ライフサイエンスコーパス: hypoglycemia

1 es good glycemic control and one that causes hypoglycemia.

2 sponse to blood glucose, mitigating risk for hypoglycemia.

3 sociated with decreases in hyperglycemia and hypoglycemia.

4 improvements in glycemia and no evidence of hypoglycemia.

5 y correlated with the adrenaline response to hypoglycemia.

6 glucose, aggravating the potential to cause hypoglycemia.

7 ed to the severity and frequency of neonatal hypoglycemia.

8 therapy in type 1 diabetes and recalcitrant hypoglycemia.

9 , the plasma ghrelin level rises, preventing hypoglycemia.

10 ted in a reduced rate of overall symptomatic hypoglycemia.

11 e counter-regulatory response (CRR) prevents hypoglycemia.

12 ult, CD36Tg mice were protected from fasting hypoglycemia.

13 may reduce the prevalence of moderate-severe hypoglycemia.

14 1 diabetes and increases the risk of severe hypoglycemia.

15 amine and the sympathetic nerve responses to hypoglycemia.

16 clamp protocol and during the last 30 min of hypoglycemia.

17 intain glucose homeostasis and guard against hypoglycemia.

18 ant literature on exogenous hyperinsulinemic hypoglycemia.

19 may contribute to the impaired detection of hypoglycemia.

20 20%]) were associated with greatest odds of hypoglycemia.

21 esponses, but not catecholamine responses to hypoglycemia.

22 latory homeostatic responses during repeated hypoglycemia.

23 d impaired cardiovascular homeostasis during hypoglycemia.

24 uces symptoms and neurohormonal responses to hypoglycemia.

25 ate preterm and term infants born at risk of hypoglycemia.

26 od had recurrent episodes of moderate-severe hypoglycemia.

27 mparable to the delay in onset of PH-induced hypoglycemia.

28 he management of iatrogenic hyperinsulinemic hypoglycemia.

29 utcomes were glucose levels and incidence of hypoglycemia.

30 ed with postexercise foods to further combat hypoglycemia.

31 increase their risk for experiencing severe hypoglycemia.

32 a potential mechanism preventing OCN-induced hypoglycemia.

33 conventional therapy, 7 patients had severe hypoglycemia.

34 lity in type 1 diabetes subjects with severe hypoglycemia.

35 ally undetected (interstitial episodes only) hypoglycemia.

36 diabetes and reduced by antecedent recurrent hypoglycemia.

37 ion during ischemic attacks and acute severe hypoglycemia.

38 ntinuous glucose monitoring group had severe hypoglycemia.

39 n effect) to defend against hyperinsulinemia-hypoglycemia.

40 gal tone remained depressed during sustained hypoglycemia.

41 aling in glucose transport was unaffected by hypoglycemia.

42 repolarization during sustained experimental hypoglycemia.

43 result, delayed the onset of fasting-induced hypoglycemia.

44 adapt to a more proinflammatory state after hypoglycemia.

45 ed plasma glucose and thus increased risk of hypoglycemia.

46 rol immediately increases the risk of severe hypoglycemia 1.5- to 3-fold.

47 was maintained at euglycemia (6.0 mmol/L) or hypoglycemia (2.5 mmol/L) for 1 h.

48 lthy volunteers were exposed to experimental hypoglycemia (2.8 mmol/L) for 120 min.

49 Those exposed to neonatal hypoglycemia (280 [58.7%]) did not have increased risk o

50 pe 1 diabetes and at least 1 risk factor for hypoglycemia, 32 weeks' treatment with insulin degludec

51 y, was associated with lower rates of severe hypoglycemia (9.55 vs 13.97 per 100 patient-years; diffe

52 Hypoglycemia, a serious risk for insulin-treated patient

53 sy were doubled among children with neonatal hypoglycemia (adjusted HR, 2.10; 95% CI, 1.90-2.33) and

54 esign to test to what extent insulin-induced hypoglycemia affects glucose uptake in skeletal muscle a

55 with type 1 diabetes face heightened risk of hypoglycemia after exercise.

56 r, longer time spent in hyperglycemia and in hypoglycemia after RYGBP compared with SG is not associa

57 At the beginning of hypoglycemia (after HIIT), brain lactate levels were ele

58 Recurrent hypoglycemia alters the cascade of physiological and beh

59 xacerbates, and whether recurrent antecedent hypoglycemia ameliorates, susceptibility to arrhythmias

60 g, had the highest risk for nausea; risk for hypoglycemia among once-weekly GLP-1RAs was similar.

61 e glucose-lowering effect and lower rates of hypoglycemia among patients who received degludec than a

62 ubset of alpha-cells for normal responses to hypoglycemia and acts via Ca(2+)-independent mechanisms.

63 in the short term, HIIT reduces awareness of hypoglycemia and attenuates hypoglycemia-induced cogniti

64 ity to serious medical complications such as hypoglycemia and diabetes.

65 y, was associated with lower risks of severe hypoglycemia and diabetic ketoacidosis and with better g

66 To determine whether rates of severe hypoglycemia and diabetic ketoacidosis are lower with in

67 Primary outcomes were rates of severe hypoglycemia and diabetic ketoacidosis during the most r

68 Severe hypoglycemia and diabetic ketoacidosis were absent in pa

69 s before and after undergoing GBP surgery to hypoglycemia and examined symptoms and hormonal and auto

70 h MDI whereas islet transplantation resolved hypoglycemia and further improved glycemic variability r

71 l" approach to glycemic control would reduce hypoglycemia and glycemic variability and appear safe.

72 n (CSII) and islet transplantation to reduce hypoglycemia and glycemic variability in type 1 diabetes

73 NEET in alpha-cells leads to fasting-induced hypoglycemia and hypersecretion of insulin during GSIS.

74 acids (FAs) when simultaneously subjected to hypoglycemia and hypoxia.

75 have shown associations between exposure to hypoglycemia and increased mortality, raising the possib

76 ponse of epinephrine and glucagon to a given hypoglycemia and increased net hepatic glucose output (N

77 en is important for the counterregulation of hypoglycemia and is reduced in individuals with type 1 d

78 croglia after sequential exposure to hypoxia/hypoglycemia and normoxia/normoglycemia (H/H-N/N).

79 was markedly blunted, resulting in profound hypoglycemia and prevalent mortality upon severe caloric

80 critical functions of ghrelin in preventing hypoglycemia and promoting survival during severe calori

81 es of negative glycemic distance or relative hypoglycemia and reduced insulin administration compared

82 th HF, given their established high risk for hypoglycemia and some uncertainties on their safety in p

83 ivation of the counterregulatory response to hypoglycemia and that impairment of glutamate metabolic

84 ell-intrinsic mechanism controls glucagon in hypoglycemia and that paracrine factors shape pulsatile

85 The advantages of GLP-1 for the avoidance of hypoglycemia and the control of body weight are attracti

86 The Children With Hypoglycemia and Their Later Development (CHYLD) Study i

87 ntromedial hypothalamus (VMH) in response to hypoglycemia and to elucidate the effects of recurrent h

88 Hypoglycemia and weight gain are common side effects of

89 with type 1 diabetes and normal awareness of hypoglycemia, and 3) healthy participants without diabet

90 lure (rescue treatment or lack of efficacy), hypoglycemia, and body weight.

91 s completely ablated during hyperinsulinemic hypoglycemia, and catecholamine signaling via cAMP-depen

92 The total incidence of adverse events (AEs), hypoglycemia, and genital and urinary infections were al

93 creases the incidence of moderate and severe hypoglycemia, and increases mortality.

94 o weight loss, does not increase the risk of hypoglycemia, and involves a novel and incompletely unde

95 e increased birth weight, transient neonatal hypoglycemia, and maturity onset diabetes of the young (

96 Cardiac autonomic regulation during hypoglycemia appears to be time dependent.

97 ), 3) STZ with antecedent recurrent (3 days) hypoglycemia ( approximately 40-45 mg/dL, 90 min) (STZ+R

98 Strategies to prevent hypoglycemia are often ineffective, highlighting the nee

99 tes (aRR, 2.42; 95% CI, 1.62-3.61), neonatal hypoglycemia (aRR, 1.53; 95% CI, 1.34-1.75), and respira

100 eater heterogeneity of repolarization during hypoglycemia as demonstrated by T-wave symmetry and prin

101 are expected to exhibit a low risk to induce hypoglycemia as well as to have a beneficial impact on b

102 Adjudicated severe hypoglycemia, as defined by the American Diabetes Associ

103 ed dysregulation of blood glucose (hyper- or hypoglycemia) associated with type 1 diabetes (T1D) has

104 precursor, N-acetylcysteine (NAC), prevented hypoglycemia-associated autonomic failure (HAAF) and imp

105 ective counterregulatory responses, known as hypoglycemia-associated autonomic failure (HAAF).

106 EA may have acute effects to protect against hypoglycemia-associated neuroendocrine and autonomic fai

107 hypoglycemia can prevent the development of hypoglycemia-associated neuroendocrine and autonomic fai

108 hrine response together with reduced EGP and hypoglycemia-associated symptoms on day 2.

109 then fell toward baseline despite maintained hypoglycemia at 1 h accompanied by reactivation of vagal

110 Median duration of hypoglycemia at less than <70 mg/dL was 43 min/d (IQR, 2

111 orted in this article, including duration of hypoglycemia at less than 70 mg/dL, measured with CGM fo

112 Together, these effects induced hypoglycemia, at least in part by increasing insulin and

113 hyperlacticacidemia on brain lactate during hypoglycemia between 1) patients with type 1 diabetes an

114 In response to hypoglycemia, BG4KO mice had impaired glucose sensing, n

115 e randomized study days: 1) hyperinsulinemic hypoglycemia (bolus insulin), 2) hyperinsulinemic euglyc

116 During hypoglycemia, brain lactate decreased approximately 30%

117 Before HIIT (baseline) and during hypoglycemia, brain lactate levels were determined conti

118 d gastric inhibitory polypeptide rose during hypoglycemia but rose less postsurgery compared with pre

119 inal physiological role in buffering against hypoglycemia, but its poor biophysical properties severe

120 patients are especially prone to IIT-induced hypoglycemia, but the mechanism remains unknown.

121 In response to insulin-induced hypoglycemia, C-peptide (absent before transplant) was a

122 Hypoglycemia can be avoided with glucagon-like peptide (

123 Severe hypoglycemia can lead to coma or death.

124 rosterone (DHEA) during episodes of repeated hypoglycemia can prevent the development of hypoglycemia

125 n of these disorders may include hypoketotic hypoglycemia, (cardio)myopathy, arrhythmia, and rhabdomy

126 Recurrent and/or antecedent hypoglycemia causes blunting of protective counterregula

127 Hypoglycemia, common in patients with type 1 diabetes, i

128 kine response to microbial stimulation after hypoglycemia compared with euglycemia, although it was l

129 similarly reduced after alprazolam or day 1 hypoglycemia compared with euglycemic control.

130 degludec is associated with a lower rate of hypoglycemia compared with insulin glargine U100 in pati

131 During hypoglycemia, compared with baseline euglycemic conditio

132 nd pre-existing diabetes, hyperglycemia, and hypoglycemia, corrected for other factors, was analyzed

133 lucose uptake in skeletal muscle and whether hypoglycemia counterregulation modulates insulin and cat

134 e Sprague-Dawley rats restores the defective hypoglycemia counterregulatory response.

135 splantation improved, and the rate of severe hypoglycemia decreased significantly as compared to cont

136 , P=0.04), as well as higher rates of severe hypoglycemia, defined as a blood glucose level below 40

137 Severe hypoglycemia dropped in SIK/IAK from 4.5 +/- 9.7 to 0.3

138 so hypoxia with iron deficiency, results in hypoglycemia due to decreased levels of hepatic pyruvate

139 which could increase their susceptibility to hypoglycemia during IIT, contraindicating its use.

140 of pre-existing diabetes, hyperglycemia, and hypoglycemia during the first 24 hours of ICU admissions

141 sulin glargine U100 group experienced severe hypoglycemia during the maintenance period (10.3%, 95% C

142 proportions of patients experiencing severe hypoglycemia during the maintenance period were 1.6% (95

143 ) and the proportion of patients with severe hypoglycemia during the maintenance period.

144 sodes and proportion of patients with severe hypoglycemia during the maintenance period.

145 insulin designed by us showed a long-lasting hypoglycemia effect with a faster onset in diabetic rats

146 n HYPOscore from 2028 to 1085 (P < 0.05) and hypoglycemia events from 24 to 8 per patient-year (P < 0

147 Severe hypoglycemia events occurred in 2 participants in each g

148 in the normal counterregulatory response to hypoglycemia explain the frequency of hypoglycemia occur

149 he case of a 66-year-old woman who developed hypoglycemia following the prolonged infiltration of a h

150 ral dextrose infusion that delays PH-induced hypoglycemia for 14 hours after surgery was identified,

151 uctions in overall and nocturnal symptomatic hypoglycemia for insulin degludec vs insulin glargine U1

152 nce period, the rates of overall symptomatic hypoglycemia for insulin degludec vs insulin glargine U1

153 le for islet transplantation, CSII decreased hypoglycemia frequency and glycemic variability compared

154 Repeated episodes of hypoglycemia further impair vascular function by additio

155 Hypoglycemia generated symptoms in patients with NAH and

156 During hypoglycemia, glucose levels reached a nadir of approxim

157 ased mortality, raising the possibility that hypoglycemia has adverse cardiovascular effects.

158 Hyperinsulinemic hypoglycemia (HI) and congenital polycystic kidney disea

159 in 12 subjects with episodic rhabdomyolysis, hypoglycemia, hyperammonemia, and susceptibility to life

160 emains uncertain whether recurrent nonsevere hypoglycemia (Hypo) results in long-term cognitive impai

161 in the development of impaired awareness of hypoglycemia (IAH) in type 1 diabetes, the capacity to t

162 in the development of impaired awareness of hypoglycemia (IAH), a condition that affects approximate

163 a (NAH), patients with impaired awareness of hypoglycemia (IAH), and healthy participants (n = 10 per

164 to a condition called impaired awareness of hypoglycemia (IAH), the cause of which is unknown.

165 sponse to moderate-to-marked insulin-induced hypoglycemia (IIH) is largely mediated by the autonomic

166 Hypoglycemia impaired insulin-stimulated glucose disposa

167 In summary, acute moderate hypoglycemia impairs fibrinolytic balance; increases pro

168 We detected relative hypoglycemia in 20 (50.0%) and nine (22.5%) patients in

169 t out to investigate the clinical problem of hypoglycemia in children with illnesses that limited the

170 may increase the risk of exercise-associated hypoglycemia in individuals with type 1 diabetes.

171 Compared with rest, HIIT reduced symptoms of hypoglycemia in patients with NAH but not in healthy par

172 in arrhythmias during spontaneous prolonged hypoglycemia in patients with T2DM.

173 sion rapidly reduces awareness of subsequent hypoglycemia in patients with type 1 diabetes and NAH, b

174 ficantly by approximately 20% in response to hypoglycemia in patients with type 1 diabetes with IAH b

175 parable pharmacology against insulin-induced hypoglycemia in rats and pigs.

176 It remains to be explored whether hypoglycemia in SCHAD CHI can be uncoupled from the syst

177 We conclude that hypoglycemia in SCHAD-CHI is islet cell-autonomous.

178 ghrelin in mediating beta blocker-associated hypoglycemia in susceptible individuals, such as young c

179 be determined whether the risk of iatrogenic hypoglycemia in T1D humans could be lessened by targetin

180 Recurrent moderate hypoglycemia in T1D, but not Control, mice significantly

181 the hypothesis that ghrelin rises to prevent hypoglycemia in the absence of glucagon function.

182 In diabetes patients, only severe hypoglycemia in the absence of hyperglycemia was associa

183 y each have been reported to protect against hypoglycemia in the fasted state, but previous data have

184 While there was a 15% incidence of hypoglycemia in the insulin group, there was only 1 mild

185 py for preventing recurrent life-threatening hypoglycemia in type 1 diabetes.

186 The counterregulatory response (CRR) to hypoglycemia in vivo and the activation of VMH GI neuron

187 crease in epinephrine release and results in hypoglycemia in vivo.

188 musculoskeletal pain or discomfort and mild hypoglycemia) in the lifestyle group and 5 in the standa

189 s' gestation with at least 1 risk factor for hypoglycemia, including diabetic mother, preterm, small,

190 Hypoglycemia increased leukocyte numbers in healthy cont

191 Of note, hypoglycemia increased the expression of markers of dema

192 In summary, severe hypoglycemia-induced cardiac arrhythmias were increased

193 t moderate hypoglycemia reduced fatal severe hypoglycemia-induced cardiac arrhythmias.

194 HIIT attenuated hypoglycemia-induced cognitive dysfunction, which was ma

195 ces awareness of hypoglycemia and attenuates hypoglycemia-induced cognitive dysfunction.

196 oes not in patients with IAH, and attenuates hypoglycemia-induced cognitive dysfunction.

197 adipocyte size, reduced lean mass, impaired hypoglycemia-induced glucagon secretion, and a lack of p

198 nts with diabetes, which may be explained by hypoglycemia-induced inflammation.

199 Hypoglycemia-induced proinflammatory changes may promote

200 tory hormone responses are key modulators of hypoglycemia-induced proinflammatory effects.

201 ly demonstrated that insulin-mediated severe hypoglycemia induces lethal cardiac arrhythmias.

202 Hypoglycemia is a major adverse effect of insulin therap

203 ient rise in glutamate levels in response to hypoglycemia is absent in RH animals.

204 Hypoglycemia is associated with increased cardiovascular

205 Prolonged neonatal hypoglycemia is associated with poor long-term neurocogn

206 Hypoglycemia is common during neonatal transition and ma

207 tive regulation is postponed when PH-induced hypoglycemia is delayed.

208 Hypoglycemia is the leading limiting factor in glycemic

209 Hypoglycemia is the most common complication of diabetes

210 type 1 diabetes mellitus (T1DM), iatrogenic hypoglycemia limits its attainment.

211 (P=0.16), and 18% patients developed serious hypoglycemia (<50 mg/dL) versus none of the controls.

212 a that is also implicated in the response to hypoglycemia, make synaptic connections with the specifi

213 y to transport lactate into the brain during hypoglycemia may be relevant in its pathogenesis.

214 compared with those with normal awareness of hypoglycemia (NAH) and healthy control subjects (n = 7 p

215 with type 1 diabetes and normal awareness of hypoglycemia (NAH), and 10 patients with type 1 diabetes

216 with type 1 diabetes and normal awareness of hypoglycemia (NAH), patients with impaired awareness of

217 cose tolerance did not increase the risk for hypoglycemia, nor did it rely upon hyperinsulinemia or b

218 lar to the life-threatening, fasting-induced hypoglycemia observed in infants treated with beta block

219 Prespecified adjudicated severe hypoglycemia occurred in 187 patients (4.9%) in the degl

220 In contrast, lethal hypoglycemia occurred in mice deficient in the GH secret

221 nse to hypoglycemia explain the frequency of hypoglycemia occurrence in T1D.

222 study was to investigate the effect of acute hypoglycemia on brain lactate concentration in patients

223 is study, we determined the acute effects of hypoglycemia on cardiovascular autonomic control.

224 ymptom counterregulatory responses following hypoglycemia on day 1.

225 During hypoglycemia on day 2, DHEA prevented blunting of all ne

226 as used to determine glucose kinetics during hypoglycemia on day 2.

227 Conversely, elucidating the effects of hypoglycemia on PHHs may provide insights into how the l

228 We characterized the effects of hypoxia/hypoglycemia on phosphorylation of signal transducer and

229 7.0% at week 24, with no episodes of severe hypoglycemia or diabetic ketoacidosis after randomizatio

230 oglobin level lower than 7.0% with no severe hypoglycemia or diabetic ketoacidosis was larger in the

231 al outcomes (emergency department visits for hypoglycemia or hyperglycemia).

232 al outcomes (emergency department visits for hypoglycemia or hyperglycemia).

233 did not differ meaningfully in CGM-measured hypoglycemia or quality-of-life outcomes.

234 SGLT-2 inhibitors offered the lowest odds of hypoglycemia (OR, 0.12 [95% CI, 0.08 to 0.18]; RD, -22%

235 ists were associated with the lowest odds of hypoglycemia (OR, 0.60 [95% CI, 0.39 to 0.94]; RD, -10%

236 sulin dose without an increase in total AEs, hypoglycemia, or genital and urinary infections.

237 ose ingestion (P=0.02) with more symptoms of hypoglycemia (P=0.04).

238 lts to a large extent from prior exposure to hypoglycemia per se, leading to a condition called impai

239 Postprandial hyperinsulinemic hypoglycemia (PHH) is often reported after Roux-en-Y gas

240 of routine prophylaxis include hyperkalemia, hypoglycemia, photosensitivity, thrombocytopenia, and mo

241 We conclude that hypoglycemia promotes mobilization of specific leukocyte

242 ve (glycemic distance, > 30% below baseline) hypoglycemia rates, insulin administration, and outcomes

243 During matched nadirs of severe hypoglycemia, rats in the STZ+RH group required a 1.7-fo

244 th high glycemic variability and problematic hypoglycemia received intraportal islet grafts under ant

245 In this model, recurrent moderate hypoglycemia reduced fatal severe hypoglycemia-induced c

246 ignal toward reduced risk of moderate-severe hypoglycemia (relative risk: liberal compared with stand

247 This glucose dependence prevents hypoglycemia, rendering GLP-1 analogs a useful and safe

248 No episodes of severe hypoglycemia requiring third-party assistance occurred d

249 (GI) neurons by low glucose after recurrent hypoglycemia (RH) in nondiabetic rats.

250 ia and to elucidate the effects of recurrent hypoglycemia (RH) on this neurotransmitter.

251 olic crises characterized by encephalopathy, hypoglycemia, rhabdomyolysis, arrhythmias, and laborator

252 ly medications with low treatment burden and hypoglycemia risk (such as metformin) are required, a lo

253 y trial involving 501 adults with at least 1 hypoglycemia risk factor treated at 84 US and 6 Polish c

254 1 adults with type 2 diabetes and at least 1 hypoglycemia risk factor who were previously treated wit

255 tes treated with insulin and with at least 1 hypoglycemia risk factor, 32 weeks' treatment with insul

256 dividuals were assessed with HbA1c, Edmonton Hypoglycemia Score (HYPOscore), continuous glucose monit

257 The mean change in Edinburgh Hypoglycemia Score during clamp was attenuated from 10.7

258 In subjects with severe hypoglycemia suitable for islet transplantation, CSII de

259 ype 1 diabetes subjects referred with severe hypoglycemia, suitable for islet transplantation.

260 nsiderations include anticipated duration of hypoglycemia, supplemental glucose, fluid management, an

261 , since the administration of lactate during hypoglycemia suppresses symptoms and counterregulation w

262 ctive glucose counterregulation and impaired hypoglycemia symptom recognition that substantially incr

263 The aware group reported higher hypoglycemia symptom scores and had higher epinephrine a

264 egulates blood glucose, as emphasized by the hypoglycemia that is induced by caloric restriction in m

265 characterized by fasting and protein-induced hypoglycemia that is unresponsive to medical therapy.

266 She subsequently experienced prolonged hypoglycemia that was managed with concentrated dextrose

267 We demonstrate that after recurrent hypoglycemia the introduction of a novel dishabituating

268 a blockers led to reduced plasma ghrelin and hypoglycemia, the latter of which is similar to the life

269 Insulinomas are beta-cell tumors that cause hypoglycemia through inappropriate secretion of insulin.

270 Mortality due to severe hypoglycemia was 5% in the STZ+RH group, 6.2-fold less t

271 However, hypoglycemia was associated with increased risk of low e

272 and for the secondary end point of nocturnal hypoglycemia was defined as an upper limit of the 2-side

273 Neonatal hypoglycemia was more common in the betamethasone group

274 Hypoglycemia was more frequent with sulfonylureas.

275 In this cohort, neonatal hypoglycemia was not associated with an adverse neurolog

276 Neonatal hypoglycemia was not associated with increased risk of c

277 The rate of severe hypoglycemia was similar in the sotagliflozin group and

278 Among once-weekly GLP-1RAs, the risk for hypoglycemia was similar, whereas taspoglutide, 20 mg, h

279 nce period, the rates of overall symptomatic hypoglycemia were 2200.9 episodes per 100 person-years'

280 The rates of nocturnal symptomatic hypoglycemia were 277.1 per 100 PYE in the insulin deglu

281 Adverse events including severe hypoglycemia were also studied.

282 Hyper- and hypoglycemia were associated with poor neurologic outcom

283 rglycemia (>/= 200 mg/dL), and patients with hypoglycemia were excluded.

284 ucagon and NHGO responses to insulin-induced hypoglycemia were reduced.

285 e, reversible neonatal liver dysfunction and hypoglycemia were seen in >40% of all cases.

286 and post-extracorporeal membrane oxygenation hypoglycemia were shown to be associated with CNS compli

287 Epinephrine levels during hypoglycemia were similar between groups.

288 ecretion induced by oral glucose could cause hypoglycemia when coupled with the levels of insulin sen

289 eurons) blocks recovery from insulin-induced hypoglycemia whereas, conversely, activation of VMN(SF1)

290 to reduce the incidence of hyperglycemia and hypoglycemia, which further reduces potential complicati

291 dity, but also causes a 4-5-fold increase in hypoglycemia, which is associated with a 9-fold increase

292 providing an alternative fuel source during hypoglycemia, which may contribute to the impaired detec

293 Infants with hypoglycemia (whole-blood glucose concentration <47 mg/d

294 association of diabetes, hyperglycemia, and hypoglycemia with 90-day mortality (n = 128,222).

295 The rate of documented hypoglycemia with a blood glucose level of 55 mg per dec

296 The rates of nocturnal symptomatic hypoglycemia with insulin degludec vs insulin glargine U

297 severe allergic reactions (antibiotics), and hypoglycemia with moderate to severe neurological effect

298 Antecedent hypoglycemia with placebo resulted in significant reduct

299 ally as effective as insulin without causing hypoglycemia, with additional benefits including improve

300 Mathematical simulations showed that hypoglycemia would occur if insulin sensitivity were not