ライフサイエンスコーパス: hypoglycemia

1 y musculoskeletal injury/discomfort and mild hypoglycemia).

2 issive for the normal CRR to insulin-induced hypoglycemia.

3 (GHSR1a), to promote food intake and prevent hypoglycemia.

4 an essential role in the protection against hypoglycemia.

5 diabetes is complicated by increased risk of hypoglycemia.

6 emia or those with recurrent versus isolated hypoglycemia.

7 arly to tramadol and has an association with hypoglycemia.

8 e variability and lower risk of postprandial hypoglycemia.

9 /dL), whereas controls were children without hypoglycemia.

10 glucose infusion rates were used to minimize hypoglycemia.

11 liver dysfunction was associated with severe hypoglycemia.

12 ce, but not the Fat-Ghr(-/-) mice, developed hypoglycemia.

13 h is sub-optimal and causes life-threatening hypoglycemia.

14 hown an association between tramadol use and hypoglycemia.

15 ion during ischemic attacks and acute severe hypoglycemia.

16 n effect) to defend against hyperinsulinemia-hypoglycemia.

17 sociated with decreases in hyperglycemia and hypoglycemia.

18 y correlated with the adrenaline response to hypoglycemia.

19 , the plasma ghrelin level rises, preventing hypoglycemia.

20 esponses, but not catecholamine responses to hypoglycemia.

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

22 conventional therapy, 7 patients had severe hypoglycemia.

23 lity in type 1 diabetes subjects with severe hypoglycemia.

24 ally undetected (interstitial episodes only) hypoglycemia.

25 diabetes and reduced by antecedent recurrent hypoglycemia.

26 ntinuous glucose monitoring group had severe hypoglycemia.

27 tes, but SUs have limitations due to risk of hypoglycemia.

28 nd was not associated with increased risk of hypoglycemia.

29 gal tone remained depressed during sustained hypoglycemia.

30 aling in glucose transport was unaffected by hypoglycemia.

31 repolarization during sustained experimental hypoglycemia.

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

33 adapt to a more proinflammatory state after hypoglycemia.

34 ed plasma glucose and thus increased risk of hypoglycemia.

35 es good glycemic control and one that causes hypoglycemia.

36 sponse to blood glucose, mitigating risk for hypoglycemia.

37 ndent insulinotropic actions without risk of hypoglycemia.

38 improvements in glycemia and no evidence of hypoglycemia.

39 issive for the normal CRR to insulin-induced hypoglycemia.

40 disorder GSD-Ib without causing symptomatic hypoglycemia.

41 stantiate the clinical relevance of relative hypoglycemia.

42 ves as a rescue medicine in the treatment of hypoglycemia.

43 al role in the counterregulatory response to hypoglycemia.

44 ecific treatment method for hyperinsulinemic hypoglycemia.

45 ed after adjustment for episodes of absolute hypoglycemia.

46 is has been suggested to be due to increased hypoglycemia.

47 alues for treatment of asymptomatic moderate hypoglycemia.

48 the first and most important defense against hypoglycemia.

49 nvolved in the counterregulatory response to hypoglycemia.

50 for the normal counterregulatory response to hypoglycemia.

51 lar events (MACEs), all-cause mortality, and hypoglycemia.

52 r for both mortality and subsequent absolute hypoglycemia.

53 ient compliance while mitigating the risk of hypoglycemia.

54 and standard BGM, respectively, were severe hypoglycemia (1 and 10), fractures (5 and 1), falls (4 a

55 with placebo (6.1% vs. 3.4%), as was severe hypoglycemia (1.5% vs. 0.3%).

56 Between baseline and 24 -hours after hypoglycemia, 15 of 140 inflammatory proteins differed i

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

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

59 events in the CGM and BGM groups were severe hypoglycemia (3 participants with an event in the CGM gr

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

61 ive patches, iontophoresis produced profound hypoglycemia (63% blood glucose drop in 3 h) without dam

62 ]), death (2 [1.0%] vs 7 [3.4%]), and severe hypoglycemia (8 [4.1%] vs 0).

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

64 from baseline (73.4 ng/mL) to 24 hours after hypoglycemia (91.7 ng/mL) was seen for urinary isoprosta

65 ncentrations compromises the defense against hypoglycemia, a common complication in diabetes therapy.

66 Acute hypoglycemia, a common occurrence in insulin-dependent d

67 healthy newborns with asymptomatic moderate hypoglycemia, a lower glucose treatment threshold (36 mg

68 Hypoglycemia, a serious risk for insulin-treated patient

69 Hypoglycemia activates GI-ERalpha(vlVMH) neurons via the

70 ystemic metabolic changes in vivo, including hypoglycemia, adipose tissue atrophy, and early mortalit

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

72 Hypoglycemia affects the electrophysiology of the heart.

73 ; however, fasted Atp7b (-/-) mice exhibited hypoglycemia after administration of insulin due to an i

74 the feasibility of a real-time, non-invasive hypoglycemia alarming system using short excerpts of ECG

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

76 r insulin therapy are limited by the risk of hypoglycemia and are associated with suboptimal glycemic

77 (CRR) system that help minimize and reverse hypoglycemia and coordination between those components a

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

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

80 Severe hypoglycemia and diabetic ketoacidosis were absent in pa

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

82 ounterregulatory response to insulin-induced hypoglycemia and glucoprivation and replicated hypoglyce

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

84 Clinical evidence suggests both hypoglycemia and glycemic variability negatively impact

85 rily a hyperglycemic agent driven by fasting/hypoglycemia and highlight the recent advances that have

86 eatures, reminders to measure blood glucose, hypoglycemia and hyperglycemia alerts, and action prompt

87 od glucose homeostasis and are used to treat hypoglycemia and hyperglycemia, respectively, in patient

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

89 Safety end points, including episodes of hypoglycemia and insulin-related adverse events, were al

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

91 tus that reduce glucose with minimal risk of hypoglycemia and potential benefits on atherosclerosis.

92 Pfkfb3 with the small molecule 3PO reversed hypoglycemia and reduced hematopoietic manifestations of

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

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

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

96 protein (CRHP) diet might reduce the risk of hypoglycemia and therefore compared the acute effects of

97 red capacity to recover from insulin-induced hypoglycemia and to a blunted CRR caused by 2-deoxy-d-gl

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

99 led to impaired intestinal barrier function, hypoglycemia, and abnormal serum metabolism, which was p

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

101 Growth hormone (GH) is secreted during hypoglycemia, and GH-responsive neurons are found in bra

102 h a strongly reduced growth rate, persistent hypoglycemia, and limited exercise capacity.

103 ) and 1024 (29.4%) had 1 or more episodes of hypoglycemia; and there were 9 (0.3%) vs 5 (0.1%) events

104 tic liver disease, pancreatic insufficiency, hypoglycemia, anemia, intermittent proteinuria, recurren

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

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

107 Rates of severe hypoglycemia are increased during pregnancy; therefore,

108 perglycemia and alpha cell responsiveness to hypoglycemia are observed only at high levels of residua

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

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

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

112 Results show that hypoglycemia, as induced by an insulin bolus, was more p

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

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

115 ting a potentially lethal condition known as hypoglycemia-associated autonomic failure (HAAF) that ma

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

117 poglycemia and glucoprivation and replicated hypoglycemia-associated autonomic failure.

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

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

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

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

122 l vs baseline), with related improvements in hypoglycemia awareness and glucose variability.

123 ovascular and/or respiratory failure, severe hypoglycemia (blood glucose < 40 mg/dL) was uncommon, bu

124 ia, including 25 (3.6%) who developed severe hypoglycemia (blood glucose < 40 mg/dL).

125 od glucose < 40 mg/dL) was uncommon, but any hypoglycemia (blood glucose < 60 mg/dL) remained common

126 Cases were children with any hypoglycemia (blood glucose < 60 mg/dL), whereas control

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

128 During hypoglycemia, brain lactate decreased approximately 30%

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

130 h associated with similar risks of MACEs and hypoglycemia but a lower risk of all-cause mortality tha

131 not only mediate the allostatic response to hypoglycemia but also modulate the homeostatic setpoint

132 is an effective therapy for life-threatening hypoglycemia, but graft function gradually declines over

133 tect glucose fluctuations and prevent severe hypoglycemia, but mechanisms mediating functions of thes

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

135 Severe hypoglycemia can lead to coma or death.

136 genetic disease, manifesting in hypoketotic hypoglycemia, cardiomyopathy, and sudden death.

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

138 ct on mortality or arrhythmias during severe hypoglycemia compared with controls.

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

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

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

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

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

144 - 3 y post-RYGB) with recurrent postprandial hypoglycemia documented by plasma glucose (PG) <=3.4 mmo

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

146 n receptors (GHSRs) exhibit life-threatening hypoglycemia during starvation-like conditions, but do n

147 tion and endogenous ghrelin protects against hypoglycemia during starvation.

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

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

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

151 ikingly, Pptc7(-/-) mice exhibit hypoketotic hypoglycemia, elevated acylcarnitines and serum lactate,

152 Severe hypoglycemia events occurred in 2 participants in each g

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

154 patients with diabetes experienced relative hypoglycemia (exposure) during their ICU admission.

155 agent and substantially reduces the risk of hypoglycemia, few studies have examined the comparative

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

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

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

159 VMN neurons activated by hypoglycemia (glucose-inhibited [GI] neurons) have been

160 th insulin-induced versus noninsulin-induced hypoglycemia had zero ICU-free days (35.8% vs 20.9%; p =

161 Hyperinsulinemic hypoglycemia (HI) and congenital polycystic kidney disea

162 tcomes, including additional CGM metrics for hypoglycemia, hyperglycemia, and glucose control; hemogl

163 ntinuous glucose monitor (Dexcom) to measure hypoglycemia, hyperglycemia, and glycemic variability fo

164 al blood conditions, including hyperglycemia/hypoglycemia, hyperoxemia/hypoxemia, and hypercarbia/hyp

165 d hypercarbia but inhibited by hypoxemia and hypoglycemia; hypocarbia had no appreciable effect.

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

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

168 Hypoglycemia impaired insulin-stimulated glucose disposa

169 acyl-ghrelin, a hormone that defends against hypoglycemia in a preclinical starvation model, is permi

170 a normal range while mitigating the risk of hypoglycemia in a type 1 diabetic mouse model.

171 erides, enhance gluconeogenesis, and prevent hypoglycemia in calorie-restricted mice, a model of fami

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

173 tudies report worse short-term outcomes with hypoglycemia in critically ill children.

174 istics, and outcome associations of relative hypoglycemia in diabetic patients with critical illness.

175 tect glucose fluctuations and prevent severe hypoglycemia in mice.

176 Hypoglycemia in MPN mouse models correlated with hyperac

177 ose levels and may be beneficial in reducing hypoglycemia in older adults with type 1 diabetes.

178 Effect of continuous glucose monitoring on hypoglycemia in older adults with type 1 diabetes: a ran

179 (-/-) mice survival after PHx, the sustained hypoglycemia in partially hepatectomized AnxA6(-/-) mice

180 rovided evidence of increased propensity for hypoglycemia in patients taking tramadol when compared t

181 es hospital length of stay and prevalence of hypoglycemia in patients with diabetic ketoacidosis and

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

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

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

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

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

187 ia, the hazard ratio for subsequent absolute hypoglycemia in the ICU was 3.5 (95% CI, 2.3-5.3).

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

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

190 It did not cause hypoglycemia in WT INSR-expressing mice.

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

192 diatric INsulin Titration protocol developed hypoglycemia, including 25 (3.6%) who developed severe h

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

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

195 Interestingly, insulin-induced hypoglycemia increases ARC POMC neuron activity.

196 Equivalent hypoglycemia, induced by lipopolysaccharide (LPS) or ins

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

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

199 We measured hypoglycemia-induced changes in endothelial parameters,

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

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

202 agus nerve is the primary mediator of severe hypoglycemia-induced fatal cardiac arrhythmias.

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

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

205 Relative hypoglycemia is a decrease in glucose greater than or eq

206 Postprandial hypoglycemia is a risk after Roux-en-Y gastric bypass (R

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

208 Hypoglycemia is associated with increased cardiovascular

209 Treatment of hyperinsulinemic hypoglycemia is challenging.

210 Hypoglycemia is common during neonatal transition and ma

211 In ICU patients with diabetes, relative hypoglycemia is common, increases with higher hemoglobin

212 e method for detecting episodes of nocturnal hypoglycemia is demonstrated with in vivo measurements m

213 ac arrhythmias during insulin-induced severe hypoglycemia is not well understood.

214 Hypoglycemia is the leading limiting factor in glycemic

215 c subunit (G6PC) and can present with severe hypoglycemia, lactic acidosis and hypertriglyceridemia.

216 Insulin-induced hypoglycemia leads to far-ranging negative consequences

217 mated by hemoglobin A1C) but not to absolute hypoglycemia levels.

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

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

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

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

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

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

224 episodes of diabetic ketoacidosis or severe hypoglycemia occurred in either group.

225 Severe hypoglycemia occurred only among patients in the intensi

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

227 verse events related to diabetes (two severe hypoglycemia, one diabetic ketoacidosis) were reported i

228 ith T2DM, between baseline and 24-hour after hypoglycemia, only one of 15 oxidative stress proteins d

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 Secondary outcomes included rates of serious hypoglycemia or hyperglycemia using ICD-9-CM and ICD-10-

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

233 eatment was well tolerated, and no events of hypoglycemia or hypotension occurred among those receivi

234 on the counterregulatory hormone response to hypoglycemia or on feeding.

235 Treatment was stopped early for hypoglycemia or other adverse events in 65 of 581 patien

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

237 etween children with severe versus nonsevere hypoglycemia or those with recurrent versus isolated hyp

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

239 but statistically significant improvement in hypoglycemia over 6 months.

240 of ghrelin, calorie-restricted mice develop hypoglycemia, owing to diminished glucose production.

241 as measured by coefficient of variation, and hypoglycemia (p for trend < 0.0001, < 0.0001, and 0.0010

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

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

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

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

246 both LPS and interleukin (IL)-1beta trigger hypoglycemia, reduce CSF glucose, and suppress spontaneo

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

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

249 tional age, macrosomia, infant birth injury, hypoglycemia, respiratory distress, 5-minute Apgar score

250 condary outcomes: large for gestational age, hypoglycemia, respiratory distress, low Apgar score, neo

251 Hypoglycemia resulted in inflammatory and oxidative stre

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

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

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

255 1 adults with type 2 diabetes and at least 1 hypoglycemia risk factor who were previously treated wit

256 male sex Relative Risk (RR) 2.88 (p = 0.03), hypoglycemia (RR) 5.7 (p = 0.004), ICU admission (RR) 14

257 esent a fail-safe system in case of impaired hypoglycemia sensing by peripherally located glucose det

258 n with the medications on the risk of severe hypoglycemia (SH), cardiovascular disease (CVD), and all

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

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

261 st aid methods of glucose administration for hypoglycemia; techniques for cooling of exertional hyper

262 ttermates underwent an insulin bolus-induced hypoglycemia test and a low-dose hyperinsulinemic-hypogl

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

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

265 After an episode of relative hypoglycemia, the hazard ratio for subsequent absolute h

266 esigned to mitigate glycemic variability and hypoglycemia through avoidance of bolus dosing, a libera

267 atory hormone to insulin, induced by fasting/hypoglycemia to raise blood glucose through action media

268 gence (AI) to automatically detect nocturnal hypoglycemia using a few heartbeats of raw ECG signal re

269 However, whether GH modulates the CRR to hypoglycemia via specific neuronal populations is curren

270 Growth hormone enhances the recovery of hypoglycemia via ventromedial hypothalamic neurons.

271 spital discharge, for patients with relative hypoglycemia was 1.9 (95% CI, 1.3-2.8) and was essential

272 Hypoglycemia was associated with fewer ICU-free days (me

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

274 Hypoglycemia was independently associated with higher mo

275 Neonatal hypoglycemia was not associated with increased risk of c

276 y bowel disease resolved, and no symptomatic hypoglycemia was observed.

277 Hypoglycemia was prevented by injection of lactate or oc

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

279 or later and identified as being at risk for hypoglycemia, we compared two threshold values for treat

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

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

282 Hyper- and hypoglycemia were associated with poor neurologic outcom

283 Methods: Six patients with hyperinsulinemic hypoglycemia were included.

284 nflammation at baseline and at 24-hours post hypoglycemia were performed: proteomic (Somalogic) analy

285 03) and relative risk (0.028; p = 0.0004) of hypoglycemia were significantly lower in the moderate-in

286 Epinephrine levels during hypoglycemia were similar between groups.

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

288 Hypoglycemia, which also stimulates hunger by activating

289 Tight glucose monitoring reduces the risk of hypoglycemia, which can result in a series of complicati

290 LPS (250 ug/kg) induced hypoglycemia, which was mimicked by interleukin (IL)-1be

291 ed in 24 patients with impaired awareness of hypoglycemia while receiving intensive insulin therapy.

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

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

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

295 ration trial to determine the association of hypoglycemia with adverse short-term outcomes in critica

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

297 The observed rates of hypoglycemia with severity of level 2 (blood glucose lev

298 rn to mothers with diabetes are screened for hypoglycemia, with a goal of preventing brain injury.

299 ms: SGLT2 inhibitors prevent both hyper- and hypoglycemia, with expectedly little net effect on HbA1C

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