ライフサイエンスコーパス: MetS

1 MetS abolished SERCA activation by GLP-1 receptor agonis

2 MetS defined by 2 criteria separately showed a similar a

3 MetS is associated with significant alterations in heart

4 MetS offspring risk for paternal smoking increased dosew

5 MetS participants had lower d6-alpha-tocopherol AUC from

6 MetS patients are strongly exposed to polypharmacy; howe

7 MetS severity seems highly heritable among whites and bl

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

9 MetS subjects have significantly lower complexity index

10 MetS subjects with a low to medium HOMA-IR exhibited red

11 MetS volunteers (n = 22) and healthy, matched controls (

12 MetS was defined according to National Cholesterol Educa

13 MetS was defined by the Joint Interim Statement criteria

14 MetS was diagnosed using the criteria defined in the Adu

15 MetS was induced in 20 swine by 6 months' feeding of a h

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

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

18 Five-hundred-seventy Saudi individuals (285 MetS and 285 controls) were enrolled in this cross-secti

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

20 h AF (age 61+/-9.6 years; persistent AF 64%; MetS 54%).

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

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

23 All MetS criteria decreased independent of diet composition

24 d report a novel variant associated with all MetS components in African Americans.

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

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

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

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

29 similar association with CA in general, and MetS defined by both the IDF and ATP III showed consiste

30 ble-blind study was conducted in healthy and MetS adults (n = 10/group) who ingested encapsulated hex

31 possibility of an association between HS and MetS.DESIGN, SETTING, AND PARTICIPANTS Cross-sectional p

32 pulation- and hospital-based study of HS and MetS.We identified 32 patients with physician-verified H

33 e their relationship with dietary intake and MetS.

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

35 nonalcoholic fatty liver disease (NAFLD) and MetS.

36 and systemic CLGI and associated obesity and MetS.

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

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

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

40 associations between the cluster scores, and MetS and each component, including hypertension, hypertr

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

42 ust accurately identify those at risk before MetS develops and must recognize subtypes and stages of

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

44 An association between MetS and supragingival plaque requires further investiga

45 Cross-sectional associations between MetS and periodontitis were examined in 657 postmenopaus

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

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

48 of dairy fat provided by milk beverages, but MetS participants had lower estimated d6-alpha-tocophero

49 tems biology methods identified 17 candidate MetS genes.

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

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

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

53 Conversely, MetS subjects without IR may be more sensitive to the de

54 50 obese patients with MS who also developed MetS.

55 lar chow, indicating that the mice developed MetS.

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

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

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

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

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

61 respectively) control-fed rats, destined for MetS, had a distinct metabolome at weaning (randomForest

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

63 nt of functional ingredients from lentil for MetS management.

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

65 The ideal patient care model for MetS must accurately identify those at risk before MetS

66 om New Zealand obese (NZO) mice, a model for MetS, compared with C57 Black 6 JAX (C57BL/6J) mice oste

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

68 er dietary alpha-tocopherol requirements for MetS adults.

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

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

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

72 associated with higher likelihood of having MetS.

73 However, MetS or its components exhibited no significant associat

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

75 76] and adulthood (d160; n = 12) to test if MetS is preceded by alterations in the metabolome.

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

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

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

79 asize either animal or plant protein improve MetS criteria similarly.

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

81 fibrillation and ventricular arrhythmias in MetS.

82 The primary endpoint was change in MetS criteria.

83 odel for investigation of retinal changes in MetS/T2D with convincing advantages over the commonly us

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

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

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

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

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

89 erstand the potential mechanisms involved in MetS-boosted tissue inflammation, our in vitro studies s

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

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

92 phisms and FA status on metabolic markers in MetS.

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

94 481 ng/g lipid weight; P = 0.01) but not in MetS+ compared with MetS- subjects.

95 ls are needed to clarify the role of nuts in MetS prevention and treatment.

96 However, mechanisms of AF recurrence in MetS remain unclear.

97 palmitic acid may play an important role in MetS-associated periodontitis by enhancing LPS-induced e

98 tion did not alter any of the plasma SPMs in MetS and control subjects.

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

100 Incident MetS was defined by the NCEP-ATP III criteria.

101 During the 23-year follow-up, 878 incident MetS cases were identified.

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

103 Of the individual MetS components, the intervention decreased risk of high

104 In this study, we induced MetS in C57BL/6 mice by feeding them high-fat diet (HFD)

105 1082639 and TGFBR2 rs3773651 SNPs influenced MetS.

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

107 Markers of later-in-life MetS included citric acid, glucosamine, myoinositol, and

108 , IUGR lineage ENS-fed rats did not manifest MetS, with significantly lower body weight (p160: 410 g)

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

110 ay abrogate IUGR-conferred multigenerational MetS.

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

112 17 that is causally associated with multiple MetS-related traits and found RGD1562963, a gene regulat

113 Neither MetS nor its other remaining MetS components were associ

114 This new MetS care model introduces both affirmed and emerging co

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

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

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

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

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

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

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

122 Panel III (ATP III) and single components of MetS, including anthropometric factors, blood pressure,

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

124 e independently related to the expression of MetS at the moment of surgery.One year after RYGB, there

125 estigated the prevalence and risk factors of MetS there.

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

127 in resistance (IR) is the central feature of MetS.

128 prospectively examined for the incidence of MetS and its five components from 1987-88 to 2010-11.

129 m was inversely associated with incidence of MetS as well as its blood lipid components.

130 longitudinally associated with incidence of MetS in American young adults.

131 A composite index of MetS as defined by the International Diabetes Federation

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

133 AT loss and has modest effects on markers of MetS.

134 ive and Lyon normotensive rats are models of MetS sensitivity and resistance, respectively.

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

136 Weight loss was the primary modifier of MetS resolution in our study population regardless of pr

137 d progressively with an increasing number of MetS components.

138 The greater the number of MetS criteria present, the greater the reduction was in

139 sheds light on the intricate pathogenesis of MetS and demonstrates that systems biology with high-thr

140 erent risk categories for the persistence of MetS (area under the curve = 0.848).

141 independently related to the persistence of MetS.

142 a significant decrease in the prevalence of MetS (63.3%-10%; P < 0.001) and in each of its component

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

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

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

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

147 e ages of 15 and 20 years, the prevalence of MetS varied between 6.0% and 7.5% in participants in the

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

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

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

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

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

153 ctors were associated with the prevalence of MetS.

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

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

156 A relation of MetS to periodontitis has been reported.

157 core can be used to predict the remission of MetS after RYGB with high accuracy.

158 multivariable analysis for the remission of MetS identified that only fasting glucose levels (OR = 1

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

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

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

162 an effective indicator for the screening of MetS.

163 ogical activity in individuals with signs of MetS.

164 ps and must recognize subtypes and stages of MetS to more effectively direct prevention and therapies

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

166 Offspring MetS risks increased with prefatherhood paternal areca n

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

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

169 o the quantity and quality of dietary fat on MetS risk factors, which suggests that targeted and pers

170 n the quality and quantity of dietary fat on MetS risk factors.

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

172 ompared with plant) and amount of protein on MetS criteria.

173 ccompany heritable IUGR, precede adult-onset MetS, and are partially amenable to dietary intervention

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

175 e replicated with the use of other pediatric MetS definitions.

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

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

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

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

180 Indicative of developmentally programmed MetS, adult F2, formerly IUGR rats, were obese (621 vs.

181 sign dietary interventions aimed at reducing MetS.

182 Neither MetS nor its other remaining MetS components were associated with a particular cluste

183 Insulin-resistant MetS subjects with more metabolic complications responde

184 Insulin-resistant MetS subjects with the highest HOMA-IR improved IR, with

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

186 Significant associations between single MetS components and CA, except for reduced high-density

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

188 lel, controlled, dietary intervention study, MetS subjects (n = 472) from 8 European countries classi

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

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

191 of those suffering from metabolic syndrome (MetS) affects this response is not established.

192 association between the metabolic syndrome (MetS) and chronic inflammatory diseases, such as psorias

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

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

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

196 nut consumption and the metabolic syndrome (MetS) and its components.

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

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

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

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

201 different definitions of metabolic syndrome (MetS) are differently associated with colorectal adenoca

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

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

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

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

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

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

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

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

210 effects of dairy fat and metabolic syndrome (MetS) health status on alpha-tocopherol pharmacokinetics

211 r for the development of metabolic syndrome (MetS) including diabetes and associated health complicat

212 Metabolic syndrome (MetS) is a cluster of cardiovascular risk factors includ

213 The metabolic syndrome (MetS) is a collection of co-occurring complex disorders

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

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

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

217 The metabolic syndrome (MetS) is associated with a chronic low-grade inflammator

218 studies have shown that metabolic syndrome (MetS) is associated with increased risk of developing pe

219 The prevalence of metabolic syndrome (MetS) is rising alarmingly in the Saudi Arabian populati

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

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

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

223 Adolescent metabolic syndrome (MetS) predicts type 2 diabetes mellitus and subclinical

224 ating chromium levels to metabolic syndrome (MetS) risk are lacking.

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

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

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

228 Metabolic syndrome (MetS), a complex cluster of risk factors for chronic dis

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

230 Metabolic syndrome (MetS), following intrauterine growth restriction (IUGR),

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

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

233 ndividuals with signs of metabolic syndrome (MetS).

234 rendering risk of adult metabolic syndrome (MetS).

235 ded for the treatment of metabolic syndrome (MetS).

236 al ingredients targeting metabolic syndrome (MetS).

237 blation in patients with metabolic syndrome (MetS).

238 ing various hallmarks of metabolic syndrome (MetS).

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

240 We conclude that MetS confers vascular resistance to GLP-1 receptor agoni

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

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

243 role in periodontitis, we hypothesized that MetS enhances LPS-induced periodontal inflammation and a

244 Recent studies suggest that MetS is a risk factor for Alzheimer disease (AD).

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

246 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).

247 ion that was significantly attenuated in the MetS (P < 0.05).

248 Additional studies in the MetS are required to determine whether SPMs affect the a

249 f SPMs in men and women with features of the MetS and in healthy matched control subjects in response

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

251 Components of the MetS such as obesity, low HDL and T2DM were associated w

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

253 Participants who had complete data on the MetS components (waist circumference, blood pressure, tr

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

255 d with cortical thickness indirectly through MetS.

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

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

258 netic determinants and mechanisms underlying MetS, an F2 intercross between Lyon hypertensive and Lyo

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

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

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

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

263 Thirty-nine obese adolescents with MetS and 51 matched adolescents without MetS received co

264 Obese adolescents with MetS had significant reductions in retinal arteriolar di

265 prior report of nondiabetic adolescents with MetS, we also uncovered cerebral WM microstructural dama

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

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

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

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

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

271 We aimed to identify factors associated with MetS in morbidly obese patients and predictors of its re

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

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

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

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

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

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

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

279 2 h.During the first 24 h, participants with MetS compared with healthy adults excreted 41% less alph

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

281 ia to periodontal bone loss in patients with MetS remains unclear.

282 L) were significantly worse in patients with MetS than healthy participants.

283 areas were observed in 46% of patients with MetS versus 8.2% patients without MetS ; P<0.0001.

284 uggesting a similar process in patients with MetS.

285 ould be regularly conducted in patients with MetS.

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

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

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

289 valuated the effect of nuts on subjects with MetS and found that they may have benefits in some compo

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

291 coronary artery disease (CAD) in swine with MetS.

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

293 mpared with healthy participants, those with MetS had lower (P < 0.05) baseline plasma alpha-tocopher

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 Volunteers with MetS had reduced plasma concentrations of the precursors

297 ic indicators to identify men and women with MetS.

298 lar diameter relative to adolescents without MetS (mean [SD] central retinal arteriolar equivalent, 1

299 with MetS and 51 matched adolescents without MetS received comprehensive endocrine, neuropsychologica

300 ients with MetS versus 8.2% patients without MetS ; P<0.0001.