chance of MetS (p = 0.009).

130 nsulinemia are consistent characteristics of MetS, but which of these features is the initiating insu

131 ratio (HR) (95% confidence interval [CI]) of MetS comparing the highest to the lowest quartiles of to

132 risk of 4 out of 5 individual components of MetS (abdominal obesity, hypertriglyceridemia, low high-

133 tS severity and the individual components of MetS among all groups, although the genetic correlations

134 s were associated with the key components of MetS and IR.

135 metabolic syndrome (MetS) and components of MetS.

136 blished for over 40 years, the definition of MetS warrants reconsideration in light of the substantia

137 ays a significant role in the development of MetS and T2DM in adult life.

138 eta cell responses during the development of MetS, as well as recent findings addressing the complexi

139 beta cell dysfunction in the development of MetS.

140 d the relationship between sex, diagnosis of MetS, presence of periodontitis, smoking, type of prosth

141 n epigenome-wide association study (EWAS) of MetS and its components, testing 1187 individuals of Eur

142 estigated the prevalence and risk factors of MetS there.

143 ysis was used to explore the risk factors of MetS.

144 ial influence on the various risk factors of MetS.

145 ic syndrome (MetS) and each manifestation of MetS is related to atrial fibrillation (AF) risks.

146 tool compound for long-term animal models of MetS.

147 dose-response relation between the number of MetS components and the presence of RE was demonstrated

148 lyzed the relationship between the number of MetS components and the severity of RE using the chi-squ

149 he severity of RE got worse as the number of MetS components increased (p < 0.001).

150 n non-MetS, higher HbA1c, SBP, and number of MetS components were linked to poorer recall performance

151 d progressively with an increasing number of MetS components.

152 We thus investigated the prevalence of MetS among a multi-ethnic population living in a low inc

153 The prevalence of MetS and IR was 8.2% and 17.1%, respectively.

154 In conclusion, the prevalence of MetS in low income rural adults of Xinjiang was high and

155 The prevalence of MetS in Xinjiang rural multi-ethnic adults was high.

156 tion definitions used, and the prevalence of MetS ranged from 60.86% to 67.06%.

157 The age-adjusted prevalence of MetS was 14.43%, 21.33%, 26.50%, and 19.89% based on the

158 The age-adjusted prevalence of MetS was 21.8%.

159 The prevalence of MetS was 40.1% in non-obese OAG and 66.0% in obese OAG.

160 The prevalence of MetS was higher in women and increased with age.

161 CDS) were used to measure the prevalence of MetS.

162 ctors were associated with the prevalence of MetS.

163 f plant foods is important for prevention of MetS in a population that habitually consumes plant food

164 tervention is effective in the prevention of MetS in adolescence.

165 ine lipids and their role on the progress of MetS, inflammation and oxidative stress.

166 The prevalence rates of MetS and RE were respectively 28.5 and 59.6%.

167 AD2 and TGFBR2 may contribute to the risk of MetS independently and through gene-gene interactions.

168 and LIPA genes may contribute to the risk of MetS independently as well as through gene-gene and gene

169 The long-term relative risk of MetS was significantly lower in the intervention group (

170 iets was associated with an elevated risk of MetS.

171 an effective indicator for the screening of MetS.

172 dysfunction correlates with the severity of MetS highlights the need to better understand beta cell

173 ogical activity in individuals with signs of MetS.

174 r study supports previous genetic studies of MetS, finding that lipid metabolism plays a key role in

175 slowed conduction on atria and ventricles of MetS-VLDL mice.

176 Offspring MetS risks increased with prefatherhood paternal areca n

177 prefatherhood on age of detecting offspring MetS at screen by using a Cox proportional hazards regre

178 ion, smoking status, or physical activity on MetS and its individual components.

179 e analysis of the effect of periodontitis on MetS used logistic regression analysis with adjustment f

180 e for 12 wk did not alter LDL cholesterol or MetS risk factors differently than an equal intake of re

181 re useful means of characterizing phenotypic MetS in genetic studies by minimizing racial differences

182 toff values for circulating BMP-9 to predict MetS was 56.6 ng/L.

183 Path models showed that PTSD predicted MetS (beta = .19, p < .001), which was associated with r

184 tic performance, respectively, in predicting MetS.

185 Adult Treatment Panel III criteria present (MetS+) or metabolic syndrome according to Adult Treatmen

186 s that constrain lipid metabolism to prevent MetS.

187 sign dietary interventions aimed at reducing MetS.

188 The comparison of persistent with resolved MetS and MUO did not reveal any difference in SigmaPCB c

189 o identify methylation loci linking separate MetS components, cg19693031 appears to represent a stron

190 Panel-III MetS and a sex- and race-specific MetS severity Z score among 3 large familial cohorts: th

191 Thus, results support MetS as a construct: the clustering of cardiometabolic v

192 (n = 13), subjects with metabolic syndrome (MetS) (n = 13), and diabetic hemodialysis (HD) patients

193 e of the criteria of the metabolic syndrome (MetS) [metabolic syndrome according to Adult Treatment P

194 ificantly lower rates of metabolic syndrome (MetS) along with better values of the high-density lipop

195 The relationship between metabolic syndrome (MetS) and Barrett's esophagus (BE) is still a challengin

196 The association of the metabolic syndrome (MetS) and component cardiovascular risk factors with the

197 based diets and incident metabolic syndrome (MetS) and components of MetS.

198 (VLDL) is a hallmark of metabolic syndrome (MetS) and each manifestation of MetS is related to atria

199 levels in subjects with Metabolic Syndrome (MetS) and examine the relationship between BMP-9 and con

200 the association between metabolic syndrome (MetS) and periodontitis among young adults, and also to

201 the relationship between metabolic syndrome (MetS) and periodontitis remains controversial.

202 Metabolic syndrome (MetS) and Type 2 diabetes mellitus (T2DM) increase risk

203 nd their impact on adult metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM).The longitudin

204 otomous criteria for the metabolic syndrome (MetS) appear heritable, it is not known whether MetS sev

205 vascular disease and the metabolic syndrome (MetS) are associated with serum concentrations of liver

206 The role of metabolic syndrome (MetS) as a preceding metabolic state for type 2 diabetes

207 Metabolic syndrome (MetS) doubles the risk of adverse cardiovascular events.

208 The metabolic syndrome (MetS) encompasses medical conditions such as obesity, hy

209 udies on the epidemic of metabolic syndrome (MetS) examined multi-ethnic adults in rural areas in Xin

210 Most previous studies on metabolic syndrome (MetS) examined urban and high income settings.

211 iple disorders including metabolic syndrome (MetS) features, though metabolomic markers have not been

212 Metabolic syndrome (MetS) has become a global public health problem affectin

213 Metabolic syndrome (MetS) has been associated with chronic damage to the car

214 eased risk of developing metabolic syndrome (MetS) has been associated with the APOA5, APOC1, BRAP, B

215 demic of obesity and the metabolic syndrome (MetS) has led to the realisation that new drug targets a

216 Metabolic syndrome (MetS) is a cluster of interrelated risk factors for card

217 k consensus was that the metabolic syndrome (MetS) is a complex pathophysiological state comprised of

218 The metabolic syndrome (MetS) is a constellation of risk factors that, if left u

219 Metabolic syndrome (MetS) is a major factor for the occurrence of cardiovasc

220 Metabolic syndrome (MetS) is a multifactorial disease cluster that consists

221 Metabolic syndrome (MetS) is one of the risk factors for all causes of morta

222 Metabolic syndrome (MetS) is thought to influence several autoimmune disease

223 kers associated with the Metabolic Syndrome (MetS) may be affected by interactions between the APOE g

224 viduals with established metabolic syndrome (MetS) or diabetes identifies CHD and ASCVD prognostic in

225 Metabolic syndrome (MetS) represents a cluster of metabolically related symp

226 nut chewing on offspring metabolic syndrome (MetS) risk in humans, on obesity and diabetes mellitus e

227 age 16/17 y; and with a metabolic syndrome (MetS) score and its components at age 16/17 y.

228 Metabolic syndrome (MetS) was defined with the joint IDF/AHA/NHBLI standard.

229 The associations of the metabolic syndrome (MetS) with intraocular pressure and primary open angle g

230 Metabolic syndrome (MetS), a complex cluster of cardiovascular risk factors,

231 Metabolic syndrome (MetS), defined by a constellation of cardiometabolic pat

232 ty (WMH) development: in metabolic syndrome (MetS), higher WMH load is often reported but the relatio

233 s in older subjects with metabolic syndrome (MetS).

234 of patients affected by metabolic syndrome (MetS).

235 s a manifestation of the metabolic syndrome (MetS).

236 al ingredients targeting metabolic syndrome (MetS).

237 ing various hallmarks of metabolic syndrome (MetS).

238 ults (aged 55-75 y) with metabolic syndrome (MetS).

239 and risk factors for the metabolic syndrome (MetS).

240 ndividuals with signs of metabolic syndrome (MetS).

241 on its relationship with metabolic syndrome (MetS).

242 opment of age-associated metabolic syndrome (MetS).

243 is often associated with metabolic syndrome (MetS).

244 iodontitis is associated with MetS, and that MetS prevalence is related to severe periodontitis.

245 In sum, this study demonstrated that MetS was associated with increased periodontal inflammat

246 Electrocardiograms demonstrated that MetS-VLDL induced prolongation of P wave (P = 0.041), PR

247 We hypothesized that MetS and inflammation may trigger the development of vas

248 We showed that MetS exacerbates group 2 PH.

249 This study suggests that MetS is significantly related to the presence and the se

250 The MetS was associated with an increased incidence of MCI a

251 the core of clinical strategies against the MetS is weight loss, induced by bariatric surgery, lifes

252 MetS of 0.24 (95% CI, 0.11-0.36) and for the MetS severity score of 0.50 (95% CI, -0.05 to 0.99).

253 narrowed when assessing heritability of the MetS severity score (JHS 0.52 [95% CI, 0.38, 0.66] and P

254 ignificantly associated with features of the MetS, including arterial hypertension [P = 0.028; OR: 2.

255 ng individuals with diabetes mellitus or the MetS with or without MCI is a promising approach in earl

256 current, and future efforts of targeting the MetS by pharmacological agents.

257 d with cortical thickness indirectly through MetS.

258 ify the molecular mechanisms linking PTSD to MetS and effective interventions to reduce PTSD-related

259 n order to understand and successfully treat MetS and associated conditions such as insulin resistanc

260 The association between risk variables, MetS, and periodontitis was tested through univariate an

261 sed risk of MCI progression to dementia were MetS (HR, 4.25; 95% CI, 1.29-14.00), diabetes mellitus (

262 with an increased risk of incident MCI were MetS (hazard ratio [HR], 1.46; 95% CI, 1.02-2.09), centr

263 iodontitis in the final logistic model were: MetS (odds ratio [OR] = 2.02; P = 0.003), number of teet

264 When MetS and periodontitis were set as observed variables in

265 Nevertheless, when MetS and periodontitis were treated as observed variable

266 S) appear heritable, it is not known whether MetS severity as assessed by a continuous MetS score is

267 s with diabetes (135 ASCVD events), 115 with MetS (175 ASCVD events), and 157 with neither (250 ASCVD

268 , dietary FA intervention in 442 adults with MetS (LIPGENE study).

269 ed over time in overweight/obese adults with MetS.

270 iation with food intake at baseline and with MetS at endpoint.

271 ssed whether these genes are associated with MetS and its individual components independently and/or

272 r 1 (TGFBR1), and TGFBR2 are associated with MetS and its individual components independently, throug

273 ntrations were significantly associated with MetS even after controlling for anthropometric variables

274 uggest that periodontitis is associated with MetS, and that MetS prevalence is related to severe peri

275 io (WHtR) were significantly associated with MetS, independent of ethnic, age, and other covariates.

276 serum concentrations in MetS+ compared with MetS- subjects (median: 58% compared with 43% and 31% co

277 ht; P = 0.01) but not in MetS+ compared with MetS- subjects.

278 in this model and are present in humans with MetS.

279 Samples comprised 122 individuals with MetS (cases) and 366 controls.

280 Our novel data suggest that individuals with MetS may benefit from personalized dietary interventions

281 is was reported, being that individuals with MetS presented worse periodontal status and higher preva

282 lenging subjects (381 older individuals with MetS) with solutions (5 concentrations) of the basic tas

283 n the differences in association of OAG with MetS and its components according to obesity status.

284 ha-tocopherol status.Adults (healthy or with MetS; n = 10/group) completed a double-blind, crossover

285 2 h.During the first 24 h, participants with MetS compared with healthy adults excreted 41% less alph

286 A total of 362 newly diagnosed patients with MetS along with healthy controls were recruited for this

287 rol adequacy, especially in populations with MetS-associated hepatic dysfunction that likely impairs

288 m zinc, copper and zinc to copper ratio with MetS in normal weight subjects.

289 During 2012-2013, 175 subjects with MetS and 226 healthy controls underwent ECG recordings o

290 y, MSE), were compared between subjects with MetS and controls.

291 d waist circumference in older subjects with MetS and identified some taste-related SNPs.

292 red with the healthy controls, subjects with MetS had significantly reduced HRV, including SDNN and p

293 y improved risk classification in those with MetS and diabetes, even if diabetes duration was longer

294 etes, 0.22 (95% CI, 0.09-0.35) in those with MetS, and 0.25 (95% CI, 0.15-0.35) in those with neither

295 healthy adults is higher than in those with MetS, thereby suggesting that the latter group has incre

296 ic indicators to identify men and women with MetS.

297 and Ansung, South Korea (2001-2016) without MetS and related chronic diseases at baseline.

298 compared with normal BMI individuals without MetS.

299 -implantitis, compared with subjects without MetS, where 26.3% of implants showed peri-implantitis an

300 Subjects with- vs. without MetS tended to have greater addiction severity.