ライフサイエンスコーパス: glucose intolerance

1 These mice develop glucose intolerance.

2 e liver deletion of STIM1 displayed systemic glucose intolerance.

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

4 ysfunction increases the tendency to develop glucose intolerance.

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

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

7 Aging is associated with glucose intolerance.

8 of gut microbiota in organophosphate-induced glucose intolerance.

9 aired insulin action and led to postprandial glucose intolerance.

10 IS and are protected against obesity-induced glucose intolerance.

11 ted energy expenditure; they also manifested glucose intolerance.

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

13 7-reactive cells coinciding with the time of glucose intolerance.

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

15 sed adipose tissue inflammation and systemic glucose intolerance.

16 ncreased fasting glucose and insulin but not glucose intolerance.

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

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

19 icited peripheral insulin responsiveness and glucose intolerance.

20 nographic abnormalities were correlated with glucose intolerance.

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

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

23 resistance but not with fasting glycemia or glucose intolerance.

24 osis, hyperleptinemia, hyperinsulinemia, and glucose intolerance.

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

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

27 e infused with sEVs from GDM women developed glucose intolerance.

28 was associated with increased body mass and glucose intolerance.

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

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

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

32 pontaneous activity, increases adiposity and glucose intolerance.

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

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

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

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

37 normalized insulin sensitivity, and reduced glucose intolerance.

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

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

40 hepatic steatosis, hypercholesterolemia, and glucose intolerance.

41 weight and adiposity that was accompanied by glucose intolerance.

42 a-cell destruction and high-fat diet-induced glucose intolerance.

43 1) in the liver promotes gluconeogenesis and glucose intolerance.

44 impaired insulin secretion, and exacerbated glucose intolerance.

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

46 rcholesterolemia, body fat accumulation, and glucose intolerance.

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

48 sted to contribute to insulin resistance and glucose intolerance.

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

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

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

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

53 tion, and metabolic abnormalities, including glucose intolerance.

54 mediates MCH-induced feeding, adiposity, and glucose intolerance.

55 ncreased FFA, and induced hypeerglycemia and glucose intolerance.

56 y acids (FFA) and produced hyperglycemia and glucose intolerance.

57 or muscle LRP2 causes insulin resistance and glucose intolerance.

58 genesis, leading to diet-induced obesity and glucose intolerance.

59 sensitivity, which contributes to whole-body glucose intolerance.

60 exhibited fasting and fed hyperglycemia and glucose intolerance.

61 2S/+ metabolic phenotype revealed late-onset glucose intolerance.

62 ibited milder hepatic insulin resistance and glucose intolerance.

63 glucose clearance in states of diet-induced glucose intolerance.

64 study indicated CRP gene is associated with glucose intolerance.

65 nt obesity-related hypertension and impaired glucose intolerance.

66 idation; and ameliorated liver steatosis and glucose intolerance.

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

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

69 orsened hyperglycemia, hyperinsulinemia, and glucose intolerance.

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

71 systemically to cause insulin resistance and glucose intolerance.

72 ces gluconeogenesis and thereby accounts for glucose intolerance.

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

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

75 Female alphaGLP-1R(-/-) mice exhibited mild glucose intolerance after an intraperitoneal glucose adm

76 ll mice are protected from hyperglycemia and glucose intolerance after long-term high-fat diet (HFD)

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

78 ight, hyperlipidemia, and severe insulin and glucose intolerance, all occurring before the onset of d

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

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

81 eatosis and inflammation, independently from glucose intolerance and adiposity, which was linked to c

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

83 BCAA catabolism and has been correlated with glucose intolerance and cardiac dysfunction.

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

85 Glucose intolerance and cortical amyloid pathology worse

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

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

88 Offspring of obese dams developed glucose intolerance and displayed increased body weight,

89 Salsalate improves glucose intolerance and dyslipidemia in type 2 diabetes

90 of T(reg) cells rescued fetal loss, maternal glucose intolerance and fetal macrosomia.

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

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

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

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

95 plasma adiponectin and increases in leptin, glucose intolerance and hyperinsulinemia.

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

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

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

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

100 1 receptor antagonist (H1RA) ameliorated the glucose intolerance and improved sleep quality in MS mic

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

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

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

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

105 Glucose intolerance and insulin resistance are associate

106 it protected mice from high-fat diet-induced glucose intolerance and insulin resistance by increasing

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

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

109 The Oral Infections, Glucose Intolerance and Insulin Resistance Study (ORIGIN

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

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

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

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

114 from gaining excessive weight and developing glucose intolerance and insulin resistance when challeng

115 s, P-selectin-deficient mice still developed glucose intolerance and insulin resistance when chronica

116 reased adiposity under basal conditions, and glucose intolerance and insulin resistance when raised o

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

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

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

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

121 ed mice and was unable to prevent or reverse glucose intolerance and insulin resistance.

122 pe that was associated with a mild degree of glucose intolerance and insulin resistance.

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

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

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

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

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

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

129 (KIKO mice) developed exercise intolerance, glucose intolerance and moderate cardiac dysfunction at

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

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

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

133 As expected, L-IRKO + GFP mice showed glucose intolerance and severe hyperinsulinemia.

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

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

136 in insulin resistance, hyperinsulinemia, and glucose intolerance and that Pg translocates to the panc

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

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

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

140 the Dlk1-Dio3 locus reduced gluconeogenesis, glucose intolerance, and fasting blood glucose levels.

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

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

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

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

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

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

147 lammation, hepatic steatosis, hyperglycemia, glucose intolerance, and insulin resistance in liver and

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

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

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

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

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

153 nduced adipose tissue inflammation, obesity, glucose intolerance, and insulin resistance.

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

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

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

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

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

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

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

164 xhibited obesity plus insulin resistance and glucose intolerance beyond that attributable to their in

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

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

167 male and female betaeIF4G1KO mice displayed glucose intolerance but normal insulin sensitivity.

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

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

170 % of energy as fat developed obesity-related glucose intolerance by 6 months.

171 tive mechanism to counteract obesity-induced glucose intolerance by decreasing food intake and promot

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

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

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

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

176 flammation, fasting blood glucose level, and glucose intolerance, compared with the continuously HF-f

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

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

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

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

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

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

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

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

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

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

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

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

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

190 3 months, before the development of systemic glucose intolerance, electroretinographic defects, or mi

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

192 size, tissue inflammation, enhanced maternal glucose intolerance, fetal macrosomia, and a long-lastin

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

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

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

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

197 otects from weight gain, insulin resistance, glucose intolerance, hepatic steatosis and hepatic infla

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

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

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

201 a-cell activity, which included whole-animal glucose intolerance, hyperglycemia, and impaired insulin

202 EPA ethyl esters prevented obesity-induced glucose intolerance, hyperinsulinemia, and hyperglycemia

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

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

205 Metabolic syndrome encompasses obesity, glucose intolerance, hypertension, and dyslipidemia; how

206 lthough HFD promoted weight gain, adiposity, glucose intolerance, hypertriglyceridemia, hepatic lipid

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

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

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

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

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

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

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

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 d body weight gain, increased adiposity, and glucose intolerance in male knockout mice, characterized

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

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

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

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

221 HF diet caused greater weight gain and glucose intolerance in middle-aged females than males.

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 atic inflammatory responses, and insulin and glucose intolerance in obese murine models.

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 D2R-OE(NAc) mice of both sexes also showed glucose intolerance in the IGTT.

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

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

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

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

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

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

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

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

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

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

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

244 CCDC3 alleviates glucose intolerance, insulin resistance and steatosis fo

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

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

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

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

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

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

251 lenge, FtMT-Adip mice are leaner but exhibit glucose intolerance, low adiponectin levels, increased r

252 Despite persistent glucose intolerance, metformin-treated guinea pigs had a

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

256 t of obese males losing weight but augmented glucose intolerance of females.

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

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

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

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

264 weight, fat mass, adiposity, and whole-body glucose intolerance (p < 0.05).

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

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

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

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

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

270 ivo analyses revealed fasting hyperglycemia, glucose intolerance, reduced sensitivity and delayed glu

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

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

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

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

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

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

277 exes of HFD-Hhip +/+ mice developed impaired glucose intolerance, that was only ameliorated in male H

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

279 nst excess weight gain, hepatic steatosis or glucose intolerance, they exhibited marked decreases in

280 the sole expression of lamin C protects from glucose intolerance through a beta-cell-adaptive transcr

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

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

283 Glucose intolerance was associated with increased left v

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

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

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

287 on treatment-reversing hepatic steatosis and glucose intolerance-were abrogated in Insp3r1 (also know

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

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

290 red glucose-stimulated insulin secretion and glucose intolerance with aging or obesity.

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

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

293 h-fat diet fed mice or aged mice exacerbated glucose intolerance with inadequate insulinemia and incr

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

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

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

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

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

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

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