ライフサイエンスコーパス: hyperglycaemia

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

2 d diacylglycerol (DG) production in diabetic hyperglycaemia.

3 D1 results in increased gluconeogenesis and hyperglycaemia.

4 ions which cause lifelong persistent fasting hyperglycaemia.

5 m the gut and thereby alleviate postprandial hyperglycaemia.

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

7 ass and markedly improving dyslipidaemia and hyperglycaemia.

8 epatic gluconeogenesis, which contributes to hyperglycaemia.

9 ar population of sympathetic neurons against hyperglycaemia.

10 with particular attention to the hazards of hyperglycaemia.

11 hich include peripheral vasoconstriction and hyperglycaemia.

12 tem/liver circuit can contribute to diabetic hyperglycaemia.

13 e of entry into proximal tubule cells during hyperglycaemia.

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

15 f the primary metabolic pathways impaired by hyperglycaemia.

16 d with increased risk of hyperlipidaemia and hyperglycaemia.

17 thways partially recovers beta-cell mass and hyperglycaemia.

18 e attributed to reduced exposure to maternal hyperglycaemia.

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

20 ay be impaired under conditions of sustained hyperglycaemia.

21 rom starches and alleviation of postprandial hyperglycaemia.

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

23 nability to maintain body temperature and by hyperglycaemia.

24 iabetes require insulin therapy for treating hyperglycaemia.

25 ncreatic diseases with varying mechanisms of hyperglycaemia.

26 is a group of diseases defined by persistent hyperglycaemia.

27 glycaemic control in the setting of chronic hyperglycaemia.

28 is warranted because of potential relapse of hyperglycaemia.

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

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

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

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

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

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

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

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

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

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

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

40 Hyperglycaemia after acute stroke is a common finding th

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

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

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

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

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

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

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

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

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

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

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

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

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

54 Chronic hyperglycaemia and microvascular disease contribute to c

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

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

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

58 Correction of hyperglycaemia and prevention of glucotoxicity are impor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 Hyperglycaemia can adversely affect outcome in criticall

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

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

77 Diabetic hyperglycaemia causes a variety of pathological changes

78 Acute hyperglycaemia causes covalent modification of CaMKII by

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

80 The cause of hyperglycaemia changes the response to hypoglycaemic dru

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

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

83 Hyperglycaemia could substantially increase the risk of

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

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

86 Maternal hyperglycaemia due to a glucokinase mutation resulted in

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

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

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

90 Hyperglycaemia during hospital admission is common in pa

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

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

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

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

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

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

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

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

99 The resultant hyperglycaemia has deleterious effects on many tissues,

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

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

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

103 Drugs for hyperglycaemia, hypertension, and dyslipidaemia were pre

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

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

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

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

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

109 Prolonged hyperglycaemia impairs vascular reactivity and inhibits

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

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

112 .04 ng ml(-1)) and increased (P < 0.05) with hyperglycaemia in both groups although to a lesser exten

113 5-HT-induced response was amplified by acute hyperglycaemia in control, but not HFD, rats.

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

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

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

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

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

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

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

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

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

123 2, provide new therapeutic targets to reduce hyperglycaemia in patients with diabetes.

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

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

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

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

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

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

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

131 Hyperglycaemia increases the production of reactive oxyg

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

133 CaMKII inhibition prevented hyperglycaemia-induced alterations.

134 Hyperglycaemia-induced changes in ASL lactate and pH wer

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

136 through promoting autophagy and ameliorating hyperglycaemia-induced NTDs.

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

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

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

140 Hyperglycaemia is a hallmark of diabetes and is largely

141 Chronic hyperglycaemia is associated with a dramatic reduction i

142 Hyperglycaemia is associated with increased risk of card

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

144 Fasting hyperglycaemia is strongly correlated with type II diabe

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

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

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

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

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

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

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

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

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

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

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

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

157 [7%]); those for combination treatment were hyperglycaemia (nine [22%] of 41 patients) and diarrhoea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Hyperglycaemia, rather than KATP channel activation, und

175 s underlying diabetes and its characteristic hyperglycaemia remain elusive.

176 but neonatal outcomes attributed to maternal hyperglycaemia remain suboptimal.

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

178 Patients with hyperglycaemia requiring treatment with insulin before a

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

180 By contrast, hyperglycaemia resulted in small but significant increas

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

182 The hyperglycaemia results from beta-cell dysfunction and is

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

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

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

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

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

188 Acute hyperglycaemia stimulates hypothalamic NPY release, whic

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

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

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

192 44 patients), neutropenia (three [7%]), and hyperglycaemia (three [7%]).

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

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

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

196 [2%] vs five [1%]) in the imatinib group and hyperglycaemia (two [<1%] vs seven [2%]) in the placebo

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

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

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

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

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

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

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

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