ライフサイエンスコーパス: glucose tolerance

1 insulin sensitivity, insulin secretion, and glucose tolerance.

2 and individuals with normal or altered oral glucose tolerance.

3 Moreover, Ad-FLD mice exhibited increased glucose tolerance.

4 CE, which was sufficient to improve systemic glucose tolerance.

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

6 ctionally modulated blood glucose levels and glucose tolerance.

7 systemic insulin administration and impaired glucose tolerance.

8 ibition of glucagon secretion contributes to glucose tolerance.

9 GLP1R agonist-induced insulin secretion and glucose tolerance.

10 g relieves diet-induced obesity and improves glucose tolerance.

11 r (GLP-1R) promotes weight loss and improves glucose tolerance.

12 cretion led to a high prevalence of impaired glucose tolerance.

13 7% have impaired fasting glucose or impaired glucose tolerance.

14 dent pathway is responsible for the enhanced glucose tolerance.

15 n plasma levels and, interestingly, improved glucose tolerance.

16 two indeterminate glycemia, and six impaired glucose tolerance.

17 nts had impaired fasting glucose or impaired glucose tolerance.

18 riceps muscles from obese mice with impaired glucose tolerance.

19 systemic deletion of Map4k4 did not improve glucose tolerance.

20 eover, mCaROCK1 mice also displayed impaired glucose tolerance.

21 adding back A. muciniphila promoted enhanced glucose tolerance.

22 All control subjects had normal glucose tolerance.

23 Homeostatic Model Assessment), and impaired glucose tolerance.

24 t that links SORLA expression to obesity and glucose tolerance.

25 ke, reduced energy expenditure, and impaired glucose tolerance.

26 from pancreatic islets and enhanced systemic glucose tolerance.

27 ut 65% of participants with CKD had impaired glucose tolerance.

28 ed peptide (Agrp) to wild-type mice enhanced glucose tolerance.

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

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

31 c gluconeogenesis without affecting systemic glucose tolerance.

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

33 ng with a 2-fold higher insulin and impaired glucose tolerance.

34 of gluconeogenesis associated with increased glucose tolerance.

35 3 subjects with cystic fibrosis had abnormal glucose tolerance (39%; P = 0.03).

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

37 hese findings indicate that despite "normal" glucose tolerance, adolescents and adults with PI-CF hav

38 number of TUNEL positive cells and improved glucose tolerance after glucose challenge.

39 d on comorbidity of alveolar bone change and glucose tolerance after HFD consumption.

40 Glucose tolerance after meal ingestion in vivo is the re

41 th the preferred compound 34 showed improved glucose tolerance after oral dosing in an oral glucose t

42 s that are associated with an improvement in glucose tolerance and a reduction in hepatic Fgf21 mRNA

43 in A. muciniphila do not show improvement in glucose tolerance and adding back A. muciniphila promote

44 sity with a phenotype that includes improved glucose tolerance and attenuated hepatic steatosis.

45 Finally, EPA feeding improved glucose tolerance and beta-cell function in a mouse mode

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

47 os in patients diagnosed with PTDM, impaired glucose tolerance and diabetes before transplantation, u

48 MS mice showed impaired glucose tolerance and disturbed sleep.

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

50 an II in mutant mice reversed alterations in glucose tolerance and glycosuria, whereas, conversely, a

51 ental effects of a maternal high-fat diet on glucose tolerance and hepatocyte glucose metabolism in f

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

53 diposity, and showed a modest improvement in glucose tolerance and improved markers of mitochondrial

54 prediabetic markers, in particular impaired glucose tolerance and insulin resistance, and first-epis

55 HFHS diet during mouse pregnancy on maternal glucose tolerance and insulin resistance, as well as, on

56 lso accompanied by a dramatic improvement in glucose tolerance and insulin resistance.

57 eit inconsistently, associated with impaired glucose tolerance and insulin resistance.

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

59 acute disruption of TrkA signaling, impairs glucose tolerance and insulin secretion in mice.

60 Furthermore, Ins2-Cre mice exhibited normal glucose tolerance and insulin secretion upon glucose sti

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

62 an obesogenic HFHS diet compromised maternal glucose tolerance and insulin sensitivity in late pregna

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

64 ive reduction of dietary BCAAs also restores glucose tolerance and insulin sensitivity to obese mice,

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

66 Consequently, KO mice have improved glucose tolerance and insulin sensitivity, and are more

67 s by inducing insulin secretion and improves glucose tolerance and insulin sensitivity.

68 y lipoprotein (VLDL) secretion, and improved glucose tolerance and insulin sensitivity.

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

70 to the third ventricle of the brain improved glucose tolerance and markedly increased hepatic insulin

71 lic health of young, growing mice, improving glucose tolerance and modestly slowing fat mass gain.

72 VC) suppresses glucose production, increases glucose tolerance and reduces food intake and body weigh

73 atment abolished the genotype differences in glucose tolerance and rGLUT2 levels, suggesting that red

74 function ameliorated the impairment in both glucose tolerance and sleep.

75 n both humans and rodents, modestly improves glucose tolerance and slows fat mass gain.

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

77 heart failure may have beneficial effects on glucose tolerance and the complications of diabetes mell

78 Unexpectedly, oral and intraperitoneal glucose tolerance and the insulin response to glycemic c

79 pregnancy may influence lipid metabolism and glucose tolerance and thus may impact the health of the

80 of growth and metabolic signalling pathways, glucose tolerance and utilization and insulin sensitivit

81 aling protein abundance by Western blotting, glucose tolerance and utilization, and insulin sensitivi

82 ering of the glucose threshold that improved glucose tolerance and/or improved insulin sensitivity, w

83 -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;

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

85 Twenty-two participants had normal glucose tolerance, and 21 participants had impaired fast

86 al of T2D, including hyperglycemia, impaired glucose tolerance, and a substantial reduction on beta c

87 ment acutely increased food intake, impaired glucose tolerance, and altered physical activity and ene

88 ncreased body weight and adiposity, impaired glucose tolerance, and elevated insulin levels.

89 ple Index Assessing Insulin Sensitivity Oral Glucose Tolerance, and HOMA-IR were high, and did not im

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

91 tes high-fat-diet-induced hepatic steatosis, glucose tolerance, and insulin resistance.

92 oid hormone T3 lowers lipid levels, improves glucose tolerance, and promotes energy expenditure to tr

93 ng levels of undercarboxylated OCN, impaired glucose tolerance, and reduced energy expenditure.

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

95 ersons without diabetes, those with impaired glucose tolerance, and those with type 2 diabetes.We sea

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

97 ablished coronary heart disease and impaired glucose tolerance, and whether the incidence of type 2 d

98 Severe infections, impaired glucose tolerance, and/or weight gain in the first year

99 iabetic while a further 55 (2%) had impaired glucose tolerance; and 218 (7%) were current smokers.

100 or central adiposity; 4) age; 5) smoking; 6) glucose tolerance; and 7) two previously reported versio

101 olic disease, as evidenced by impairments in glucose tolerance as early as 24 h into the HFD.

102 Kcne2 deletion in mice impaired glucose tolerance as early as 5 wk of age in pups fed a

103 fenugreek was not as effective at improving glucose tolerance as was four days of voluntary wheel ru

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

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

106 ht gain than wild-type animals, and improved glucose tolerance, better insulin sensitivity and marked

107 in 9-39 abolished the observed difference in glucose tolerance between control and knockout mice.

108 Liraglutide significantly improved glucose tolerance, body weight, and cardiometabolic dist

109 vity were still affected, the improvement in glucose tolerance by cIH was abolished in muscle-specifi

110 sulin sensitivity while improving whole-body glucose tolerance by promoting specific activation of th

111 lated insulin release (by 60%; P < 0.01) and glucose tolerance (by 20%; P < 0.01).

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

113 ts with type 2 diabetes mellitus or impaired glucose tolerance, canakinumab had no effect compared wi

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

115 (2+)]i and proinsulin and higher insulin and glucose tolerance compared with control littermates afte

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

117 rom high fat-fed trained dams had normalized glucose tolerance, decreased fasting insulin, and decrea

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

119 exhibit urinary glucose wasting and improved glucose tolerance, despite euglycemia and normal insulin

120 t (HFD), body weight (BW) gain, and impaired glucose tolerance development are associated with alveol

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

122 While glucose tolerance did not differ between genotypes at ba

123 Insulin secretion and glucose tolerance did not differ significantly between g

124 HId), and a more than twofold improvement in glucose tolerance (disposition index).

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

126 The acute anorectic and glucose tolerance effects of peripherally dosed GLP-1RA

127 The primary end point was change in glucose tolerance estimated by a 75-g oral glucose toler

128 system containing E6 significantly improved glucose tolerance for 96 h.

129 yperglycemia, hyperinsulinemia, and impaired glucose tolerance from 12 weeks of age without significa

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

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

132 ion index [DI]) in obese youth with impaired glucose tolerance (IGT) versus normal glucose tolerance

133 entifying impaired fasting glucose, impaired glucose tolerance (IGT), and NODAT.

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

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

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

137 age resulted in time-dependent worsening of glucose tolerance, impairment of insulin secretion, and

138 Glucose tolerance improved in the liraglutide group comp

139 Pharmacological Sirt6 inhibition improves glucose tolerance in a type 2 diabetes mouse model.

140 High-fat diet equally worsened glucose tolerance in AgRP and POMC IR KO mice and their

141 E6, has significantly improved half-life and glucose tolerance in an oral glucose tolerance test in r

142 ism for the observed glycosuria and improved glucose tolerance in ArcPOMC-deficient mice.

143 ty acutely increases food intake and worsens glucose tolerance in chow-fed rodents and causes excess

144 Exendin-4 is used to clinically improve glucose tolerance in diabetic patients due to its abilit

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

146 n of StarD10 in the adult beta cell improved glucose tolerance in high fat-fed animals.

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

148 h/day) on whole-body insulin sensitivity and glucose tolerance in lean mice.

149 treatment increased hematocrit and improved glucose tolerance in male and female mice, we observed a

150 ls, enhanced insulin signaling, and improved glucose tolerance in mice fed a high-fat diet.

151 t genetic deletion of A2AARs caused impaired glucose tolerance in mice fed an HFD.

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

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

154 e the in vitro digestibility and the in vivo glucose tolerance in mice.

155 to increased insulin signaling and improved glucose tolerance in obesity.

156 Lorcaserin treatment also improved glucose tolerance in olanzapine-fed mice.

157 ransplantation of Tg adipose tissue improved glucose tolerance in recipient mice supporting a role of

158 ry but are inversely variant with insulin or glucose tolerance in the HFD model of T2DM suggesting no

159 de 1 (GLP-1) and insulin levels and improved glucose tolerance in wild-type and Gpr119(betacell-/-) m

160 anges, hormone levels, body fat content, and glucose tolerance) in the exposed females when they reac

161 and normal control subjects, all with normal glucose tolerance, in order to identify early pathophysi

162 roup differences in stool energy content and glucose tolerance increased, and between-group differenc

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

164 Unexpectedly, cIH improved whole-body glucose tolerance independently of changes in body weigh

165 improved diabetic markers (fasting glucose, glucose tolerance, insulin tolerance, GLP-1 and insulin

166 an and a number of physiological parameters (glucose tolerance, insulin tolerance, indirect calorimet

167 In cystic fibrosis, abnormal glucose tolerance is associated with decreased lung func

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

169 Abnormal glucose tolerance is notably prevalent among young child

170 nts with coronary heart disease and impaired glucose tolerance is unknown.

171 or 10 d was well tolerated and improved oral glucose tolerance, it increased the expression of the gl

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

173 anslational evidence indicates that abnormal glucose tolerance may begin in early life.

174 erence 0.30 [95% CI 0.18 to 0.42]), impaired glucose tolerance (mean difference 1.31 [0.37 to 2.25]),

175 ialogue between IFNgamma, A. muciniphila and glucose tolerance might be an evolutionally conserved me

176 ollowed up after 5 y to determine changes in glucose tolerance (n = 167 for NGT, n = 174 for IGT, and

177 newly diagnosed T2D patients and 2105 normal glucose tolerance (NGT) individuals.

178 In the transition from normal glucose tolerance (NGT) to type 2 diabetes mellitus (T2D

179 paired glucose tolerance (IGT) versus normal glucose tolerance (NGT).

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

181 ]), and the number of patients with impaired glucose tolerance (odds ratio 5.44 [2.63 to 11.27]), but

182 adiposity and reduced glucose production and glucose tolerance of HFHS dams.

183 9(-/-) mice displayed normal body weight and glucose tolerance on a regular chow (RC) diet.

184 ht also be useful for patients with impaired glucose tolerance or diabetes.

185 iteria for impaired fasting glucose/impaired glucose tolerance or diabetes.

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

187 ndividuals, particularly those with impaired glucose tolerance or type 2 diabetes.

188 n when compared with individuals with normal glucose tolerance (P </= 0.014).

189 a robustly enhanced insulin sensitivity and glucose tolerance, phenotypes mimicked by a selective Vp

190 Three hundred two subjects with varying glucose tolerance received an oral glucose tolerance tes

191 versed with impaired insulin sensitivity and glucose tolerance, reduced insulin signaling in liver, e

192 The glucose tolerance response after HFD significantly varie

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

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

195 After a screening examination during which glucose tolerance status was determined, subjects were s

196 otal body and liver fat accumulation, better glucose tolerance, stronger hepatic insulin-dependent PK

197 lower CNS penetration, and activity in oral glucose tolerance studies was demonstrated.

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

199 = .03), plasma glucose levels after an oral glucose tolerance test (Hedges g = 0.61; 95% CI, 0.16 to

200 and subsequently assessed by intraperitoneal glucose tolerance test (IPGTT).

201 erance was measured using an intraperitoneal glucose tolerance test (IPGTT).

202 tion in humans during an in-vivo Intravenous Glucose Tolerance Test (IVGTT).

203 g to identifying IGT/NODAT using 2-hour oral glucose tolerance test (n = 66), fructosamine was the mo

204 from prediabetes onset and the average oral glucose tolerance test (OGTT) 2-h glucose measurement ov

205 h varying glucose tolerance received an oral glucose tolerance test (OGTT) and euglycemic insulin cla

206 tracer and labeled glucose infusion and oral glucose tolerance test (OGTT) before and 6 months after

207 glucose beverage consumption during an oral glucose tolerance test (OGTT) for 400 northern European

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

209 ained, in addition to 0-hour and 2-hour oral glucose tolerance test (OGTT) results, with measurement

210 blood glucose measured 2 h after a 75 g oral glucose tolerance test (OGTT), compared first between th

211 placebo (PLC) 30 minutes before a 75-g oral glucose tolerance test (OGTT).

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

213 cose during the first 30 minutes of the oral glucose tolerance test 2 years later.

214 d 10 healthy control subjects to a 75-g oral glucose tolerance test and a corresponding isoglycemic i

215 d disposition index were measured after oral glucose tolerance test and isoglycemic IV glucose inject

216 Participants underwent an oral glucose tolerance test and retinal imaging at 26-28 week

217 cose during the first 30 minutes of the oral glucose tolerance test and using the area under the curv

218 body surface area burned, underwent an oral glucose tolerance test at discharge.

219 The glucose tolerance test clarified that the complex retain

220 asma glucose >/=200 mg/dL during a 75-g oral glucose tolerance test had a definite diagnosis of type

221 test (GCT) followed by a 75-gram 2-hour oral glucose tolerance test if GCT result was >/=7.8 mmol/L.

222 d half-life and glucose tolerance in an oral glucose tolerance test in rodents.

223 n glucose tolerance estimated by a 75-g oral glucose tolerance test result.

224 In addition, body weight records and a glucose tolerance test revealed no differences between W

225 The glucose tolerance test showed major improvement of the g

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

227 Oral glucose tolerance test was considered the gold standard

228 ulinemic-euglycemic clamp and an intravenous glucose tolerance test were performed.

229 ol participants underwent a 6-hour 75-g oral glucose tolerance test with ECG recording and blood samp

230 total of 1,437 individuals underwent an oral glucose tolerance test with measurements of circulating

231 All underwent an oral glucose tolerance test, a liver panel, and a lipid profi

232 ose and lipid levels, the results of an oral glucose tolerance test, and blood pressure were used to

233 on (O-BP) using a clinical examination, oral glucose tolerance test, and gene expression and DNA meth

234 RSM with three predonation RFs (oral glucose tolerance test, basal insulin, fasting plasma gl

235 glucose (beta = 0.46, P = 0.00090) post oral glucose tolerance test, but only the latter passed Bonfe

236 levels, plasma glucose levels after an oral glucose tolerance test, fasting plasma insulin levels, i

237 levels, plasma glucose levels after an oral glucose tolerance test, fasting plasma insulin levels, i

238 assessment of insulin resistance and an oral glucose tolerance test-based index (Matsuda insulin sens

239 In the independent cohort, only oral glucose tolerance test-derived indexes were associated w

240 glucose, fasting glucose or insulin, or oral glucose tolerance test-derived measures.

241 men with type 2 diabetes before and after a glucose tolerance test.

242 ose homeostasis measured by means of an oral glucose tolerance test.

243 ulin-modified frequently sampled intravenous glucose tolerance test.

244 ucose tolerance after oral dosing in an oral glucose tolerance test.

245 e measures assessed by using a standard oral glucose tolerance test.

246 ucose) in the basal state and during an oral glucose tolerance test.

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

248 nd 2-hour glucose was measured after an oral glucose tolerance test.

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

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

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

252 mption (P = 0.07) and glycemia after an oral-glucose-tolerance test (P = 0.10) trended toward being l

253 ered questionnaires, by fasting and 2-h oral-glucose-tolerance test blood glucose measurement at re-e

254 ning in the early postpartum period via oral glucose tolerance testing after GDM, which is a time-con

255 Glucose tolerance testing at discharge offers an opportu

256 ulin stainings and performed intraperitoneal glucose tolerance testing in transgenic mice overexpress

257 Oral glucose tolerance testing with glucose, insulin, and C-p

258 orrelated with glucose responses during oral glucose tolerance testing, HbA1c, beta-cell function, an

259 d IR in the obese subjects was documented by glucose tolerance testing.

260 was measured by nonfasting blood glucose and glucose tolerance testing.

261 ation of glucose disposal during intravenous glucose tolerance tests (IVGTT) remains critical for str

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

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

264 function, we performed oral and intravenous glucose tolerance tests on mutation carriers and matched

265 All underwent oral glucose tolerance tests pre-LTx and serially post-LTx.

266 Glucose tolerance tests showed that Syn-1A-betaKO mice e

267 Oral glucose tolerance tests were administered at the same ti

268 Intravenous glucose tolerance tests were performed before and after

269 by nuclear magnetic resonance spectroscopy, glucose tolerance tests, and plasma analyses.

270 g or non-fasting plasma glucose levels, oral glucose tolerance tests, hemoglobin A1C levels, and/or a

271 nsulin secretion, as measured by intravenous glucose tolerance tests, using up to 5,567 individuals w

272 by nonfasting blood glucose measurements and glucose tolerance tests.

273 ic-euglycemic clamp and intravenous and oral glucose tolerance tests.

274 Insulin kinetics were calculated from oral glucose tolerance tests.

275 mps), and insulin secretion [via intravenous-glucose-tolerance tests (IVGTTs)].Fifty-four participant

276 sures collected from frequently sampled oral-glucose-tolerance tests (OGTTs).Twenty-seven of 29 recru

277 e activity in aged mice resulted in impaired glucose tolerance that could be attributed to peripheral

278 ncreased plasma levels of GLP1, insulin, and glucose tolerance; these effects were amplified in mice

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

280 ant harbored within the TCF7L2 locus impairs glucose tolerance through effects on glucagon as well as

281 failure underlies the transition of impaired glucose tolerance to overt diabetes; endoplasmic reticul

282 in sensitivity, clearance, and secretion and glucose tolerance using hyperinsulinemic-euglycemic clam

283 This impaired glucose tolerance was caused by a decrease in insulin se

284 Furthermore, intraperitoneal glucose tolerance was improved in animals receiving SCHA

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

286 Glucose tolerance was measured in (nocturnal) mice expos

287 BW changes were assessed, and glucose tolerance was measured using an intraperitoneal

288 st year after renal transplantation.Impaired glucose tolerance was not associated with either overall

289 s, demonstrating that beta cell function and glucose tolerance were impaired within the first two day

290 energy expenditure, food intake, and insulin/glucose tolerance were measured regularly, and tissues w

291 either type 2 diabetes mellitus or impaired glucose tolerance were randomized to receive placebo (n

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

293 nd body weight; their energy expenditure and glucose tolerance were unaffected.

294 including insulin autoantibodies and normal glucose tolerance, were enrolled in Canada, the United S

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

296 kedly reduced fat accumulation, and improved glucose tolerance, which can be eliminated by an antagon

297 lipids, and insulin (P < 0.05) and improved glucose tolerance, which was associated with increased V

298 ice with PAHSAs lowers glycemia and improves glucose tolerance while stimulating glucagon-like peptid

299 impaired insulin secretion, deterioration of glucose tolerance with either aging and/or high-fat feed

300 , treated mice showed significantly improved glucose tolerance with enhanced serum insulin levels, re