ライフサイエンスコーパス: hyperglycaemia

1 ted (epistaxis and the DLTs of diarrhoea and hyperglycaemia).

2 crete lactate into ASL, which is elevated in hyperglycaemia.

3 nability to maintain body temperature and by hyperglycaemia.

4 iabetes require insulin therapy for treating hyperglycaemia.

5 ncreatic diseases with varying mechanisms of hyperglycaemia.

6 is a group of diseases defined by persistent hyperglycaemia.

7 glycaemic control in the setting of chronic hyperglycaemia.

8 is warranted because of potential relapse of hyperglycaemia.

9 D1 results in increased gluconeogenesis and hyperglycaemia.

10 ions which cause lifelong persistent fasting hyperglycaemia.

11 m the gut and thereby alleviate postprandial hyperglycaemia.

12 p1r+/+ mice would result in exercise-induced hyperglycaemia.

13 ass and markedly improving dyslipidaemia and hyperglycaemia.

14 epatic gluconeogenesis, which contributes to hyperglycaemia.

15 ar population of sympathetic neurons against hyperglycaemia.

16 with particular attention to the hazards of hyperglycaemia.

17 hich include peripheral vasoconstriction and hyperglycaemia.

18 tem/liver circuit can contribute to diabetic hyperglycaemia.

19 e of entry into proximal tubule cells during hyperglycaemia.

20 nts, that are licensed for the management of hyperglycaemia.

21 d with increased risk of hyperlipidaemia and hyperglycaemia.

22 revented among individuals with intermediate hyperglycaemia.

23 ay be impaired under conditions of sustained hyperglycaemia.

24 enograft models at doses that did not induce hyperglycaemia.

25 9%) presented with some form of intermediate hyperglycaemia.

26 mellitus (T2DM) in people with non-diabetic hyperglycaemia.

27 ified in the PlGF promoter also increased in hyperglycaemia.

28 Calphabeta inhibition in ACS associated with hyperglycaemia.

29 ccur during a heart attack by stress-induced hyperglycaemia.

30 indices of beta-cell function in those with hyperglycaemia.

31 of individuals identified with intermediate hyperglycaemia.

32 d diacylglycerol (DG) production in diabetic hyperglycaemia.

33 e attributed to reduced exposure to maternal hyperglycaemia.

34 f the primary metabolic pathways impaired by hyperglycaemia.

35 thways partially recovers beta-cell mass and hyperglycaemia.

36 tailed by dose-limiting side effects such as hyperglycaemia.

37 rom starches and alleviation of postprandial hyperglycaemia.

38 f having diabetes (5.29, 95% CI 2.61-10.70), hyperglycaemia (1.86, 1.38-2.50), and renal insufficienc

39 pina (most common were neutropenia [29%] and hyperglycaemia [10%]; nine [21%] grade 5 adverse events,

40 ts included electrolyte disturbances (n=15), hyperglycaemia (11), infections (six), mucositis (four),

41 pina (most common were neutropenia [29%] and hyperglycaemia [14%]; no grade 5 adverse events) and in

42 buparlisib group vs the placebo group) were hyperglycaemia (17 [22%] of 76 vs two [3%] of 78), anaem

43 monotherapy were diarrhoea (15 [37%] of 41), hyperglycaemia (17 [41%]), and weight loss (8 [20%]); th

44 The most common adverse events were hyperglycaemia (21 [33%] for treatment with 40 mg pasire

45 d group vs 29 [6%] of 526 in the KRd group), hyperglycaemia (23 [4%] vs 34 [6%]), diarrhoea (23 [5%]

46 e associated with combination treatment were hyperglycaemia (27 [66%] of 41]), diarrhoea (19 [46%]),

47 ] vs 3 [1%]), anaemia (19 [6%] vs 53 [17%]), hyperglycaemia (3 [1%] vs 16 [5%]), and hypomagnesaemia

48 te aminotransferase (51 [18%] vs four [3%]), hyperglycaemia (35 [12%] vs none), hypertension (16 [6%]

49 neuropathy is linked with dyslipidaemia and hyperglycaemia(4), the contribution of inflammation to p

50 vs 1 [1%]), fatigue (7 [3%] vs 1 [1%]), and hyperglycaemia (7 [3%] vs 0).

51 ate aminotransferase (103 [18%] vs 16 [3%]), hyperglycaemia (88 [15%] vs one [<1%]), and rash (45 [8%

52 AKH secretion in corpora cardiaca and caused hyperglycaemia, a hallmark feature of diabetes mellitus.

53 ents with diabetes might also develop stress hyperglycaemia-a fact overlooked in many studies compari

54 y risk factors of metabolic syndrome include hyperglycaemia, abdominal obesity, dyslipidaemia, and hi

55 With the exception of hyperglycaemia, adverse events were generally similar be

56 tment option for T2DM patients to ameliorate hyperglycaemia, adverse lipid metabolism and blood press

57 Hyperglycaemia after acute stroke is a common finding th

58 owth and birth weight in addition to causing hyperglycaemia after birth.

59 associated with diabetes are attributable to hyperglycaemia alone and are reversed when blood glucose

60 operties of five definitions of intermediate hyperglycaemia (also known as prediabetes) on the basis

61 dy demonstrated high prevalence of transient hyperglycaemia and a significant TB/DM and TB/IGR associ

62 sion, bradycardia, femoral vasoconstriction, hyperglycaemia and an increase in haemoglobin, catechola

63 ealth on combined prevalence of intermediate hyperglycaemia and diabetes (aOR 0.93, 0.74-1.16) or the

64 bilisation on the prevalence of intermediate hyperglycaemia and diabetes among the general adult popu

65 The success of a strategy using new-onset hyperglycaemia and diabetes as a screening tool to ident

66 bidities are linked with insulin resistance, hyperglycaemia and dyslipidaemia(3-7), aberrant non-esse

67 isease, increasing the risk of hypertension, hyperglycaemia and dyslipidaemia, recognized as the meta

68 known for its therapeutic effect on obesity, hyperglycaemia and dyslipidaemia; however, its effect on

69 metabolic disorder characterized by chronic hyperglycaemia and dysregulation in metabolism, is uncle

70 ce to insulin, leading to hyperinsulinaemia, hyperglycaemia and enlarged fatty liver.

71 of pregnancy, and prevalence of undiagnosed hyperglycaemia and even overt diabetes in young women is

72 Dose-limiting toxic effects included hyperglycaemia and fever with decreased neutrophil count

73 f type-1 diabetes mellitus (T1DM), including hyperglycaemia and glucose intolerance with mild insulin

74 There was no grade 4 hyperglycaemia and grade 3 cases were asymptomatic.

75 d this model and found it developed obesity, hyperglycaemia and hyperinsulinaemia.

76 redox balance in T2DM hearts during peaks of hyperglycaemia and increased workload.

77 tissue injury, interstitial fluid overload, hyperglycaemia and inflammation.

78 Exposure of blood vessel organoids to hyperglycaemia and inflammatory cytokines in vitro induc

79 fter, the diagnosis of clinical disease with hyperglycaemia and insulin dependence.

80 utcomes is not well understood, but maternal hyperglycaemia and insulin resistance are both implicate

81 ammation in metabolic tissues, fatty livers, hyperglycaemia and insulin resistance recapitulating met

82 es many of the metabolic symptoms, including hyperglycaemia and insulin resistance.

83 HF groups were obese, with fat accumulation, hyperglycaemia and insulin resistance.

84 eatosis and was more effective at correcting hyperglycaemia and lowering haemoglobin A1c levels than

85 Chronic hyperglycaemia and microvascular disease contribute to c

86 reby suggesting a causal association between hyperglycaemia and mortality risk.

87 accelerate the effect of maternal ageing, so hyperglycaemia and obesity do not simply explain the mec

88 We conclude that hyperglycaemia and P. aeruginosa induce a metabolic shif

89 almost half of adults as having intermediate hyperglycaemia and poorly predicts diabetes.

90 Correction of hyperglycaemia and prevention of glucotoxicity are impor

91 sensitivity and glucose homeostasis, linking hyperglycaemia and SIRT1 downregulation.

92 ) in TB patients and the association between hyperglycaemia and TB at enrolment and 3 months after TB

93 olment in newly diagnosed DM, but persistent hyperglycaemia and TB/DM association in HIV-1-infected p

94 rmed the strong relationship between chronic hyperglycaemia and the development and progression of di

95 mpact of chronic preconditioning of cells to hyperglycaemia and transient switching of cultured endot

96 omplex process, and its disruption can cause hyperglycaemia and type II diabetes mellitus.

97 After STZ, PAD4-/- and WT mice developed hyperglycaemia and weight loss, yet only WT neutrophils

98 group (with six patients having grade 3 or 4 hyperglycaemia) and none of 49 in the placebo group.

99 n ratio, increased liver glucose production, hyperglycaemia, and a greater capillary density in order

100 al symptoms, colitis, adrenal insufficiency, hyperglycaemia, and hypokalaemia.

101 glucokinase mutation, in in vitro models of hyperglycaemia, and in islets from type-2 diabetic patie

102 ed agents in the treatment of dyslipidaemia, hyperglycaemia, and insulin resistance.

103 e neutropenia, one (3%) patient with grade 4 hyperglycaemia, and one (3%) patient with grade 2 bronch

104 s and exemestane (the most common were rash, hyperglycaemia, and stomatitis, which each affected two

105 history of diabetic ketoacidosis and chronic hyperglycaemia appear to be more injurious than previous

106 ies have suggested that patients with stress hyperglycaemia are at higher risk of adverse consequence

107 ion of the Glp1r results in exercise-induced hyperglycaemia associated with an excessive increase in

108 or its signalling cascade may be affected by hyperglycaemia associated with gestational diabetes, res

109 Among 2470 adults with intermediate hyperglycaemia at baseline, 2100 (85%) were followed-up

110 ype 2 diabetes in a cohort with intermediate hyperglycaemia at baseline.

111 Acute hyperglycaemia at the time of a heart attack worsens the

112 y (ie, early gestational diabetes defined by hyperglycaemia before 20 weeks of gestation).

113 ls had impaired glucose tolerance or fasting hyperglycaemia but, after adjusting for age and sex, the

114 the other three definitions of intermediate hyperglycaemia, but their sensitivity is low.

115 ho presented with reactive hypoglycaemia and hyperglycaemia, but who was subsequently cured by surger

116 al diabetes, and is thought to contribute to hyperglycaemia by leading to impaired beta cell function

117 al for beta-cell function and can ameliorate hyperglycaemia by remodelling local vasculature and secr

118 al genotype and indirectly, through maternal hyperglycaemia, by the maternal genotype.

119 Hyperglycaemia can adversely affect outcome in criticall

120 contains elevated lactate concentrations and hyperglycaemia can also increase ASL lactate.

121 thiazolidinediones (TZDs) as a treatment for hyperglycaemia can be difficult to assess because of the

122 uggests that the damaging cardiac effects of hyperglycaemia can be reversed by selective PKC inhibiti

123 Chronic hyperglycaemia causes a dramatic decrease in mitochondri

124 Diabetic hyperglycaemia causes a variety of pathological changes

125 Acute hyperglycaemia causes covalent modification of CaMKII by

126 retinopathy, the underlying mechanism of how hyperglycaemia causes retinal microvascular damage remai

127 The cause of hyperglycaemia changes the response to hypoglycaemic dru

128 stroke, but it is unclear whether sustained hyperglycaemia contributes to the development of cerebro

129 In both cases, extreme hyperglycaemia could not be controlled by conventional a

130 Hyperglycaemia could substantially increase the risk of

131 hy, or prevalent fasting versus postprandial hyperglycaemia, could also be considered in treatment de

132 Intermediate hyperglycaemia defined without an oral glucose tolerance

133 e particularly informative--ie, the roles of hyperglycaemia, diabetic dyslipidaemia (other than the c

134 lts suggest that vascular responses to acute hyperglycaemia differ based on the study population (i.e

135 We assessed the prevalence of hyperglycaemia (DM and impaired glucose regulation (IGR)

136 rately controlled type 2 diabetes treated by hyperglycaemia drugs or insulin.

137 Maternal hyperglycaemia due to a glucokinase mutation resulted in

138 Glp1r-/- mice displayed exercise-induced hyperglycaemia due to an excessive increase in Ra but no

139 s with type 2 diabetes often exhibit fasting hyperglycaemia due to elevated gluconeogenesis; compound

140 Diabetes is characterized by hyperglycaemia due to impaired insulin secretion and abe

141 Hyperglycaemia during hospital admission is common in pa

142 be in remission at 2 years had a relapse of hyperglycaemia during the follow-up period (BPD 52.6% [9

143 besity (assessed using waist circumference), hyperglycaemia, dyslipidaemia and hypertension, highligh

144 ucocorticoid excess include central obesity, hyperglycaemia, dyslipidaemia, electrolyte abnormalities

145 Acute intravenous glucose-induced hyperglycaemia enhanced brachial artery flow-mediated di

146 adverse events in both cohorts combined were hyperglycaemia (five [10%]), lipase elevation (three [6%

147 atment-related grade 3-4 adverse events were hyperglycaemia (five [16%] of 32 patients), nausea (thre

148 ximately 1,000 genes yield approximately 160 hyperglycaemia 'flyabetes' candidates that we classify u

149 en diagnosed with late gestational diabetes (hyperglycaemia from 24 weeks to 28 weeks of gestation).

150 rough a reduction in both mean time spent in hyperglycaemia (glucose concentration >10.0 mmol/L; 31.6

151 dependently segregating loci predisposing to hyperglycaemia, glucose intolerance or altered insulin s

152 The general consensus now is that excessive hyperglycaemia (>10 mmol/L) and severe hypoglycaemia (<2

153 ulation should be limited to avoid excessive hyperglycaemia (>10 mmol/L).

154 hen sensor glucose values were suggestive of hyperglycaemia (>8.0 mmol/L) (15.9%, 10.7-21.0; p<0.0001

155 galy, irrespective of presence or absence of hyperglycaemia, had similar degree of insulin resistance

156 Hyperglycaemia has a powerful association with adverse p

157 Although hyperglycaemia has been determined as the most important

158 The resultant hyperglycaemia has deleterious effects on many tissues,

159 Definition of the genetic basis of hyperglycaemia has implications for patient management.

160 Other vascular factors, such as hyperglycaemia, have now been approached as a continuum

161 esponse to hyperglycaemia Using experimental hyperglycaemia (HG) in vitro, we demonstrate that ECs di

162 ol, and entirely prevents the development of hyperglycaemia, hyperlipidemia and atherosclerosis.

163 ristics of impaired metabolic health such as hyperglycaemia, hypertension and subclinical inflammatio

164 Drugs for hyperglycaemia, hypertension, and dyslipidaemia were pre

165 tion as insulin sensitizers and can decrease hyperglycaemia, hypertriglyceridaemia and hyperinsulinae

166 The mechanisms by which hyperglycaemia (i.e. 11 mM) attenuates hyperthermia are

167 five laboratory definitions of intermediate hyperglycaemia: IGT (2 h plasma glucose >=7.8 mmol/L [>=

168 se uptake in muscle, leading to postprandial hyperglycaemia, impaired glucose tolerance and T2D.

169 Here we show that chronic hyperglycaemia impairs glucose metabolism and alters exp

170 Our findings demonstrate that hyperglycaemia impairs the actions of human insulin on u

171 Prolonged hyperglycaemia impairs vascular reactivity and inhibits

172 d patients were anaemia in 16 (9%) patients, hyperglycaemia in 18 (10%), hypophosphataemia in 16 (9%)

173 and is more effective in the suppression of hyperglycaemia in a maltose loading test than miglitol,

174 whether the adverse clinical association of hyperglycaemia in ACS can be replicated in preclinical c

175 .04 ng ml(-1)) and increased (P < 0.05) with hyperglycaemia in both groups although to a lesser exten

176 5-HT-induced response was amplified by acute hyperglycaemia in control, but not HFD, rats.

177 There is long-established evidence that hyperglycaemia in diabetes is associated with adverse pe

178 ic SREBP1c-CRY1 signalling may contribute to hyperglycaemia in diabetic animals.

179 We recorded relapse of hyperglycaemia in eight (53%) of the 15 patients who ach

180 ucose production in hepatocytes in vitro and hyperglycaemia in fasting mice in vivo.

181 Thus, we hypothesize that exercise-induced hyperglycaemia in Glp1r-/- mice is due to excessive hepa

182 This implies that exercise-induced hyperglycaemia in Glp1r-/- mice results from the loss of

183 Exercise also induces hyperglycaemia in Glp1r-/- mice.

184 lycaemia in one patient on 60 mg once daily, hyperglycaemia in one patient on 150 mg twice weekly, an

185 of 40 DLT-evaluable patients (diarrhoea and hyperglycaemia in one patient on 60 mg once daily, hyper

186 ity (IS) and beta-cell dysfunction result in hyperglycaemia in patients of acromegaly.

187 2, provide new therapeutic targets to reduce hyperglycaemia in patients with diabetes.

188 Although it seems sensible to control hyperglycaemia in patients with neurological injury, the

189 -bolus insulin regimen for the management of hyperglycaemia in patients with type 2 diabetes admitted

190 evalence of type 2 diabetes and intermediate hyperglycaemia in the overall population at the end of t

191 evalence of type 2 diabetes and intermediate hyperglycaemia in the PLA group compared with the contro

192 ther the prediabetes phenotype is defined by hyperglycaemia in the postprandial state (impaired gluco

193 ion in pathology we investigated the role of hyperglycaemia in the regulation of PlGF production in e

194 types previously associated with gestational hyperglycaemia in the third trimester disrupt regulatory

195 evelopment of high-fat-diet-induced diabetic hyperglycaemia in wild-type mice, but not in Trpm5(-/-)

196 lymphopenia were dose-limiting toxicities); hyperglycaemia (in patient number 7); hypokalaemia, hypo

197 ephalus, seizures, venous thrombotic events, hyperglycaemia, increased blood pressure, fever, and inf

198 coronary heart disease, but also with modest hyperglycaemia, increased bodyweight, and modestly incre

199 Hyperglycaemia increases the production of reactive oxyg

200 Acute hyperglycaemia (induced by intravenous glucose) enhanced

201 pathway-specific inhibitors prevent various hyperglycaemia-induced abnormalities.

202 CaMKII inhibition prevented hyperglycaemia-induced alterations.

203 Hyperglycaemia-induced changes in ASL lactate and pH wer

204 knockdown attenuates tunicamycin-induced and hyperglycaemia-induced ER stress and apoptosis.

205 through promoting autophagy and ameliorating hyperglycaemia-induced NTDs.

206 All seem to reflect a single hyperglycaemia-induced process of overproduction of supe

207 We now report that hyperglycaemia-induced repression of miR-30c increases P

208 These data indicate hyperglycaemia induces metabolic changes in beta-cells t

209 In diabetic mouse skin, hyperglycaemia inhibits the expression of IL-17-induced

210 Hyperglycaemia is a hallmark of diabetes and is largely

211 Chronic hyperglycaemia is associated with a dramatic reduction i

212 Hyperglycaemia is associated with increased risk of card

213 Hyperglycaemia is implicated in driving endothelial dysf

214 standard in clinical practice that excessive hyperglycaemia is not acceptable.

215 Acute hyperglycaemia is not limited to diabetic patients and c

216 Hyperglycaemia is one such complication in the intensive

217 Fasting hyperglycaemia is strongly correlated with type II diabe

218 So-called stress hyperglycaemia is usually defined as hyperglycaemia reso

219 Prediabetes (intermediate hyperglycaemia) is a high-risk state for diabetes that i

220 R-129-2, which mediate the teratogenicity of hyperglycaemia leading to NTDs.

221 ints included hypoglycaemia and uncontrolled hyperglycaemia leading to treatment failure.

222 size that increased airway glucose caused by hyperglycaemia leads to increased bacterial loads.

223 ll patients with type 2 diabetes and chronic hyperglycaemia, liberal glycemic control appears to atte

224 e ranges that can be used for discriminating hyperglycaemia likely to be caused by a GCK mutation and

225 Clinical and experimental data suggest that hyperglycaemia lowers the ischaemic neuronal threshold i

226 This study provides the first evidence that hyperglycaemia may increase influenza severity by damagi

227 c beta-cell replication, but the presence of hyperglycaemia may increase the hypoxic susceptibility o

228 We describe classification of stress hyperglycaemia, mechanisms of harm, and management strat

229 ns and identification of patients at risk of hyperglycaemia might be needed.

230 Diabetes and hyperglycaemia models were adjusted for potential confou

231 was designed to determine whether hypo- and hyperglycaemia modulate the hypoxic ventilatory response

232 SGA, n = 34) and (c) whose mothers developed hyperglycaemia (n = 59).

233 -abiraterone group and in two patients (<1%; hyperglycaemia [n=1] and chemical pneumonitis [n=1]) in

234 management of incident cases of non-diabetic hyperglycaemia (NDH) and T2D.

235 [7%]); those for combination treatment were hyperglycaemia (nine [22%] of 41 patients) and diarrhoea

236 ur [5%] of 76 in the intervention group) and hyperglycaemia (observed in seven [9%] of 77 vs seven [9

237 group, and diabetic ketoacidosis and severe hyperglycaemia occurred in one participant each in the C

238 the most common grade 3-4 adverse event was hyperglycaemia, occurring in one (<1%) of 320 patients g

239 effects of the hypoxic stress of OSA and the hyperglycaemia of type 2 diabetes on haemodynamic and me

240 output is a major aetiological factor in the hyperglycaemia of type-2 diabetes mellitus and other dis

241 microl) abolished the inhibitory effects of hyperglycaemia on gastric distension-induced pyloric rel

242 nervous system in modulating the effects of hyperglycaemia on gastric distension-induced pyloric rel

243 n in CGM-measured mean glucose (p=0.005) and hyperglycaemia (on four metrics: p=0.007 for >180 mg/dL

244 eversible grade 3 neutropenia (two), grade 4 hyperglycaemia (one), and grade 4 increases in aminotran

245 injury (two), diarrhoea (three), rash (two), hyperglycaemia (one), loss of consciousness (one), sepsi

246 receptor distribution was amplified by acute hyperglycaemia only in control rats.

247 atients with pancreatic cancer who also have hyperglycaemia or diabetes has previously been under app

248 of leptin synthesis is reproduced by either hyperglycaemia or hyperlipidaemia, which also increase t

249 ic excursions and, consequently, the risk of hyperglycaemia or hypoglycaemia.

250 Two diabetes-related serious adverse events (hyperglycaemia or ketosis without acidosis) resulting in

251 FFA and microbiota that, even in absence of hyperglycaemia or overt endotoxaemia, synergistically in

252 or PLA were INT$316 per case of intermediate hyperglycaemia or type 2 diabetes prevented and $6518 pe

253 orial and likely include effects of obesity, hyperglycaemia, oxidative stress, and accumulation of ad

254 ssociated with long-standing diabetes, acute hyperglycaemia per se has effects on gastric emptying.

255 The extent to which hyperglycaemia per se underlies these alterations remain

256 lar function and obscure the effect of acute hyperglycaemia per se.

257 Hyperglycaemia, rather than KATP channel activation, und

258 Acute hyperglycaemia readily induces robust ROS production in

259 s underlying diabetes and its characteristic hyperglycaemia remain elusive.

260 but neonatal outcomes attributed to maternal hyperglycaemia remain suboptimal.

261 anisms behind the mild stimulating effect of hyperglycaemia remain to be elucidated.

262 Patients with hyperglycaemia requiring treatment with insulin before a

263 stress hyperglycaemia is usually defined as hyperglycaemia resolving spontaneously after dissipation

264 By contrast, hyperglycaemia resulted in small but significant increas

265 tate where glucose homeostasis is preserved, hyperglycaemia results during exercise in GLUT4(-/-) due

266 The hyperglycaemia results from beta-cell dysfunction and is

267 In a mouse model of human neonatal diabetes, hyperglycaemia results in marked glycogen accumulation,

268 emia (three [7%]); those for everolimus were hyperglycaemia (seven [17%] of 42 patients), stomatitis

269 and 4 adverse events in the safety set were hyperglycaemia (seven [8%] of 92 patients), rash (four [

270 In HEK293 cells, hyperglycaemia significantly enhanced [(3) H]ryanodine b

271 In HEK293 cells, hyperglycaemia significantly enhanced [(3) H]ryanodine b

272 Acute hyperglycaemia stimulates hypothalamic NPY release, whic

273 te the ventilatory response to hypoxia, with hyperglycaemia suppressing the hypoxic response and hypo

274 e 3-4 non-haematological adverse events were hyperglycaemia (ten [55%] patients), hypokalaemia (six [

275 o showed more severe glucose intolerance and hyperglycaemia than Mc4r KO.

276 Hyperglycaemia that develops during pregnancy and resolv

277 ns, including weight gain and rare events of hyperglycaemia, that could affect maternal, fetal, and p

278 44 patients), neutropenia (three [7%]), and hyperglycaemia (three [7%]).

279 of 41 patients), diarrhoea (three [7%]), and hyperglycaemia (three [7%]); those for everolimus were h

280 of individuals identified with intermediate hyperglycaemia through a cross-sectional survey at basel

281 b/db mice, overexpression of CRY1 attenuates hyperglycaemia through reduction of hepatic FOXO1 protei

282 odification of brain proteins link Abeta and hyperglycaemia to cognitive dysfunction in MetS/T2DM and

283 [2%] vs five [1%]) in the imatinib group and hyperglycaemia (two [<1%] vs seven [2%]) in the placebo

284 ey were dehydration (two individuals [10%]), hyperglycaemia (two [10%]), and increased concentrations

285 acebo group), nausea (two [2%] vs none), and hyperglycaemia (two [2%] vs none).

286 with few grade 3-4 adverse events including hyperglycaemia (two [4%] patients, grade 3), nausea (one

287 ion to how this influences their response to hyperglycaemia Using experimental hyperglycaemia (HG) in

288 1) respectively, and the insulin response to hyperglycaemia was abolished in shams but not affected i

289 Hyperglycaemia was reported by 12 of 106 (11%) patients

290 y between treatment modality and severity of hyperglycaemia, we cannot exclude that treatment-related

291 Diabetes and hyperglycaemia were collectively evaluated as dysglycaem

292 ions in utero and others exposed to maternal hyperglycaemia were compared to a control group with res

293 Cells habituated to hyperglycaemia were energetically quiescent.

294 and control type 2 diabetes and intermediate hyperglycaemia, which together affect roughly a third of

295 VAN) activity in vivo before and after acute hyperglycaemia, while electrophysiological recordings fr

296 in keeping with the clinical association of hyperglycaemia with an adverse outcome in ACS.

297 No episodes of severe hypoglycaemia or hyperglycaemia with ketonaemia occurred in either group.

298 No episodes of severe hypoglycaemia or hyperglycaemia with ketonaemia occurred in either study

299 ues can target both fasting and postprandial hyperglycaemia, with the added advantage of being premix

300 pe 2 diabetes among people with intermediate hyperglycaemia within the study population.