ライフサイエンスコーパス: glucose tolerance

1 n sensitive, insulin resistant, and impaired glucose tolerance).

2 ated in some low-BMI individuals with normal glucose tolerance.

3 uded 256 with diabetes and 133 with a normal glucose tolerance.

4 e common hepatic artery (CHADN) in improving glucose tolerance.

5 ls, accompanied by a striking improvement in glucose tolerance.

6 y and contribute importantly to postprandial glucose tolerance.

7 n via an anti-alpha-klotho antibody impaired glucose tolerance.

8 neither daily chow intake nor body weight or glucose tolerance.

9 males treated with PCB-77 exhibited impaired glucose tolerance.

10 osure-induced insulin resistance and greater glucose tolerance.

11 types such as reduced adiposity and improved glucose tolerance.

12 ht, fat mass, and insulin level and improved glucose tolerance.

13 more, are hyperlipidemic, and have impaired glucose tolerance.

14 sis, liver injury, and fibrosis and improved glucose tolerance.

15 modest enhancement in insulin secretion and glucose tolerance.

16 H2Ab1 which, in contrast, revealed improved glucose tolerance.

17 ain and plasma insulin levels and to improve glucose tolerance.

18 5A show reduced dietary intake and preserved glucose tolerance.

19 enhanced insulin release and restored normal glucose tolerance.

20 r1 knockout mice was accompanied by improved glucose tolerance.

21 insulin sensitivity, insulin secretion, and glucose tolerance.

22 body-positive at-risk children with impaired glucose tolerance.

23 ntly in IFG, but not in subjects with normal glucose tolerance.

24 es, improved insulin sensitivity, and better glucose tolerance.

25 c gluconeogenesis without affecting systemic glucose tolerance.

26 human paired box gene PAX6 lead to impaired glucose tolerance.

27 with markers of lipid oxidation and reduced glucose tolerance.

28 luding blood glucose levels, and insulin and glucose tolerance.

29 sedentary mice reproduces the improvement of glucose tolerance.

30 n mRNA in vivo but has only minor effects on glucose tolerance.

31 pression of gluconeogenic genes and impaired glucose tolerance.

32 ) restores systemic insulin sensitivity and glucose tolerance.

33 lic syndrome, including obesity and impaired glucose tolerance.

34 d exhibited improved insulin sensitivity and glucose tolerance.

35 defect in insulin action to maintain normal glucose tolerance.

36 atosis, lowered insulin levels, and improved glucose tolerance.

37 g significant weight loss, VSG also improves glucose tolerance.

38 ed a high-fat diet, resulting in ameliorated glucose tolerance.

39 ventions, except VSG, significantly improved glucose tolerance.

40 metrics of body weight, hyperlipidemia, and glucose tolerance.

41 t-diet-induced obesity and markedly improved glucose tolerance.

42 eta-cell mass but are insufficient to impair glucose tolerance.

43 ave previously been associated with impaired glucose tolerance(2), insulin resistance(3) and mitochon

44 t present with low blood pressure and normal glucose tolerance(4).

45 nts with coronary heart disease and impaired glucose tolerance, acarbose did not reduce the risk of m

46 e preconception/gestation group had worsened glucose tolerance and an increase in resident (CD11c(-))

47 fail to expand adaptively and show impaired glucose tolerance and beta-cell dysfunction.

48 l littermates, knockout mice showed impaired glucose tolerance and circulating leptin, GLP-1, and ins

49 e administration of recombinant IF1 improved glucose tolerance and down-regulated blood glucose level

50 tion, not sphingomyelin hydrolysis, improved glucose tolerance and dyslipidemia.

51 differences in body composition, weight, and glucose tolerance and estimates of IS.

52 , including circulating triglyceride levels, glucose tolerance and FGF21 levels.

53 l bile acid (BA) metabolism improve systemic glucose tolerance and hepatic metabolic homeostasis are

54 expression in islets from donors with normal glucose tolerance and hyperglycemia (including T2D).

55 he inflammatory impact of a high fat diet on glucose tolerance and insulin resistance.

56 ent mice have been shown to exhibit impaired glucose tolerance and insulin secretion, but the underly

57 Mice lacking TrkB.T1 show impaired glucose tolerance and insulin secretion.

58 wever, the Fndc5 mutant mice exhibit reduced glucose tolerance and insulin sensitivity and have lower

59 ptor signaling were associated with improved glucose tolerance and insulin sensitivity as well as wit

60 observed, Lin28aKI(VMH) mice showed improved glucose tolerance and insulin sensitivity compared with

61 cumulate body fat and develop impairments in glucose tolerance and insulin sensitivity despite develo

62 Glucose tolerance and insulin sensitivity improved (P <

63 PAHSAs reduce ambient glycemia and improve glucose tolerance and insulin sensitivity in insulin-res

64 rt the first evidence for initially improved glucose tolerance and insulin sensitivity in response to

65 ntrol and LIMP2 KO mice maintained a similar glucose tolerance and insulin sensitivity up to 6 months

66 In HFD-fed obese mice systemic glucose tolerance and insulin sensitivity were improved

67 ly, ATM Exos obtained from lean mice improve glucose tolerance and insulin sensitivity when administe

68 ron-specific deletion, had impaired systemic glucose tolerance and insulin sensitivity when exposed t

69 ts mice from diet-induced obesity, improving glucose tolerance and insulin sensitivity with reduced s

70 t, Foxp3creInsrfl/fl mice exhibited improved glucose tolerance and insulin sensitivity, effects assoc

71 tions, AdipoGR-KO mice exhibited an improved glucose tolerance and insulin sensitivity.

72 ipocyte PPARg cistrome resulting in impaired glucose tolerance and insulin sensitivity.

73 diet-induced obesity and improves whole-body glucose tolerance and insulin sensitivity.

74 In conclusion, glucose tolerance and insulin-stimulated glucose uptake

75 who were healthy other than having impaired glucose tolerance and obesity, were enrolled and 25 comp

76 test at baseline and after 2 years to assess glucose tolerance and oral beta-cell function (oDI(cpep)

77 ckout and NOX4betaKO mice exhibited impaired glucose tolerance and peripheral insulin resistance.

78 ne pancreatic beta-cells results in impaired glucose tolerance and reduced insulin secretion, both in

79 mutant mice displayed significantly impaired glucose tolerance and reduced insulin sensitivity when m

80 ng that even 1 night of shift work decreases glucose tolerance and that circadian disruption is linke

81 these associations among adults with normal glucose tolerance and with prediabetes.

82 -10 g/L (95% CI: -12.90, -7.10 g/L; impaired glucose tolerance) and -6 g/L (95% CI: -8.47, -3.53 g/L;

83 LD with impaired fasting glucose or impaired glucose tolerance) and were randomly assigned into exerc

84 lycaemia in the postprandial state (impaired glucose tolerance) and/or fasting state (impaired fastin

85 nists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicki

86 uced inflammation in fat and liver, improved glucose tolerance, and improved systemic insulin sensiti

87 normoglycemia and vascularization, improved glucose tolerance, and increased insulin content.

88 , culminating in reduced energy expenditure, glucose tolerance, and insulin sensitivity.

89 was sufficient to increase running distance, glucose tolerance, and mitochondrial activity similar to

90 is associated with higher body fat, impaired glucose tolerance, and reduced insulin secretion in firs

91 uman plasma, decreases food intake, improves glucose tolerance, and stimulates GPR119-dependent GLP-1

92 -known apelin effects, such as angiogenesis, glucose tolerance, and vasodilatation.

93 temically to promote insulin sensitivity and glucose tolerance; as a class, these lipids are referred

94 inhibition showed a transient improvement in glucose tolerance at 5 weeks of HFD whereas it lost this

95 We assessed oral glucose tolerance at baseline and after 4 weeks of high-

96 sified as having either diabetes or a normal glucose tolerance at enrollment.

97 s a compensatory response to maintain normal glucose tolerance but is impaired in individuals with T2

98 t of type 2 diabetes in people with impaired glucose tolerance, but whether this leads subsequently t

99 CHADN improved glucose tolerance by ~60% in part because of enhanced in

100 trains of mice which differ in adiposity and glucose tolerance, C57BL/6J and WSB/EiJ.

101 ess to GLP1R agonists, resulting in improved glucose tolerance, cAMP production, and insulin secretio

102 gh glucose tolerance levels, confirming that glucose tolerance can be achieved by the substitution of

103 icipants (N = 973) with different weight and glucose tolerance categories were recruited.

104 3 months postsurgery and the improvement in glucose tolerance caused by CHADN continued.

105 fcantly lesser effect or no effect at all on glucose tolerance compared to rGDF11, consistent with da

106 reated participants (63.8%) developed normal glucose tolerance compared with 8 placebo-treated partic

107 of IR, IRS-1, and Akt in muscle and improved glucose tolerance compared with controls.

108 educe serum cholesterol levels, and increase glucose tolerance compared with mice on the same diet fe

109 dams produced female offspring with impaired glucose tolerance compared with offspring of chow-fed da

110 sulted in decreased beta cell mass, impaired glucose tolerance, defective insulin secretion, and incr

111 festyle intervention in people with impaired glucose tolerance delayed the onset of type 2 diabetes a

112 including increased meal frequency, impaired glucose tolerance, delayed gastric emptying, and increas

113 ads to increased insulin levels and improved glucose tolerance, dependent upon glucagon-like peptide

114 lt life and allows the maintenance of normal glucose tolerance despite insulin resistance.

115 6a-(KGKY-knockin) mice demonstrated improved glucose tolerance, despite impaired insulin sensitivity

116 ats housed at 5 degrees C for 28 h, and yet, glucose tolerance did not change, owing to a doubling of

117 While glucose tolerance did not differ between genotypes at ba

118 heir pancreatic pericytes exhibited impaired glucose tolerance due to compromised beta-cell function

119 evented weight regain and resulted in better glucose tolerance during a high-fat diet-induced regain

120 7 administration to obese male mice impaired glucose tolerance during weight loss.

121 ned the effects of statins on hyperglycemia, glucose tolerance, fatty acid accumulation and insulin s

122 2 (-/-) mice exhibited greater impairment in glucose tolerance following streptozotocin exposure than

123 nd categorized into quartiles) with impaired glucose tolerance (IGT) and gestational diabetes mellitu

124 n is central to the pathogenesis of impaired glucose tolerance (IGT) and type 2 diabetes.

125 orize up to 40% of individuals with impaired glucose tolerance (IGT) or frank diabetes based on the r

126 a large group of subjects with NGT, impaired glucose tolerance (IGT), and T2DM.

127 timing and type 2 diabetes (T2D) or impaired glucose tolerance (IGT), with and without adjustment for

128 ed with intervention in people with impaired glucose tolerance (IGT).

129 evels are observed in subjects with impaired glucose tolerance (IGT).

130 l glucose tolerance (NGT; n = 190), impaired glucose tolerance (IGT; n = 209), and diabetes (n = 230)

131 al glucose tolerance [NGT], 57 with impaired glucose tolerance [IGT], and 207 with type 2 diabetes me

132 independently to IF1-mediated improvement of glucose tolerance impairment.

133 ct of statins on (a) whether they can worsen glucose tolerance in a high sucrose fed animal model and

134 y weight by 3-17% and significantly improved glucose tolerance in aged mice fed a chow (~30% vs. sali

135 Antibody injection improved glucose tolerance in D734A INSR-expressing mice and redu

136 ping syndrome, and potentially for improving glucose tolerance in diabetes mellitus/metabolic syndrom

137 ignificantly lower blood glucose and improve glucose tolerance in diet-induced obese mice.

138 ke BAT phenotype is not linked to heightened glucose tolerance in female mice.

139 -like BAT phenotype is coupled with enhanced glucose tolerance in female mice.

140 perimentally confirm the structural basis of glucose tolerance in GH1 beta-glucosidases but also demo

141 results provide new clues to understand the glucose tolerance in GH3 beta-glucosidases.

142 in either group, but did transiently improve glucose tolerance in high fat-fed mice.

143 NAD(+) levels without affecting fat mass or glucose tolerance in HNKO or WT animals.

144 anied with inflammation but does not disrupt glucose tolerance in lean mice, and 3) exercise and low-

145 lin-GHSR axis mediating insulin secretion or glucose tolerance in lean, chow-fed adult mice.

146 ult mice greatly impairs insulin release and glucose tolerance in mice fed with a calorie-rich diet.

147 GB-IL(dist) improves oral glucose tolerance in mice made obese with high-fat diet.

148 e and that circadian disruption is linked to glucose tolerance in mice.

149 2, but not whole-body PAK1 knockout, impairs glucose tolerance in mice.

150 se-stimulated insulin secretion and improved glucose tolerance in NOD mice.

151 ce, and 3) exercise and low-fat diet improve glucose tolerance in obese mice but these effects do not

152 ia chronic mild cold stress does not improve glucose tolerance in obese mice, 2) silencing of the Pnp

153 h fat diet-impaired placental efficiency and glucose tolerance in offspring.

154 GB-IL induced weight loss and improved oral glucose tolerance in Tgr5(-/-), but not Fxr(Delta/E) mic

155 acid synthase (Fas) expression and improves glucose tolerance in the adult offspring.

156 sion of sEVs and determined their effects on glucose tolerance in vivo and islets and skeletal muscle

157 L-cell number and GLP-1 levels and improved glucose tolerance in vivo.

158 me 7 conferred weight reduction and improved glucose tolerance in znt7-KO male mice.

159 nd DLL4 in adult beta-cells display improved glucose tolerance, increased glucose-stimulated insulin

160 in females and was associated with improved glucose tolerance, increased metabolism, energy expendit

161 y functions as a 'glucose sink' and improves glucose tolerance independently of body weight loss.

162 rted into four groups (lean and obese normal glucose tolerance, insulin sensitive, insulin resistant,

163 ct, at 0.125 ug ABA/kg body weight, improves glucose tolerance, insulin sensitivity and fasting blood

164 ted from the plasma of trained mice improves glucose tolerance, insulin sensitivity, and decreases pl

165 e association between the rs4343 variant and glucose tolerance is modulated by dietary fat intake.

166 ity, even in the absence of an impairment of glucose tolerance, is associated with lowering of hepati

167 normal intrahepatic triglyceride (IHTG) and glucose tolerance (lean-NL; n = 14), (b) obese subjects

168 The tailored enzyme displayed high glucose tolerance levels, confirming that glucose tolera

169 sity and liver triglycerides, with decreased glucose tolerance, liver NAD(+) levels and citrate synth

170 old Swedish women with different GTS [normal glucose tolerance (NGT; n = 190), impaired glucose toler

171 Subjects (104 with normal glucose tolerance [NGT], 57 with impaired glucose tolera

172 Glucose tolerance normalized in one abnormal glucose tol

173 14), (b) obese subjects with normal IHTG and glucose tolerance (obese-NL; n = 24), and (c) obese subj

174 During weight loss, PCB-77 impaired glucose tolerance of males.

175 9(-/-) mice displayed normal body weight and glucose tolerance on a regular chow (RC) diet.

176 , increased energy expenditure, and improved glucose tolerance on chow, high-fat, and FFDs.

177 estyle interventions in people with impaired glucose tolerance on the incidence of diabetes, its comp

178 glucose, plasma insulin or glucagon levels, glucose tolerance or arginine tolerance.

179 diet presented no significant difference in glucose tolerance or insulin secretion compared with mic

180 ns were similar for participants with normal glucose tolerance or prediabetes.

181 extracellular vesicles in people with normal glucose tolerance or type 2 diabetes.

182 uals with impaired fasting glucose, impaired glucose tolerance, or both [22 women, 17 men; mean +/- S

183 s on extent of upregulation of FAHFA levels, glucose tolerance, or insulin sensitivity in mice, indic

184 male/six female; seven normal/five abnormal glucose tolerance (oral glucose tolerance test 1-h gluco

185 ose on body weight, ingestive behaviors, and glucose tolerance over a 12-wk intervention in adults (1

186 mirabegron treatment included improved oral glucose tolerance (P < 0.01), reduced hemoglobin A1c lev

187 Slowed gastric emptying and improved oral glucose tolerance produced by a nanomolar-potency inhibi

188 ngagement on ILC2s significantly ameliorates glucose tolerance, protects against insulin-resistance o

189 Glucose tolerance reclassification after delivery is rec

190 However, glucose tolerance remained normal without insulin resist

191 olar bone volume changes and increased BW or glucose tolerance response.

192 ght-independent improvements in glycemia and glucose tolerance secondary to augmented insulin respons

193 study was to explore how diet is related to glucose tolerance status (GTS) and to future development

194 Glucose tolerance status and prediabetes were defined ac

195 covariates, and missing data for measures of glucose tolerance status at follow-up visits were exclud

196 eline, missing data for baseline measures of glucose tolerance status, missing data for baseline homo

197 opositivity and different BMI categories, or glucose tolerance status.

198 Glucose tolerance normalized in one abnormal glucose tolerance subject.

199 lin-modified, frequently sampled intravenous glucose tolerance test (FSIGT), we estimated hepatic ver

200 object recognition, grip strength, rotarod, glucose tolerance test (GTT) and insulin tolerance test

201 ield test, ABA paradigm, and intraperitoneal glucose tolerance test (IGTT).

202 diac structure and function, intraperitoneal glucose tolerance test (IPGTT) for glucose metabolism, i

203 lin concentrations during an intraperitoneal glucose tolerance test (ipGTT).

204 ose tolerance test (OGTT) and an intravenous glucose tolerance test (IVGTT) were performed between th

205 insulin-clamp (40 mU/m(2) . min) and an oral glucose tolerance test (OGTT) (75 g) on separate days.

206 d women aged 50-65 were subjected to an oral glucose tolerance test (OGTT) and a mixed-meal test (MMT

207 In this prospective clinical study, an oral glucose tolerance test (OGTT) and an intravenous glucose

208 , hemoglobin A1C, body composition, the oral glucose tolerance test (oGTT) and the Sweet Taste Test (

209 (GDM) is conventionally confirmed with oral glucose tolerance test (OGTT) in 24 to 28 weeks of gesta

210 Diagnosis is usually performed using an oral glucose tolerance test (OGTT), although a non-fasting, g

211 ted controls were evaluated using a 2-h oral glucose tolerance test (OGTT), with 7 samples of plasma

212 lin required to clear glucose during an oral glucose tolerance test (OGTT).

213 k diabetes based on the rarely utilized oral glucose tolerance test (OGTT).

214 normal/five abnormal glucose tolerance (oral glucose tolerance test 1-h glucose >=155 and 2-h glucose

215 ual intravenous [6,6-2H2]-, oral 13C-labeled glucose tolerance test and a polysomnographic recording

216 amily history of T2DM (FH+) received an oral glucose tolerance test and two-step hyperglycemic clamp

217 diate hyperglycaemia defined without an oral glucose tolerance test as impaired fasting glucose (IFG)

218 Participants underwent an oral glucose tolerance test at baseline and after 2 years to

219 SG or RYGB were studied with an intravenous glucose tolerance test before surgery and at 5-12% weigh

220 Nemos) with sham stimulation during an oral glucose tolerance test in a randomized, single-blind, cr

221 On the basis of the glucose tolerance test known to be a clinically relevant

222 A 2-hour oral glucose tolerance test of >=140 mg/dL remains the most c

223 se metabolism observed in an intraperitoneal glucose tolerance test on male C57BL/6J mice supported t

224 HFD worsened glucose tolerance test results and caused increased adip

225 ocyte size; for mice on an HFD, SAP improved glucose tolerance test results and reduced adipocyte siz

226 Finally, an intravenous glucose tolerance test revealed higher insulin sensitivi

227 The glucose tolerance test showed major improvement of the g

228 irst-phase insulin release on an intravenous glucose tolerance test that was higher than the threshol

229 sulinemic-euglycemic clamp and a 3-hour oral glucose tolerance test were performed to evaluate insuli

230 in, 30 min before and during the entire oral glucose tolerance test with stimulation cycles of 30 s o

231 curve for glucose, and insulin from an oral glucose tolerance test) analysed in the intention-to-tre

232 d aSAT, S(I) (frequently sampled intravenous glucose tolerance test), body composition (dual-energy X

233 ecognition is crucial, and the modified oral glucose tolerance test, but not gastric emptying testing

234 During the oral glucose tolerance test, overfeeding significantly increa

235 s score was combined with results of an oral glucose tolerance test, the AUC reached 82.4% (80.9-83.9

236 ion for blood and urine sampling and an oral glucose tolerance test.

237 underwent hemoglobin A1c testing and an oral glucose tolerance test.

238 after surgery, as assessed by an intravenous glucose tolerance test.

239 phenotypes were derived from a 5-point oral glucose tolerance test.

240 al of diabetes; mice were then given an oral glucose tolerance test.

241 Insulin sensitivity was assessed by oral glucose tolerance test.

242 assessed by a frequently sampled intravenous glucose tolerance test.RESULTSChronic mirabegron therapy

243 p with measurement of glucose turnover; oral glucose tolerance test; and a liver biopsy.

244 lucose and insulin during an intraperitoneal glucose tolerance test; and Glut4 and ApoE expression in

245 After 6 wk, a 75-g oral-glucose-tolerance test (13C-labeled) and a subsequent fa

246 273), and whose mothers had a 2-h 75-g oral-glucose-tolerance test (OGTT) at 26-28 weeks of gestatio

247 )) of 22.4 +/- 0.8 were subjected to an oral-glucose-tolerance test (OGTT) on 4 separate days with th

248 At each visit, an oral-glucose-tolerance test (OGTT) was performed.

249 etone monoester (KE) drink before a 2-h oral-glucose-tolerance test (OGTT) would lower blood glucose

250 Postinfusion, a 240-min oral-glucose-tolerance test (OGTT; 75 g) was administered.

251 with improved insulin response after an oral glucose-tolerance test (P = 9.8 x 10(-5)), whereas abnor

252 An oral-glucose-tolerance test was performed pre- and postinterv

253 ongitudinal cohort of women with GDM who had glucose tolerance tested during the early postpartum per

254 blood glucose measurements, intraperitoneal glucose tolerance testing (IPGTT), and human C-peptide s

255 identify high risk women for subsequent oral glucose tolerance testing improves dysglycemia detection

256 oid hormone, vitamin D, and response to oral glucose tolerance testing were similar.

257 According to oral glucose tolerance testing, approximately 14% of patients

258 ned glucose intolerant as determined by oral glucose tolerance testing.

259 erum insulin; HbA1c; glucose dynamics during glucose tolerance testing; or in pancreatic islet area o

260 ntagonist exendin(9-39)NH(2) During 4-h oral glucose tolerance tests (75 g) combined with an ad libit

261 n research visits including 2-hour 75-g oral glucose tolerance tests (OGTTs) at study baseline (6-9 w

262 postchallenge change in glucagon during oral glucose tolerance tests (OGTTs), hypothesizing that high

263 ng blood glucose concentrations and 2-h oral glucose tolerance tests among a cross-section of adults

264 e and after beta3-AR agonist treatment, oral glucose tolerance tests and euglycemic clamps were perfo

265 sulting in impaired insulin secretion during glucose tolerance tests as well as hyperglycemic clamps.

266 Oral glucose tolerance tests at baseline and after 1 year of

267 All women underwent 75-g oral glucose tolerance tests at ~26 weeks of gestation; we us

268 ues in response to a glucose load applied in glucose tolerance tests on different days, promoted gluc

269 Oral glucose tolerance tests were administered at the same ti

270 etric parameters and frequently sampled oral glucose tolerance tests were performed before and after

271 Intravenous glucose tolerance tests were performed before and after

272 questionnaires, clinical measurements, oral glucose tolerance tests, and laboratory examinations wer

273 Oral glucose tolerance tests, mixed-meal tolerance tests, and

274 diabetes was performed with the use of oral glucose-tolerance tests at 6-month intervals.

275 Since 2-hour glucose is an indicator of glucose tolerance, this study indicated CRP gene is asso

276 ression of patients from a state of impaired glucose tolerance to full blown type 2 diabetes (T2D).

277 ges and CD8(+) effector T cells, and loss of glucose tolerance under standard diet conditions.

278 signaling, insulin sensitivity, and systemic glucose tolerance was consistent with functional MRI dat

279 Furthermore, whole-body glucose tolerance was improved by compound A treatment,

280 Systemic glucose tolerance was improved in obese GR-deficient mic

281 By contrast, glucose tolerance was mildly impaired in mice lacking PA

282 Glucose tolerance was not significantly affected by any

283 However, no improved glucose tolerance was observed in NNMT(-/-) mice.

284 Glucose tolerance was quantified during weight gain (wee

285 strate utilization, insulin sensitivity, and glucose tolerance were all elevated in the IIA+ mice giv

286 hepatic insulin resistance and impairment of glucose tolerance were further aggravated in KO mice.

287 However, weight loss and glucose tolerance were improved in response to VSG in PP

288 gy intake, energy expenditure, appetite, and glucose tolerance were measured at baseline.

289 nts with coronary heart disease and impaired glucose tolerance were randomly assigned (1:1), in block

290 tch transcriptional activity showed improved glucose tolerance when subjected to high-fat diet feedin

291 ients with CF with normal to mildly impaired glucose tolerance, whereas incretin secretion remained u

292 e a mild phenotype with a slight decrease in glucose tolerance, whereas patients with the ZnT8 R325W

293 ed the L lactis subsp cremoris had increased glucose tolerance while on the Western-style diet compar

294 tational diabetes mellitus and have impaired glucose tolerance whilst cholestatic.

295 se) for 6 years for 577 adults with impaired glucose tolerance who usually receive their medical care

296 es that better identify people with impaired glucose tolerance, who benefit from the currently availa

297 that parkin is not an essential regulator of glucose tolerance, whole-body energy metabolism, or mito

298 27 knockout mice exhibited slightly worsened glucose tolerance with lower plasma insulin levels while

299 ed HFD-induced hyperlipidemia and stabilized glucose tolerance without affecting body weight.

300 ropeptide (ODN) reduces feeding and improves glucose tolerance, yet the contribution of endogenous AC