ライフサイエンスコーパス: glucose intolerance

1 study indicated CRP gene is associated with glucose intolerance.

2 nographic abnormalities were correlated with glucose intolerance.

3 s, impaired insulin signaling, and increased glucose intolerance.

4 rs responded poorly to glucose, resulting in glucose intolerance.

5 resistance but not with fasting glycemia or glucose intolerance.

6 osis, hyperleptinemia, hyperinsulinemia, and glucose intolerance.

7 l clock ablation in adult mice caused severe glucose intolerance.

8 high-fat diet-induced insulin resistance or glucose intolerance.

9 was associated with increased body mass and glucose intolerance.

10 rleukin [IL]-6, and lipopolysaccharide), and glucose intolerance.

11 adiol levels, abnormal fat accumulation, and glucose intolerance.

12 ation, leading to reduced beta-cell mass and glucose intolerance.

13 rweight and obese subjects, some of whom had glucose intolerance.

14 pontaneous activity, increases adiposity and glucose intolerance.

15 atosis and inflammation, as well as systemic glucose intolerance.

16 d with wild-type mice, both groups developed glucose intolerance.

17 orsened hyperglycemia, hyperinsulinemia, and glucose intolerance.

18 ed with beta cell loss, hypoinsulinemia, and glucose intolerance.

19 ent of insulin and osteocalcin cross-talk in glucose intolerance.

20 er, mice fed HF/HS+INDO exhibited pronounced glucose intolerance.

21 normalized insulin sensitivity, and reduced glucose intolerance.

22 et-induced adiposity, hepatic steatosis, and glucose intolerance.

23 es obesity and protects against diet-induced glucose intolerance.

24 hepatic steatosis, hypercholesterolemia, and glucose intolerance.

25 weight and adiposity that was accompanied by glucose intolerance.

26 impaired insulin secretion, and exacerbated glucose intolerance.

27 joint markers of insulin resistance (IR) and glucose intolerance.

28 s produced by ATMs can exacerbate whole-body glucose intolerance.

29 sted to contribute to insulin resistance and glucose intolerance.

30 ice from diet-induced insulin resistance and glucose intolerance.

31 le insulin resistance, to the development of glucose intolerance.

32 t diet-induced obesity, hyperleptinemia, and glucose intolerance.

33 t, wild-type mice became obese and developed glucose intolerance.

34 rted to impair insulin secretion, leading to glucose intolerance.

35 eatment, particularly those with preexisting glucose intolerance.

36 and protected from diet-induced obesity and glucose intolerance.

37 mice, we observe exacerbated weight gain and glucose intolerance.

38 diet-induced systemic insulin resistance and glucose intolerance.

39 FD-induced whole-body insulin resistance and glucose intolerance.

40 inflammation, spontaneous hyperglycemia, and glucose intolerance.

41 also causes heightened oxidative stress and glucose intolerance.

42 ith beta-islet cell destruction and systemic glucose intolerance.

43 from high-fat diet (HFD)-induced obesity and glucose intolerance.

44 lowed weight gain, it failed to protect from glucose intolerance.

45 vated hyperleptinemia, hyperinsulinemia, and glucose intolerance.

46 S component traits, such as hypertension and glucose intolerance.

47 nt7 KO mice fed the high fat diet had severe glucose intolerance.

48 systemically to cause insulin resistance and glucose intolerance.

49 ted protection against high-fat-diet-induced glucose intolerance.

50 d obesity and age- and high fat diet-induced glucose intolerance.

51 dullin in mice with pancreatic cancer led to glucose intolerance.

52 ces gluconeogenesis and thereby accounts for glucose intolerance.

53 g baseline C15:0/C17:0 with the prognosis of glucose intolerance.

54 These mice develop glucose intolerance.

55 e liver deletion of STIM1 displayed systemic glucose intolerance.

56 protected from diet-induced weight gain and glucose intolerance.

57 ysfunction increases the tendency to develop glucose intolerance.

58 dietary Zn(2+) supplementation also induced glucose intolerance.

59 en in SERT deficiency-associated obesity and glucose intolerance.

60 Aging is associated with glucose intolerance.

61 of gut microbiota in organophosphate-induced glucose intolerance.

62 aired insulin action and led to postprandial glucose intolerance.

63 nt obesity-related hypertension and impaired glucose intolerance.

64 ted energy expenditure; they also manifested glucose intolerance.

65 ment of inflammation, colorectal cancer, and glucose intolerance.

66 7-reactive cells coinciding with the time of glucose intolerance.

67 idation; and ameliorated liver steatosis and glucose intolerance.

68 o-thirds of burn patients had some degree of glucose intolerance.

69 sed adipose tissue inflammation and systemic glucose intolerance.

70 ncreased fasting glucose and insulin but not glucose intolerance.

71 d insulin signalling in WAT as the basis for glucose intolerance.

72 ater body weight gain, body fat content, and glucose intolerance.

73 icited peripheral insulin responsiveness and glucose intolerance.

74 lyses assessed the score's ability to detect glucose intolerance (90-min MMTT glucose >/=8 mmol/L) an

75 Both MODY groups exhibited glucose intolerance after oral glucose (most pronounced

76 ent mice were protected from obesity-induced glucose intolerance and adipose tissue fibrosis.

77 obesity and associated complications such as glucose intolerance and adipose tissue inflammation and

78 e copy of KD-mTOR mutant transgene developed glucose intolerance and beta-cell insulin secretion defe

79 he pancreas in the 3xTg-AD mouse, leading to glucose intolerance and contributing to a pathologic sel

80 Glucose intolerance and cortical amyloid pathology worse

81 been indicated to curb diet-induced obesity, glucose intolerance and delay the onset of type 2 diabet

82 e less severe disease, which may progress to glucose intolerance and diabetes in later life (e.g., SU

83 lta subunit in pancreatic islets, results in glucose intolerance and diabetes without affecting insul

84 Salsalate improves glucose intolerance and dyslipidemia in type 2 diabetes

85 us metabolic abnormalities, characterized by glucose intolerance and enhanced hepatic gluconeogenesis

86 deficiency increases susceptibility to both glucose intolerance and HCC, partially by increasing IL-

87 ike adipocyte formation in iWAT, and develop glucose intolerance and high fat-induced hepatic steatos

88 DKO also showed more severe glucose intolerance and hyperglycaemia than Mc4r KO.

89 Furthermore, PTG overexpression reversed the glucose intolerance and hyperinsulinemia caused by the H

90 sults showed that Adipoq(-/-) dams developed glucose intolerance and hyperlipidemia in late pregnancy

91 y high-fat diet (HF), such as dyslipidaemia, glucose intolerance and hypertension.

92 MODY1, including adult-onset hyperglycemia, glucose intolerance and impaired glucose-stimulated insu

93 de, to treatment with a thiazide can prevent glucose intolerance and improve blood pressure control.

94 , cathepsin K knockout alleviated whole-body glucose intolerance and improved insulin-stimulated Akt

95 1 receptor antagonist (H1RA) ameliorated the glucose intolerance and improved sleep quality in MS mic

96 doses equipotent on blood pressure, prevents glucose intolerance and improves control of blood pressu

97 variable and shows greater discrimination of glucose intolerance and insulin independence after trans

98 la: see text] A score <20 and >/=15 detected glucose intolerance and insulin independence, respective

99 ) and fat mass ( approximately 64%) and show glucose intolerance and insulin insensitivity.

100 expression of beta(2)AR in aged mice rescued glucose intolerance and insulin release both in vivo and

101 Glucose intolerance and insulin resistance are associate

102 tained into adulthood, which correlated with glucose intolerance and insulin resistance in HFD offspr

103 ith all-trans-retinoic acid (RA) ameliorates glucose intolerance and insulin resistance in obese mice

104 an HFD remain insulin-sensitive, but develop glucose intolerance and insulin resistance in response t

105 orylation correlates with the development of glucose intolerance and insulin resistance in rodents, n

106 Glucose intolerance and insulin resistance of Lrictor(KO

107 ORIGINS (the Oral Infections, Glucose Intolerance and Insulin Resistance Study) cross

108 We determined that the severity of glucose intolerance and insulin resistance that mice dev

109 The same measures of glucose intolerance and insulin resistance were also cor

110 iRNA-containing exosomes (Exos), which cause glucose intolerance and insulin resistance when administ

111 ion in both white and brown adipose tissues, glucose intolerance and insulin resistance while exhibit

112 spective cohort with multiple assessments of glucose intolerance and insulin resistance, measures of

113 Protein hyperacetylation is associated with glucose intolerance and insulin resistance, suggesting t

114 HFD become obese after 12 weeks and exhibit glucose intolerance and insulin resistance.

115 ay be effective in reversing obesity-related glucose intolerance and insulin resistance.

116 of adipogenic transcription factors but lack glucose intolerance and insulin resistance.

117 Conversely, Lin28aKD(VMH) mice displayed glucose intolerance and insulin resistance.

118 We observed that these mice displayed glucose intolerance and insulin resistance.

119 conveyed resistant to obesity, and improved glucose intolerance and insulin sensitivity in mice fed

120 Antioxidant treatment significantly reduced glucose intolerance and markers of inflammation and oxid

121 ypercortisolism, adrenocortical hyperplasia, glucose intolerance and mature-onset obesity, reminiscen

122 The aim of this study was to examine whether glucose intolerance and MS identified late after transpl

123 cal impact of unacylated ghrelin (UnAG) in a glucose intolerance and PAD mouse model.

124 Blockading IL-6 overexpression averts glucose intolerance and partially deters HCC development

125 ockout mice exhibited significant whole-body glucose intolerance and peripheral insulin resistance, c

126 g-II(-/-)) are protected from age-associated glucose intolerance and reveal greater glucose induced-i

127 Dynamin 2 deletion in beta cells caused glucose intolerance and substantial reduction of the sec

128 l fat mass rises significantly with age, and glucose intolerance and systemic insulin resistance deve

129 abolic perturbations prior to development of glucose intolerance and T2DM.

130 ifferentially expressed between HS rats with glucose intolerance and those with normal glucose regula

131 fficking proteins that accompany symptoms of glucose intolerance and weight gain.

132 ented the development of insulin resistance, glucose intolerance, and abnormal weight gain in cortico

133 marked improvements in insulin sensitivity, glucose intolerance, and cardiovascular abnormalities.

134 alling in the liver and adipose tissue (AT), glucose intolerance, and enhanced progression to steatoh

135 ut (DKO) mice are refractory to weight gain, glucose intolerance, and hepatic steatosis when challeng

136 ing and increases in body mass, fat content, glucose intolerance, and hepatic steatosis with advancin

137 t exhibit hyperinsulinemia, hyperleptinemia, glucose intolerance, and hepatic steatosis, with increas

138 causes insulin resistance, hyperinsulinemia, glucose intolerance, and hyperglycemia and diminishes th

139 etabolic syndrome disorders such as obesity, glucose intolerance, and hypertension.

140 adipogenesis, induced insulin resistance and glucose intolerance, and increased hepatic steatosis in

141 olic disorders, including hepatic steatosis, glucose intolerance, and inflammation.

142 a mice were more susceptible to diet-induced glucose intolerance, and insulin action measured in isol

143 measures of hyperglycemia, hyperinsulinemia, glucose intolerance, and insulin resistance in 197 parti

144 arkedly increases susceptibility to obesity, glucose intolerance, and insulin resistance specifically

145 metabolic syndrome, including hyperglycemia, glucose intolerance, and insulin resistance when maintai

146 w early increased body weight and adiposity, glucose intolerance, and insulin resistance when placed

147 ing water ameliorated fasting hyperglycemia, glucose intolerance, and insulin resistance with consequ

148 deficiency of AC5 protects against obesity, glucose intolerance, and insulin resistance, supporting

149 JNK1 has been implicated in obesity, glucose intolerance, and insulin resistance.

150 m high-fat diet (HFD)-induced obesity, blood glucose intolerance, and insulin resistance.

151 , changes in the gut microbiota, insulin and glucose intolerance, and levels of tissue inflammation w

152 abolic disorders such as insulin resistance, glucose intolerance, and nonalcoholic steatohepatitis.

153 lipidemia, steatohepatitis, atherosclerosis, glucose intolerance, and obesity in metabolically compro

154 Adult beta(2)AR(-/-) mice featured glucose intolerance, and pancreatic islets isolated from

155 interleukin-6 (IL-6) expression, early-onset glucose intolerance, and progressive steatosis and dyspl

156 knockout mice exhibit insulin resistance and glucose intolerance, and Sesn3 transgenic mice were prot

157 olved in SERT deficiency-induced obesity and glucose intolerance, and suggest approaches to restore 1

158 ly to the development of insulin resistance, glucose intolerance, and type 2 diabetes.

159 years old were more likely to have obesity, glucose intolerance, and/or hypertension compared to you

160 offspring of LP0.5-exposed mothers exhibited glucose intolerance as a result of an insulin secretory

161 how that JNK activation in beta-cells led to glucose intolerance as a result of impaired capacity to

162 rovement of dexamethasone-induced whole-body glucose intolerance as well as insulin resistance in HDA

163 fed an LPD developed abdominal adiposity and glucose intolerance associated with a 5-fold up-regulati

164 led to fasting hyperglycemia and more severe glucose intolerance associated with defective insulin se

165 in beta-cells resulted in hyperglycemia and glucose intolerance associated with reduced and delayed

166 ion of human AD transgenes led to peripheral glucose intolerance, associated with pancreatic human Ab

167 cking either p300 or CBP in islets developed glucose intolerance attributable to impaired insulin sec

168 e, in 19 BD patients with insulin resistance/glucose intolerance (BD + IR/GI), 14 BD subjects with T2

169 High-fat diet enhanced glucose intolerance, brain soluble Abeta, and memory imp

170 yte population that promotes weight gain and glucose intolerance but are defined by the M2 marker CD3

171 reduced lipid-induced hepatic steatosis and glucose intolerance, but these effects were not observed

172 PDAC has been linked with obesity and glucose intolerance, but whether changes in circulating

173 % of energy as fat developed obesity-related glucose intolerance by 6 months.

174 er NIK in obesity promotes hyperglycemia and glucose intolerance by increasing the hyperglycemic resp

175 In the setting of pre-established glucose intolerance caused by diet-induced insulin resis

176 vents may be enhanced when heart failure and glucose intolerance coexist and may be attenuated when d

177 ore likely to progress to a higher degree of glucose intolerance compared to those without MS (58% vs

178 ty, hyperleptinemia, reduced metabolism, and glucose intolerance compared with ovariectomized WT fema

179 PREP knockdown mice (Prep(gt/gt)) exhibited glucose intolerance, decreased fasting insulin, increase

180 defects, including fasting hyperglycemia and glucose intolerance, decreased insulin levels, and eleva

181 -/-) mice are protected against diet-induced glucose intolerance despite enhanced adiposity and the p

182 CerS2 null mice exhibited glucose intolerance despite normal insulin secretion fro

183 wn to wound macrophages in a murine model of glucose intolerance (diet-induced obese).

184 (a model of T1DM), including hyperglycemia, glucose intolerance, diminished islet insulin storage, a

185 nsgene [RIPCre;KD-mTOR (Homozygous)] develop glucose intolerance due to a defect in beta-cell functio

186 HFD-fed GPR43 knockout (KO) mice develop glucose intolerance due to a defect in insulin secretion

187 mitoNEET induction causes hyperglycemia and glucose intolerance due to activation of a Parkin-depend

188 Adult Tshz1(+/-) mice display glucose intolerance due to defects in glucose-stimulated

189 ensing, specifically in the ARC, resulted in glucose intolerance due to deficient insulin secretion a

190 Animals genetically lacking adipsin have glucose intolerance due to insulinopenia; isolated islet

191 energy homeostasis but developed late-onset glucose intolerance due to reduced insulin secretion, wh

192 3 months, before the development of systemic glucose intolerance, electroretinographic defects, or mi

193 ulted in decreased weight gain but increased glucose intolerance, epicardial adipose tissue (EAT) inf

194 l CaMKII inhibition dramatically exacerbates glucose intolerance following exposure to a high fat die

195 th obesity increased from 8% to 26% and with glucose intolerance from 9% to 25%.

196 e indications of weight loss or treatment of glucose intolerance (from pre-diabetes to diabetes).

197 in a pregnant diet-induced model of impaired glucose intolerance/gestational diabetes mellitus (IGT/G

198 hages (ATMs) directly contribute to systemic glucose intolerance has not been determined.

199 The HTF-C diet caused glucose intolerance, hepatic steatosis, and induced hepa

200 nistration completely corrected HFru-induced glucose intolerance, hepatic steatosis, and the impaired

201 in, dyslipidemia, hyperinsulinemia, and mild glucose intolerance, however, this was not aggravated fu

202 circulating GC excess are protected from the glucose intolerance, hyperinsulinemia, hepatic steatosis

203 osphate levels, activated ChREBP, and caused glucose intolerance, hyperinsulinemia, hypertriglyceride

204 mice were also characterized by significant glucose intolerance (ie, impaired glucose utilization).

205 ting glucose level in 7 patients (3.2%), and glucose intolerance in 6 patients (2.7%).

206 system and increases abdominal adiposity and glucose intolerance in a sex- and time-specific fashion,

207 mice against diet-induced hyperglycemia and glucose intolerance in an M3R-dependent fashion.

208 A in association with supportive evidence of glucose intolerance in at least a subset of such childre

209 KC) constrains food intake, weight gain, and glucose intolerance in both rats and mice.

210 esis, thereby resulting in hyperglycemia and glucose intolerance in casein-injected mice.

211 omocysteine induced hyperhomocysteinemia and glucose intolerance in control, but not SHP-null, mice.

212 xidation and ameliorated liver steatosis and glucose intolerance in diet-induced obese mice, but thes

213 s hepatic glucose production and exacerbates glucose intolerance in diet-induced obese mice.

214 optosis, insufficient insulin secretion, and glucose intolerance in female rather than male mice.

215 ic pathway contributes to the progression of glucose intolerance in individuals with diabetes.

216 , improved insulin sensitivity, and improved glucose intolerance in mice after the establishment of o

217 tes induced exaggerated body weight gain and glucose intolerance in mice exposed to a high-fat diet.

218 sion in skeletal muscle prevents obesity and glucose intolerance in mice, although the underlying mec

219 but only feeding of SFAs was accompanied by glucose intolerance in mice.

220 ive regulator MDM2, impairs GSIS, leading to glucose intolerance in mice.

221 hypercholesterolemia, insulin resistance and glucose intolerance in murine models of obesity and T2DM

222 type 2 diabetes, such as severe insulin and glucose intolerance in muscle and the liver, excessive p

223 on of MC4Rs specifically in the LHA improves glucose intolerance in obese MC4R-null mice without affe

224 verexpression of SIRT1 reduces steatosis and glucose intolerance in obese mice.

225 HGP and protected against hyperglycemia and glucose intolerance in obese mice.

226 We conclude that the gradual development of glucose intolerance in patients with the SUR1-E1506K mut

227 et tissue (pancreas), and the development of glucose intolerance in rat insulin promoter-glycoprotein

228 effectively prevents insulin resistance and glucose intolerance in rats fed a high-fat diet (HFD).

229 MS is a risk factor for the progression of glucose intolerance in renal transplant recipients in th

230 eeks, effectively improved hyperglycemia and glucose intolerance in streptozotocin, high-fat diet-fed

231 with CF may contribute to the development of glucose intolerance in the CF pediatric population, and

232 ssion in beta cells does not account for the glucose intolerance in the Tcf7l2 overexpression mouse m

233 pancreas, and propranolol treatment reversed glucose intolerance in these mice.

234 urbed, partly accounting for the HCV-induced glucose intolerance in these mice.

235 ased apoptosis (0.1 vs. 0.6%; P < 0.01), and glucose intolerance in transgenic mice.

236 hypercholesterolemia, insulin resistance and glucose intolerance in type 2 diabetes mellitus (T2DM),

237 diacylglycerol but not ceramide), and severe glucose intolerance in WT mice alone.

238 High-fat diet caused glucose intolerance in WT mice but did not further worse

239 ontributed to worsening of hyperglycemia and glucose-intolerance in these mice.

240 ased fasting insulin and glucose, as well as glucose intolerance, in C57BL/6 mice.

241 ice developed hyperlipidemia, hyperglycemia, glucose intolerance, increased adiposity, and steatosis,

242 sal temperature dysregulation (hot flashes), glucose intolerance, increased appetite and reduced meta

243 ral TGF-beta excess caused hyperglycemia and glucose intolerance independent of a change in body weig

244 on of the IR (L-Insulin Receptor KO) induces glucose intolerance, insulin resistance and prevents the

245 CCDC3 alleviates glucose intolerance, insulin resistance and steatosis fo

246 TG mice fed a high-fat diet (HFD) normalized glucose intolerance, insulin resistance, and dyslipidemi

247 culating lipids, Nck2-deficient mice develop glucose intolerance, insulin resistance, and hepatic ste

248 Heterozygous db mice (db/+) present with glucose intolerance, insulin resistance, and increased w

249 of related disorders that includes obesity, glucose intolerance, insulin resistance, dyslipidemia, a

250 al UVR significantly suppressed weight gain, glucose intolerance, insulin resistance, nonalcoholic fa

251 tion of PI3Kgamma ablation in obesity-driven glucose intolerance is largely a result of its leptin-de

252 endotoxemia, glucose insulinotropic peptide, glucose intolerance, lipogenesis, and metabolic inflexib

253 The alphaXBPKO mice exhibited glucose intolerance, mild insulin resistance, and an ina

254 ere significantly protected from HFD-induced glucose intolerance observed in pfn wild-type mice.

255 ce in WT mice but did not further worsen the glucose intolerance observed in standard chow-fed SOD1-n

256 8(+) T cells in the pancreas, and consequent glucose intolerance observed in the context of priming b

257 over two weeks did not alter body weight or glucose intolerance of obese mice.

258 drugs are associated with the development of glucose intolerance or deterioration in glycemic control

259 t mice lacking FoxM1 in the pancreas display glucose intolerance or diabetes with only a 60% reductio

260 The fraction of older donors accepted with glucose intolerance or hypertension remains small and fo

261 studies, we found no consistent evidence of glucose intolerance or insulin resistance during pregnan

262 D pathology or 11C-PiB beta-amyloid load and glucose intolerance or insulin resistance in subjects wh

263 tion in liver, Tsc1 deletion failed to cause glucose intolerance or promote hyperinsulinemia in mixed

264 ificantly associated with the progression of glucose intolerance (OR 3.5, CI 1.2-9.9, P=0.01), as was

265 related disorders including liver steatosis, glucose intolerance, or elevated serum levels of estroge

266 ition impairs the induction of the obese and glucose intolerance phenotypes.

267 With this in mind, surveillance of glucose intolerance post discharge should be considered.

268 ed in mice to reverse insulin resistance and glucose intolerance prior to reduction of obesity.

269 ve adiposity, severe insulin resistance, and glucose intolerance--quite reminiscent of the phenotype

270 This was associated with development of glucose intolerance, reduced HDL cholesterol, and increa

271 sity and hyperinsulinemia, although systemic glucose intolerance remained largely unaffected.

272 tive stress caused by SOD1 ablation leads to glucose intolerance secondary to beta-cell dysfunction.

273 Set(Delta)beta mice exhibited glucose intolerance similar to Pdx1-deficient mice, and

274 The glucose intolerance study showed only C17:0 correlated w

275 in SERT (-/-) mice reversed the obesity and glucose intolerance, supporting a role for estrogen in S

276 etaAb counteracted beta-cell dysfunction and glucose intolerance, supporting the notion that preventi

277 ess hormones, hyperglycemia, leptinemia, and glucose intolerance that are associated with global chan

278 insulinemia, impaired insulin secretion, and glucose intolerance that rapidly progresses to overt dia

279 y, DHHC7 KO mice developed hyperglycemia and glucose intolerance, thereby confirming that DHHC7 repre

280 ocin or its analogs reduced the magnitude of glucose intolerance through improving insulin secretion.

281 se model overexpressing Tcf7l2, resulting in glucose intolerance, to infer the contribution of Tcf7l2

282 Glucose intolerance was associated with increased left v

283 Glucose intolerance was defined as follows: (1) prediabe

284 elopment of obesity, insulin resistance, and glucose intolerance was monitored, and the effect of ind

285 d aPKC activities in muscle improved, as did glucose intolerance, weight gain, hepatosteatosis, and h

286 for Galpha(z) are protected from developing glucose intolerance when fed a high fat (45 kcal%) diet.

287 f Gal3 to mice causes insulin resistance and glucose intolerance, whereas inhibition of Gal3, through

288 Genetic ablation of SOD1 caused glucose intolerance, which was associated with reduced i

289 patients with mutant leaky RyR2 present with glucose intolerance, which was heretofore unappreciated.

290 Accelerated onset of glucose intolerance with elevated insulin levels, cardia

291 duced obesity in mice results in more marked glucose intolerance with evidence for enhanced hepatic G

292 ellitus (T1DM), including hyperglycaemia and glucose intolerance with mild insulin resistance.

293 phate for 180 days confirms the induction of glucose intolerance with no significant change in acetyl

294 Interestingly, betaTFG KO displayed marked glucose intolerance with reduced insulin secretion.

295 ibited hyperglucagonemia, hyperglycemia, and glucose intolerance, with 71% reduction of beta-cell mas

296 iabetes mellitus (GDM) is defined as varying glucose intolerance, with first onset or recognition in

297 .v. injection of FGF19 dramatically improved glucose intolerance within 2 hours.

298 ted from diet-induced insulin resistance and glucose intolerance without accompanying changes in adip

299 These RIPcre(+)fak(fl/fl) mice exhibited glucose intolerance without changes in insulin sensitivi

300 l as other metabolic phenotypes (obesity and glucose intolerance), worsened.