ライフサイエンスコーパス: hyperglycemia

1 rgency department visits for hypoglycemia or hyperglycemia).

2 rgency department visits for hypoglycemia or hyperglycemia).

3 d hepatic gluconeogenic activity and fasting hyperglycemia.

4 entiated beta-cells after exposure to severe hyperglycemia.

5 ges parallel those that occur in response to hyperglycemia.

6 but protects mice from high-fat diet-induced hyperglycemia.

7 kinase degradation, which becomes induced in hyperglycemia.

8 pment of hepatic steatosis, dyslipidemia and hyperglycemia.

9 to loss of insulin production and resultant hyperglycemia.

10 onsidered most likely to be a consequence of hyperglycemia.

11 ssion of ZIP7 and ZnT7 were also observed in hyperglycemia.

12 n may be an important consequence of chronic hyperglycemia.

13 absorption, in order to manage postprandial hyperglycemia.

14 esity with associated insulin resistance and hyperglycemia.

15 tients in the 33 degrees C treatment arm had hyperglycemia.

16 5 protected ZDF rats from beta-cell loss and hyperglycemia.

17 etes is the most common form of drug-induced hyperglycemia.

18 y disease (DKD) is a serious complication of hyperglycemia.

19 e in decreasing, or in some cases resolving, hyperglycemia.

20 er results in constitutive CREB activity and hyperglycemia.

21 abnormalities were strongly correlated with hyperglycemia.

22 s hepatic and circulating TGs and normalizes hyperglycemia.

23 in-producing ss cells which leads to chronic hyperglycemia.

24 lbuminuria upon streptozotocin (STZ)-induced hyperglycemia.

25 d by tamoxifen injection, caused progressive hyperglycemia.

26 itically ill patients typically present with hyperglycemia.

27 rapy have been associated with high rates of hyperglycemia.

28 ress-induced release of sCD93 is impaired by hyperglycemia.

29 of obesity-associated insulin resistance and hyperglycemia.

30 of glucose-glycogen homeostasis, leading to hyperglycemia.

31 idney grafts resulted in immediate return to hyperglycemia.

32 mprove the treatment of stroke patients with hyperglycemia.

33 had muscle weakness, and 90.9% vs 81.5% had hyperglycemia.

34 role in the development of ER stress during hyperglycemia.

35 isk directly associated with the severity of hyperglycemia.

36 tance, but only MAFB decreased under chronic hyperglycemia.

37 n immature beta-cells promotes acute fasting hyperglycemia.

38 exacerbation of this injury in conditions of hyperglycemia.

39 nemia is a pertinent contributor to diabetic hyperglycemia.

40 -stimulated insulin secretion during chronic hyperglycemia.

41 secretion dysregulation in diabetes fosters hyperglycemia.

42 267 (27.1%) had mild, and 201 (20.4%) severe hyperglycemia.

43 food ingredients for regulating postprandial hyperglycemia.

44 lin antagonist, significantly contributes to hyperglycemia.

45 2 mice, but not in C57BL/6J, with comparable hyperglycemia.

46 ges were replicated in wild-type mice during hyperglycemia.

47 zes body temperature and causes postprandial hyperglycemia.

48 ge diabetes in individuals with uncontrolled hyperglycemia.

49 nd proteomic profiles prior to appearance of hyperglycemia.

50 s on retinal neurovascular injury induced by hyperglycemia.

51 including hematologic toxicities (19 [40%]), hyperglycemia (12 [25%]), and pneumonia (7 [15%]).

52 patients in euglycemia (71-140 mg/dL), mild hyperglycemia (141-199 mg/dL), and severe hyperglycemia

53 ation with intrauterine exposure to maternal hyperglycemia, a common metabolic pregnancy complication

54 odified insulin peptide R22E did not prevent hyperglycemia, accelerated disease onset, increased its

55 atherosclerosis, but the mechanism by which hyperglycemia accelerates lesion development is not well

56 Prolonged hyperglycemia activates the formation of advanced glycat

57 Despite the transient hyperglycemia, advanced atherosclerosis was observed at

58 Understanding how chronic hyperglycemia affects primary human hepatocytes (PHHs) c

59 Our study used T1D mice with severe hyperglycemia along with significant deficits in echocar

60 Chronic hyperglycemia also decreased brain cell proliferation in

61 sleeping time with the risks of obesity and hyperglycemia among 1263 offspring aged 1-5 years of mot

62 r activity or sleeping time with the risk of hyperglycemia among offspring born to GDM mothers in Tia

63 ce on everolimus in breast cancer has placed hyperglycemia among the most common high grade adverse e

64 stridium butyricum CGMCC0313.1 (CB0313.1) on hyperglycemia and associated metabolic dysfunction in tw

65 robiotic for the prevention and treatment of hyperglycemia and associated metabolic dysfunction.

66 cellular protein, as a putative link between hyperglycemia and atherosclerotic complications in diabe

67 cardiovascular disease, but the link between hyperglycemia and atherothrombotic disease is not comple

68 ve role, whereas TMEM132C was upregulated in hyperglycemia and correlated negatively with insulin sec

69 and PRR14L were downregulated in donors with hyperglycemia and correlated positively with insulin sec

70 Mechanistically, we showed that hyperglycemia and diabetes decreased PKM2 tetramer forma

71 , hyperinsulinemia, glucose intolerance, and hyperglycemia and diminishes the plasma membrane localiz

72 Hyperglycemia and dyslipidemia contribute to glucolipoto

73 l. uncover a previously unknown link between hyperglycemia and enhanced platelet production and react

74 Diet-induced postprandial hyperglycemia and fasting hyperinsulinemia significantly

75 and it is activated postprandially by portal hyperglycemia and fructose through dissociation from GKR

76 Finally, DHHC7 KO mice developed hyperglycemia and glucose intolerance, thereby confirmin

77 se abnormalities contributed to worsening of hyperglycemia and glucose-intolerance in these mice.

78 In a mouse model combining hyperglycemia and hypercholesterolemia (streptozotocin d

79 Hyperglycemia and hyperinsulinemia also impaired the PI3

80 in LMCs and provide the first evidence that hyperglycemia and hyperinsulinemia promote insulin resis

81 cemic control and to reduce the incidence of hyperglycemia and hypoglycemia, which further reduces po

82 of the vGMS was associated with decreases in hyperglycemia and hypoglycemia.

83 deletion in the adult mouse beta-cell caused hyperglycemia and hypoinsulinemia.

84 widely used in cancer treatment that promote hyperglycemia and identify dietary interventions that re

85 d male ZDF rats prevented the development of hyperglycemia and improved metabolic parameters similar

86 tective pathways were uncovered for managing hyperglycemia and include augmentation of fibroblast gro

87 evidence for an association between current hyperglycemia and infection risk in type 2 diabetes pati

88 ed by reduced plasma LPS level, and improved hyperglycemia and insulin resistance.

89 rely burned patients for postburn control of hyperglycemia and insulin resistance.

90 ent effects by which leptin reverses fasting hyperglycemia and ketoacidosis in a rodent model of DKA

91 x6 in beta cells of adult mice led to lethal hyperglycemia and ketosis that were attributed to loss o

92 model of periodontitis in mice with chronic hyperglycemia and lack of leukocyte p47(phox) (Akita/Ncf

93 Moreover, betaMcl-1KO mice displayed higher hyperglycemia and lower pancreatic insulin content after

94 istration of NRTN and liraglutide normalized hyperglycemia and other metabolic parameters, demonstrat

95 redisposed to altered beta-cell function and hyperglycemia and place it as a critical regulator of fe

96 eatic beta-cell toxin streptozotocin induced hyperglycemia and raised plasma ghrelin levels in wild-t

97 cells was associated with attenuation of the hyperglycemia and TGF-beta1-induced enhanced ROS product

98 whether a lack of suppression contributes to hyperglycemia and thus to the development of diabetes.

99 of gut microbiota in organophosphate-induced hyperglycemia and to unravel the molecular mechanism beh

100 ese data demonstrate a possible link between hyperglycemia and vascular disease states associated wit

101 oE(-/-):Ins2(+/Akita) mice presented chronic hyperglycemia, and atherosclerosis appeared to be advanc

102 ty were predictors of the stable reversal of hyperglycemia, and decline in insulin autoantibody posit

103 from obesity, including insulin resistance, hyperglycemia, and dyslipidemia, can further impact tumo

104 at diet-induced ailments, including obesity, hyperglycemia, and hepatosteatosis.

105 is accompanied by neutropenia, lympocytosis, hyperglycemia, and higher reticulocyte counts, along wit

106 ne the association of pre-existing diabetes, hyperglycemia, and hypoglycemia during the first 24 hour

107 sion to analyze the association of diabetes, hyperglycemia, and hypoglycemia with 90-day mortality (n

108 90-day mortality and pre-existing diabetes, hyperglycemia, and hypoglycemia, corrected for other fac

109 terized by a 50% decrease in plasma insulin, hyperglycemia, and insulin resistance (IR), as well as m

110 st S961 to induce severe insulin resistance, hyperglycemia, and ketonemia in mice.

111 n of CB1R are protected from beta-cell loss, hyperglycemia, and nephropathy that are present in ZDF l

112 etes is characterized by insulin resistance, hyperglycemia, and progressive beta cell dysfunction.

113 Hyperglycemia- and hyperinsulinemia-induced insulin resi

114 anisms underlying the detrimental effects of hyperglycemia are largely unclear.

115 gainst chemotoxicity, yet drugs that promote hyperglycemia are widely used in cancer treatment.

116 A growing body of evidence supports hyperglycemia as a putative contributor to several brain

117 nce intervals [CI]) of childhood obesity and hyperglycemia associated with different levels of indoor

118 The multivariable-adjusted ORs of hyperglycemia associated with different levels of sleepi

119 Western blotting demonstrated that chronic hyperglycemia-associated oxidative stress inhibits nucle

120 of childhood insulin on the BMI-MetS and BMI-hyperglycemia associations was estimated at 19.2% (p < 0

121 Male sex, overweight, and hyperglycemia at admission were associated with undiagno

122 echanisms that control the renal response to hyperglycemia at the efferent arteriole.

123 Hyperglycemia augments a branch pathway in glycolysis, t

124 The multivariable-adjusted ORs of hyperglycemia based on different levels of indoor activi

125 Hyperglycemia, based on the FCG level, at enrollment was

126 We propose hyperglycemia be managed promptly after LTx.

127 tions, weaning failure, muscle weakness, and hyperglycemia (blood glucose level >150 mg/dL [to conver

128 ession triggers brain hypoxia and subsequent hyperglycemia, both of which precede slower changes in b

129 Genes whose expression changed in hyperglycemia but not after short-term glucose exposure,

130 to ZDF rats also prevents beta-cell loss and hyperglycemia but not nephropathy.

131 c BP and modulated the renal RE responses to hyperglycemia but without impacting the RAAS or NO level

132 DNA, are formed not only in the presence of hyperglycemia, but also in diseases associated with high

133 report that sustained inflammation promotes hyperglycemia by targeting the mevalonate pathway.

134 Under hyperglycemia, cAMP production and PKA activity were mar

135 nephropathy, although it does not affect the hyperglycemia caused by the Akita mutation.

136 Intracellular hyperglycemia causes excessive ROS production.

137 ined under fasting, 230 mg/dL, and 340 mg/dL hyperglycemia clamp conditions.

138 (STZ), hep-tg animals developed less severe hyperglycemia compared with wild-type, an effect likely

139 In type 2 diabetes (T2DM), dyslipidemia and hyperglycemia damage DRG neurons and induce mitochondria

140 e mutant beta-cells were tightly linked with hyperglycemia, decreased beta-cell proliferation, reduce

141 Thus, sustained SHP-1 expression caused by hyperglycemia despite systemic glucose normalization cou

142 After initiation, it takes years before hyperglycemia develops in patients at risk for type 1 di

143 When Ager was deleted, hyperglycemia did not aggravate ischemic brain damage an

144 Critically ill children with hyperglycemia did not benefit from tight glycemic contro

145 , we sought to determine the role of chronic hyperglycemia due to insulinopenia on alloimmunity using

146 r branching angle, suggesting that transient hyperglycemia during pregnancy may cause small-vessel dy

147 iabetes mellitus (GDM), a state of transient hyperglycemia during pregnancy, and retinal microvascula

148 ucose-lowering agents and insulin), control (hyperglycemia, dyslipidemia and hypertension) and chroni

149 ors include metabolic abnormalities, such as hyperglycemia, elevated triglyceride levels, low high-de

150 igned critically ill children with confirmed hyperglycemia (excluding patients who had undergone card

151 The duration and severity of hyperglycemia exposure were estimated as the number of y

152 rediabetes, IR, and duration and severity of hyperglycemia exposure.

153 Over a period of 8 weeks of hyperglycemia, GLO1 overexpression delayed and limited t

154 ark symptoms of MODY1, including adult-onset hyperglycemia, glucose intolerance and impaired glucose-

155 od2 (-/-) HFD mice developed hyperlipidemia, hyperglycemia, glucose intolerance, increased adiposity,

156 ld hyperglycemia (141-199 mg/dL), and severe hyperglycemia (>/= 200 mg/dL), and patients with hypogly

157 Overt hyperglycemia (>250 mg/dL) manifested 6 weeks after the

158 1) with stratification by center (n = 8) and hyperglycemia (>5.6 mmol/L).

159 Surprisingly, chronic hyperglycemia had little effect on primary T-cell reacti

160 adily rejected islet allografts, and chronic hyperglycemia had no impact on the magnitude or quality

161 Hyperglycemia (HG) stimulates the production of reactive

162 tional risk factors, including hypertension, hyperglycemia, hypercholesterolemia, and high circulatin

163 iet, deletion of PKD1 in beta-cells worsened hyperglycemia, hyperinsulinemia, and glucose intolerance

164 Doubly heterozygous mice exhibit progressive hyperglycemia, hyperinsulinemia, and impaired glucose to

165 herapeutics depend on experimental models of hyperglycemia, hyperinsulinemia, and insulin resistance.

166 ompensatory beta-cell replication when acute hyperglycemia/hyperinsulinemia is induced.

167 e in Iran, the estimated national control of hyperglycemia, hyperlipidemia and hypertension (especial

168 .3% of patients with diabetes had controlled hyperglycemia, hyperlipidemia and hypertension, respecti

169 mia, or it could develop as a consequence of hyperglycemia (i.e., glucotoxicity).

170 ical abnormalities typical of T2D, including hyperglycemia, impaired glucose tolerance, and a substan

171 nt in 64 (65.3%), hypotension in 67 (68.4%), hyperglycemia in 17 (18.1%), and fever in 37 (37.8%).

172 1, alanine transaminase elevation in 1, and hyperglycemia in 2 participants.

173 Induced GI insulin(+) cells can suppress hyperglycemia in a diabetic mouse model for at least 6 m

174 pleotropic effects by which leptin reverses hyperglycemia in a non-DKA rodent model of T1D.

175 ads to the early development of postprandial hyperglycemia in CF.

176 deficiency accelerates the normalization of hyperglycemia in chemically induced diabetic recipient m

177 Hyperglycemia in db pigs, even without ischemia, induced

178 omising tool with the potential to attenuate hyperglycemia in diabetes mellitus.

179 n action in skeletal myocytes contributes to hyperglycemia in diabetes.

180 ations and normalizes insulin resistance and hyperglycemia in high-fat diet (HFD)-induced obesity.

181 titutively activated PKA and did not improve hyperglycemia in mice with hyperglucagonemia.

182 e-specific expression of Ad36E4ORF1 improves hyperglycemia in mice.

183 nce deletion or inhibition of GcgRs corrects hyperglycemia in models of diabetes.

184 iency dramatically accelerated insulitis and hyperglycemia in NOD mice along with a substantial reduc

185 r improves insulin sensitivity and decreases hyperglycemia in obese mice.

186 Chronic oral nitrite treatment improved hyperglycemia in obese ZSF1 rats by a process that requi

187 The only drug-related adverse event was hyperglycemia in patients with diabetes; this event was

188 esults in notable weight loss and alleviates hyperglycemia in patients with type 2 diabetes (T2D).

189 S is superior to medical therapy in reducing hyperglycemia in persons with type 2 diabetes, and has b

190 ed the insulin requirement to prevent severe hyperglycemia in STZ rats.

191 enhanced the filtration fraction response to hyperglycemia in T1D patients through larger increases i

192 itors was significantly decreased by chronic hyperglycemia in the injured brain of fish.

193 otein expression was elevated in response to hyperglycemia in the retina of diabetic rodents.

194 Hyperglycemia in type 2 diabetes and obesity is caused b

195 Hyperglycemia in type 2 diabetes mellitus has been linke

196 be a promising therapeutic target to reduce hyperglycemia in type 2 diabetes.

197 ucose production (EGP) is the main source of hyperglycemia in type 2 diabetes.

198 rom donors with normal glucose tolerance and hyperglycemia (including T2D).

199 ouse model of ischemic stroke, we found that hyperglycemia increased the infarct volume and decreased

200 Hyperglycemia increases ICCs via oxidative metabolism-de

201 haracterized, and manipulated a new model of hyperglycemia-induced atherosclerosis: the apolipoprotei

202 ceptor substrate 2 (IRS2), we confirmed that hyperglycemia-induced beta-cell proliferation requires I

203 l-molecule PKM2 activator, TEPP-46, reversed hyperglycemia-induced elevation in toxic glucose metabol

204 domain (ASC), or pro-IL-1beta prevented the hyperglycemia-induced enhancement of reactive species pr

205 Critical role of the cAMP-PKA pathway in hyperglycemia-induced epigenetic activation of fibrogeni

206 TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.

207 ctivation in pancreatic alpha cells enhances hyperglycemia-induced PC1 expression thereby releasing G

208 NTDs are associated with hyperglycemia-induced protein misfolding and Caspase-8-i

209 adriamycin-induced nephropathy and mice with hyperglycemia-induced renal injury.

210 We also investigated hyperglycemia-induced signaling in the ICC lineage and I

211 TGR5 activation augmented a hyperglycemia-induced switch from glucagon to GLP-1 synt

212 ogression was accompanied with inhibition of hyperglycemia-induced TSP-1 expression and reduced prote

213 onance energy transfer sensors, we show that hyperglycemia induces a marked redistribution of cellula

214 Hyperglycemia induces beta-cell replication, but the mec

215 as caloric restriction, ketogenic diet, and hyperglycemia influence the inflammatory response, but h

216 Corticosterone-induced hyperglycemia, insulin resistance, and changes in muscle

217 Hyperglycemia is a major pathogenic factor that promotes

218 n of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure.

219 Admission hyperglycemia is associated with adverse outcome of seps

220 Preoperative hyperglycemia is associated with adverse postoperative o

221 Inpatient hyperglycemia is common and is linked to adverse patient

222 The resultant hyperglycemia is deleterious to the normal function of m

223 Transient hyperglycemia is frequent during tuberculosis, and DM ne

224 IRAB-B hyperglycemia is normalized in mice treated with exendin

225 tients with preexisting diabetes and chronic hyperglycemia is unknown.

226 ings indicate that the genetic background of hyperglycemia is unrecognized in the vast majority of fa

227 The resulting hyperglycemia is very difficult to treat, and patients a

228 eas diabetes influences host immune defense, hyperglycemia itself does not cause generalized alloimmu

229 glucose in the presence of hyperinsulinemic hyperglycemia later in the same day, indicating that bre

230 cell proliferation was not affected by acute hyperglycemia, later proliferation of neural progenitors

231 in rats induces release of stress hormones, hyperglycemia, leptinemia, and glucose intolerance that

232 a-dicarbonyls and AGER as mediators by which hyperglycemia lowers the number of protective noninflamm

233 uggests that factors other than intrauterine hyperglycemia may contribute to the decreased PPARGC1A e

234 ive vigilance and a lower threshold to treat hyperglycemia may explain this finding.

235 st that immune compromise in diabetes due to hyperglycemia may not apply to cellular rejection of tra

236 key mechanism behind organophosphate-induced hyperglycemia, mediated by the organophosphate-degrading

237 Here we found that in response to hyperglycemia, neutrophil-derived S100 calcium-binding p

238 control offspring and insulin resistance and hyperglycemia occur.

239 T2D, and t-PA predicted 5-year transition to hyperglycemia (odds ratio 1.30, 95% CI 1.02-1.65).

240 r previous studies show hypothyroxinemia and hyperglycemia of the alcohol-consuming pregnant rat, whi

241 re is limited understanding of the impact of hyperglycemia on brain dysfunction in the zebrafish mode

242 at exploring the impact of acute and chronic hyperglycemia on brain homeostasis and neurogenesis.

243 nd telencephalic injury model, the impact of hyperglycemia on brain repair mechanisms was investigate

244 reduced body weight gain and protected from hyperglycemia on high-fat diet.

245 une-compromised state, the impact of chronic hyperglycemia on host alloimmunity is not clear.

246 e the impact of free fatty acids compared to hyperglycemia on mitochondrial transport, primary adult

247 he evolutionary conserved adverse effects of hyperglycemia on neurogenesis and brain healing in zebra

248 Here we characterize the effect of chronic hyperglycemia on Nrf2 signaling within a diabetic cutane

249 We characterized the effects of chronic hyperglycemia on the Keap1/Nrf2 pathway within models of

250 This is in part attributed to the effects of hyperglycemia on vascular endothelial and smooth muscle

251 Hyperglycemia or blockade of insulin signaling reduces t

252 insulin secretion rate in response to basal hyperglycemia or insulin resistance, and shows that beta

253 t be causally involved in the development of hyperglycemia, or it could develop as a consequence of h

254 volving metabolic abnormalities secondary to hyperglycemia, oxidative stress, and activation of trans

255 The db/db mice developed hyperglycemia, oxidative stress, and nephropathy at age

256 events downstream of GPVI are influenced by hyperglycemia, oxidative stress, and shear stress.

257 retinal morphological alteration induced by hyperglycemia, particularly preserving survival of retin

258 nset of hyperglycemia within 6 h, and severe hyperglycemia persists for 2 weeks.

259 interdependent oxidative stress response to hyperglycemia perturbs neutrophil cytoskeletal stability

260 ate contributed to an insulin resistance and hyperglycemia phenotype.

261 in immunoprecipitation assays confirmed that hyperglycemia promoted phospho-p65 or phospho-CREB and C

262 Whether hyperglycemia promotes platelet production and whether e

263 STZ causing severe and rapid development of hyperglycemia related to the catastrophic loss of insuli

264 This work reveals that hyperglycemia represents a condition in which cells are

265 lar to NOD mice and humans, characterized by hyperglycemia requiring lifelong exogenous insulin thera

266 Hyperglycemia resulted in increased infarct size in a mo

267 a cell mass in the RIP-DTR mouse, a model of hyperglycemia resulting from diphtheria toxin induced be

268 The binding is reversible in the setting of hyperglycemia, resulting in fast release of insulin and

269 e superoxide production in mice with chronic hyperglycemia results in interstitial pneumonia and incr

270 a model of type 2 diabetes (T2D), developing hyperglycemia, severe insulin resistance and diabetic pe

271 induced diabetes; however, despite levels of hyperglycemia similar to those of WT STZ mice, TLR4KO ST

272 CC lineage and gastric organotypic cultures, hyperglycemia stimulated proliferation by mitogen-activa

273 tion and reversed the detrimental effects of hyperglycemia, suggesting new avenues to treat stroke pa

274 monocytes blocked the detrimental effect of hyperglycemia, suggesting that monocytes are required.

275 (0.510 vs 0.190, p < 0.001), and greater in hyperglycemia than in normoglycemia groups (0.503 vs 0.2

276 n of insulin-producing beta cells leading to hyperglycemia that, in turn, specifically affects a pati

277 m resulting from insulin resistance leads to hyperglycemia, the hallmark of type 2 diabetes mellitus

278 ogenesis, promoting fasting and postprandial hyperglycemia through increased fatty acid delivery to t

279 zyme of glycogen metabolism can combine with hyperglycemia to directly hyperinhibit glycogen phosphor

280 transient and optimal degree of postprandial hyperglycemia to efficiently enhance insulin-induced cha

281 il8, and tnfalpha) in the brain and chronic hyperglycemia to impair expression of genes involved in

282 d sensitivity to weight gain, steatosis, and hyperglycemia to wild type germ free mice.

283 resolution prevents from morbid obesity and hyperglycemia under dietary overload conditions.

284 emia after correcting excessive postprandial hyperglycemia using treatment with a sodium-glucose cotr

285 Hyperglycemia was also independently associated with poo

286 ciation of tuberculosis and its outcome with hyperglycemia was assessed using logistic regression ana

287 Severe, but not mild, admission hyperglycemia was associated with increased 30-day morta

288 , only severe hypoglycemia in the absence of hyperglycemia was associated with increased 90-day morta

289 Early postoperative hyperglycemia was associated with increased readmission,

290 sed plasma ghrelin levels in wild-type mice, hyperglycemia was averted in similarly treated Gcgr(-/-)

291 The proportion of hyperglycemia was higher in the 33 degrees C group compa

292 Acute hyperglycemia was shown to promote gene expression of pr

293 genesis from those likely to be secondary to hyperglycemia, we exposed islets from human donors to no

294 ata, greater severity and longer duration of hyperglycemia were independently associated with longer

295 These abnormalities, with the exception of hyperglycemia, were attenuated in db/dbhnRNP F-transgeni

296 liraglutide resulted in some alleviation of hyperglycemia, whereas NRTN was not as effective despite

297 Treating 10-week-old ZDF rats with sustained hyperglycemia with liraglutide resulted in some alleviat

298 In this model, separate treatment of hyperglycemia with rosiglitazone or hypertension with li

299 single dose of IRAB-B induces rapid onset of hyperglycemia within 6 h, and severe hyperglycemia persi

300 etes revealed that single oral doses lowered hyperglycemia within 60 min, enhanced insulin-stimulated