ライフサイエンスコーパス: hypoglycemic

1 sulinemic (0.2 units kg(-1) min(-1)), severe hypoglycemic (10-15 mg/dL) clamps for 3 h with continuou

2 cemia can be fatal, hyperinsulinemic, severe hypoglycemic (10-15 mg/dL) clamps were performed in Spra

3 littermate controls were subjected to graded hypoglycemic (100, 70, 50, and 30 mg/dl) hyperinsulinemi

4 = 10 per group) underwent a hyperinsulinemic-hypoglycemic (2.6 mmol/L) clamp, either after a HIIT ses

5 ing hyperinsulinemic-euglycemic (5.0 mmol/L)-hypoglycemic (2.6 mmol/L) clamps in 11 healthy participa

6 All participants underwent a hypoglycemic (2.8 mmol/L) clamp after performing a bout

7 tep hyperinsulinemic euglycemic (5.0 mmol/L)-hypoglycemic (2.8 mmol/L) glucose clamp.

8 e imaging during euglycemic (5.0 mmol/L) and hypoglycemic (2.8 mmol/L) hyperinsulinemic clamps, we co

9 A 2-h hyperinsulinemic [hypoglycemic (2.8 mmol/l) or euglycemic (5.0 mmol/l)] cl

10 l/L) or hyperinsulinemic (812 +/- 50 pmol/L)-hypoglycemic (2.9 +/- 0.1 mmol/L) clamps.

11 Hyperinsulinemic euglycemic (5 mmol/L) and hypoglycemic (3 mmol/L) [1-(13)C]glucose clamps were per

12 tted to hyperglycemic (40% glucose i.v.) and hypoglycemic (5 U/kg insulin i.v.) challenges.

13 In vivo hyperinsulinemic-hypoglycemic (50 mg dl(-1)) clamp studies were performed

14 that in the VA: 35.3% versus 12.7% for oral hypoglycemics, 50.7% versus 18.2% for statins, 42.5% ver

15 ion 92.4 +/- 2.3 mg/dl) and hyperinsulinemic-hypoglycemic (52.9 +/- 4.8 mg/dl) clamps separated by at

16 hyperinsulinemic euglycemic (92+/-3 mg/dL) - hypoglycemic (53+/-1 mg/dL) clamp.

17 nsulinemic euglycemic (90 mg/dL x 1 h), then hypoglycemic (54 mg/dL x 2 h) clamps, in the morning and

18 olyphenol-enriched DSF exhibited significant hypoglycemic activities in C57bl/6J mice, and cranberry

19 ither taking no medication or taking an oral hypoglycemic agent (with or without insulin) were classi

20 >/= 7.0 mmol/L) >/= 30 days apart, (ii) oral hypoglycemic agent use for >/= 30 consecutive days, (iii

21 load glucose >/=200 mg/dL, HbA1c >/=6.5%, or hypoglycemic agent use.

22 onic obstructive pulmonary disease, use of a hypoglycemic agent, lower activity level, higher New Yor

23 tory of angina pectoris or asthma, no use of hypoglycemic agent, more activity level, and lower New Y

24 , oral antiplatelet agents (13.3%), and oral hypoglycemic agents (10.7%).

25 Basal insulin can be added to oral hypoglycemic agents (generally stopping sulfonylureas) i

26 r, age 18 years or older, taking 0 to 3 oral hypoglycemic agents (metformin, thiazolidinedione, sulfo

27 sions or patients taking any insulin or oral hypoglycemic agents 1 month or later after kidney transp

28 etes was ascertained by using information on hypoglycemic agents and serum glucose.

29 The newer oral hypoglycemic agents are also in use and have mechanisms

30 insulin monotherapy, is the addition of oral hypoglycemic agents associated with benefits (measured b

31 t amelioration of hyperglycemia by different hypoglycemic agents forestalled PI-producing ATM accumul

32 alpha-amylase, a therapeutic target for oral hypoglycemic agents in type-2 diabetes.

33 Only the associations with systemic hypoglycemic agents were greater than 1 mm Hg, a thresho

34 n of rosiglitazone, compared with other oral hypoglycemic agents, among 2393 long-term hemodialysis p

35 ns: the first (control) while receiving oral hypoglycemic agents, and the second after the addition o

36 ose not fasting), the use of insulin or oral hypoglycemic agents, or self-reported history.

37 Compared with patients prescribed other oral hypoglycemic agents, patients prescribed rosiglitazone h

38 vels, lived in Eastern Europe or were taking hypoglycemic agents, were more likely to have impaired Q

39 ogues, antihypertensive agents, statins, and hypoglycemic agents, whereas in spite of the prominent r

40 P4 inhibitors) and were noninferior to other hypoglycemic agents.

41 theobromine in DFCP were associated with the hypoglycemic and anti-inflammatory effects observed.

42 the protein tyrosine phosphatase OST-PTP are hypoglycemic and are protected from obesity and glucose

43 Hypoxic mice became hypoglycemic and displayed impaired hepatic glucose prod

44 First, we found that DeltaNesp55(m) mice are hypoglycemic and have reduced stomach-to-body weight rat

45 genus, it was widely popular because of its hypoglycemic and hypolipidemic properties but various ca

46 The hypoglycemic and insulin-like effects of CE and CDSF may

47 ansplantation using stepped hyperinsulinemic-hypoglycemic and paired hyperinsulinemic-euglycemic clam

48 of patient-days classified as hyperglycemic, hypoglycemic, and at-goal (all measurements >/=3.9 and <

49 of age and became malnourished, underweight, hypoglycemic, and hypothermic.

50 tative RT-PCR and immunoblots in recurrently hypoglycemic animals revealed that GAD(65) mRNA and prot

51 ls decreased in both control and recurrently hypoglycemic animals with the onset of hypoglycemia, the

52 re more than threefold higher in recurrently hypoglycemic animals.

53 d can potentially minimize the occurrence of hypoglycemic anomalies.

54 will introduce measures of adherence to oral hypoglycemic, antihypertensive, and cholesterol-lowering

55 lic triterpene from Olea europaea L., exerts hypoglycemic, antioxidant, cardioprotective and antitumo

56 inemic (0.2 units x kg(-1) x min(-1)) severe hypoglycemic ( approximately 11 mg/dl) clamp for 60 or 9

57 c-euglycemic (approximately 8.5 mmol/l) and -hypoglycemic (approximately 3.0 mmol/l) clamps were done

58 on AMPK to suppress oxidative stress in the hypoglycemic bone marrow environment.

59 n stores, which can defend the brain against hypoglycemic brain damage but may aggravate brain damage

60 arked hypoglycemia and provide evidence that hypoglycemic brain neuronal death is in fact increased b

61 Mice rendered hypoglycemic by a null mutation in the glucagon receptor

62 d cerebral cortex are uniquely vulnerable to hypoglycemic cell death, and oxidative stress is a key e

63 Here we show that in the hypoglycemic chicken retina, spontaneous episodes of SD

64 Day 2 consisted of a single 2-h hypoglycemic clamp (2.9 mmol/L) following either DHEA (1

65 During the subsequent hypoglycemic clamp (all measurements from baseline to th

66 < 0.02, n = 5) during a 2-h hyperinsulinemic-hypoglycemic clamp (glucose concentration 57.2 +/- 9.7 m

67 C]acetate infusion during a hyperinsulinemic-hypoglycemic clamp (n = 8).

68 -25) after GBP surgery with hyperinsulinemic-hypoglycemic clamp (stepwise to plasma glucose 2.7 mmol/

69 d with a stepped hyperinsulinemic euglycemic-hypoglycemic clamp and behavioral measures of interest i

70 However, at the end of the hypoglycemic clamp concentrations all of the above menti

71 zes glucagon and corticosterone responses to hypoglycemic clamp in diabetic rats.

72 pinephrine secretion during hyperinsulinemic/hypoglycemic clamp in rats.

73 consisted of a single-step hyperinsulinemic-hypoglycemic clamp of 2.9 mmol/l.

74 BA(A)) receptor agonist muscimol, prior to a hypoglycemic clamp or under baseline conditions.

75 min(-1))-hypoglycemic clamp studies before and after 6 weeks of f

76 bose to lower A1C to 6.7% and 2-day repeated hypoglycemic clamp studies before and after intensive th

77 ion of ephrinA5-Fc before a hyperinsulinemic hypoglycemic clamp study caused a reduction in the gluco

78 Subsequently, a hyperinsulinemic-hypoglycemic clamp study was performed.

79 ects participated in a single 2-day repeated hypoglycemic clamp study.

80 re measured during baseline and a subsequent hypoglycemic clamp taking place in the morning.

81 nses to hypoglycemia were assessed using the hypoglycemic clamp technique.

82 explored using the in vivo hyperinsulinemic-hypoglycemic clamp technique.

83 Subsequently, these rats underwent a hypoglycemic clamp to assess hormone responses.

84 ts and nondiabetic control subjects during a hypoglycemic clamp using (13)C magnetic resonance spectr

85 hormones measured at the end of the 240-min hypoglycemic clamp were not affected by TSD it can be sp

86 2 consisted of a single 2-h hyperinsulinemic-hypoglycemic clamp.

87 related hormones during a subsequent 240-min hypoglycemic clamp.

88 fter 6 weeks, subjects returned for a second hypoglycemic clamp.

89 ine methiodide (BIC) before performance of a hypoglycemic clamp.

90 fusion followed by a 2-hour hyperinsulinemic/hypoglycemic clamp.

91 Day 1 consisted of morning and afternoon 2-h hypoglycemic clamps (2.9 mmol/L) with 800 mg of DHEA or

92 ) x min(-1)) euglycemic clamps (5.1 mmol/l), hypoglycemic clamps (2.9 mmol/l), or euglycemic clamps w

93 in synaptic activity during hyperinsulinemic hypoglycemic clamps (55 mg/dl [3.0 mmol/l]) in the naive

94 On day 2, subjects underwent stepped hypoglycemic clamps (nadir 60 mg/dL) with evaluation of

95 se to acute insulin-induced hypoglycemia and hypoglycemic clamps after modulation of brain NO signali

96 required lower glucose infusion rates during hypoglycemic clamps and displayed enhanced glucagon rele

97 Instead, lack of a glucagon response during hypoglycemic clamps identified impaired counterregulatio

98 ek later, animals underwent hyperinsulinemic-hypoglycemic clamps in which the hypoglycemic nadir, 2.4

99 otomy (TSV) were exposed to hyperinsulinemic-hypoglycemic clamps where glycemia was lowered slowly ov

100 g and afternoon 2-h euglycemic or 2.9 mmol/L hypoglycemic clamps with or without 1 mg alprazolam give

101 afternoon 2-h hyperinsulinemic-euglycemic or hypoglycemic clamps with or without 1 mg alprazolam give

102 l were studied with stepped hyperinsulinemic-hypoglycemic clamps, using hormone concentrations and gl

103 ine-specific neurotoxin and hyperinsulinemic-hypoglycemic clamps, we found that sympathoadrenal CRRs

104 ay 2 involved similar morning euglycemic and hypoglycemic clamps, with saline infusion, on all three

105 n metabolism during and after euglycemic and hypoglycemic clamps.

106 Hypoglycemic coma and brain injury are potential complic

107 ent, 2-deoxyglucose (2-DG), under normal and hypoglycemic conditions and also after MAN lesioning wit

108 acellular Glu sustained cell viability under hypoglycemic conditions and increased GOT-mediated metab

109 ow that the degeneration of the macula under hypoglycemic conditions can be prevented by blocking ree

110 recurrent hypoglycemia under euglycemic and hypoglycemic conditions in a rat model and to test the h

111 ificantly different comparing euglycemic and hypoglycemic conditions in patients with T1DM.

112 ucose contribution to brain metabolism under hypoglycemic conditions that restored metabolic activity

113 advantage of preserving brain function under hypoglycemic conditions without causing deleterious hype

114 nversely related to the HbA1C and was, under hypoglycemic conditions, approximately 45% higher than t

115 that CD8(+) TILs reprogram under hypoxic and hypoglycemic conditions, regaining effector function by

116 h a truncated tricarboxylic acid cycle under hypoglycemic conditions.

117 surement of low glucose concentrations under hypoglycemic conditions.

118 w the brain to function normally under acute hypoglycemic conditions.

119 evel of the VMH under both normoglycemic and hypoglycemic conditions.

120 cancer (PC-E1) were subjected to hypoxic and hypoglycemic conditions.

121 Insulin action and hypoglycemic counter-regulatory and insulin secretory ph

122 5-h-fasted mice to assess insulin action and hypoglycemic counter-regulatory responsiveness.

123 Hypoglycemic detection at the portal-mesenteric vein (PM

124 The critical locus for hypoglycemic detection shifts away from the portal-mesen

125 been highlighted by the discovery of a novel hypoglycemic disorder in children, the hyperinsulinism-h

126 be corrected by treating cells with the oral hypoglycemic drugs sulfonylureas, which we have shown pr

127 mass index, glycated hemoglobin, use of oral hypoglycemic drugs, and smoking.

128 es glucose uptake in adipocytes and has oral hypoglycemic effect in wild-type C57BL/6J mice and db/db

129 n site (S436A) demonstrate resistance to the hypoglycemic effect of both insulin and metformin.

130 ex I abundance and sensitized animals to the hypoglycemic effect of metformin.

131 al IRs also resulted in a delay in the acute hypoglycemic effect of systemic insulin administration a

132 d for blueberry, demonstrating the potential hypoglycemic effect of the juices.

133 The samples showed a higher in vitro hypoglycemic effect than individual or mixed standards,

134 Pancreatic clamp studies revealed that this hypoglycemic effect was due to a decrease of hepatic glu

135 commonly used antirheumatic medication, has hypoglycemic effects and may reduce the risk of diabetes

136 er evaluated for its hypotriglyceridemic and hypoglycemic effects in high-fructose diet (HFD)-induced

137 -Tf exhibited a slow, but sustained, in vivo hypoglycemic efficacy and long plasma half-life.

138 in the insulin group, there was only 1 mild hypoglycemic episode (6%) in the metformin group, P < 0.

139 Neonatal hypoglycemic episode, defined as at least 1 consecutive

140 who were stratified according the number of hypoglycemic episodes (< 60 mg/dL glucose) they experien

141 ed dapagliflozin groups had a higher rate of hypoglycemic episodes (56.6% vs. 51.8%), events suggesti

142 3.77 to -2.64],P < .001) and fewer confirmed hypoglycemic episodes (episodes/patient-year exposure, 2

143 oints were the rate of nocturnal symptomatic hypoglycemic episodes (severe or blood glucose confirmed

144 nd point was the rate of overall symptomatic hypoglycemic episodes (severe or blood glucose confirmed

145 owest blood glucose concentration, number of hypoglycemic episodes and events, and negative interstit

146 Fewer hypoglycemic episodes and less weight gain occurred in p

147 s included the rate of nocturnal symptomatic hypoglycemic episodes and proportion of patients with se

148 ercent of all recipients were free of severe hypoglycemic episodes at 1 year.

149 Hypoglycemic episodes correlate with injury severity and

150 od glucose-confirmed (<56 mg/dL) symptomatic hypoglycemic episodes during the maintenance period.

151 odes were recorded, with moderate and severe hypoglycemic episodes grouped together.

152 Patients with one or more hypoglycemic episodes had longer hospitalization, as wel

153 and reduces weight without increasing major hypoglycemic episodes in patients with inadequately cont

154 Whether minor hypoglycemic episodes increase risk of dementia is unkno

155 Three severe hypoglycemic episodes occurred during the closed-loop ph

156 llitus (T1DM) experience, on average, 2 to 3 hypoglycemic episodes per week.

157 ts with type 2 diabetes, a history of severe hypoglycemic episodes was associated with a greater risk

158 3.33]), and the proportions of patients with hypoglycemic episodes were 22.5% vs 31.6% (difference, -

159 2.85]), and the proportions of patients with hypoglycemic episodes were 9.7% vs 14.7% (difference, -5

160 e (< 4.0 mmol/L) and severe (</= 2.2 mmol/L) hypoglycemic episodes were recorded, with moderate and s

161 Group C (three patients with fasting hypoglycemic episodes) displayed very low rates of insul

162 ur patients with fasting and/or postprandial hypoglycemic episodes) showed qualitatively normal respo

163 Group B (three patients with fasting hypoglycemic episodes) was mainly characterized by large

164 ved mean glycemic levels, with less frequent hypoglycemic episodes, among both adults and adolescents

165 ld contribute to arrhythmias during clinical hypoglycemic episodes.

166 ine U100 in reducing the rate of symptomatic hypoglycemic episodes.

167 41), or 3 or more (3+; n = 17) prior severe hypoglycemic episodes.

168 isodes of diabetic ketoacidosis and frequent hypoglycemic episodes.

169 near-normal glycemic control without severe hypoglycemic episodes.

170 ions often result in adverse weight gain and hypoglycemic episodes.

171 change in body weight, and rate of confirmed hypoglycemic episodes.

172 red glucose levels and frequent asymptomatic hypoglycemic episodes.

173 ted in a reduced rate of overall symptomatic hypoglycemic episodes.

174 Atf4 null mice are hypoglycemic, even before substantial changes in fat con

175 stratified based on whether they developed a hypoglycemic event (random glucose level < 60 mg/dL) dur

176 ents (all in the control group) had a severe hypoglycemic event; no patients had diabetic ketoacidosi

177 Forty severe hypoglycemic events (<2.2 mmol/L [<40 mg/dL]) occurred d

178 aggressive control had a higher incidence of hypoglycemic events (4 vs 30; P < 0.0001).

179 The primary end points were the number of hypoglycemic events (defined as a sensor glucose value o

180 glycemic control increases the incidence of hypoglycemic events and does not result in any significa

181 ed more QALYs (16.68 vs. 16.58) due to fewer hypoglycemic events and fewer medications.

182 ll transplant recipients were free of severe hypoglycemic events and maintained hemoglobin A1c (HbA1c

183 tegy is expected to present a lower risk for hypoglycemic events compared to KATP channel blockers.

184 onylurea to insulin was associated with more hypoglycemic events compared with insulin alone, but thi

185 Hypoglycemic events from 1980-2002 were collected and re

186 sity score-matched patients with one or more hypoglycemic events had greater inflammatory and metabol

187 Severe hypoglycemic events have been associated with increased

188 The baseline rate of severe and moderate hypoglycemic events in the pump-only group was 20.7 vs 1

189 Nocturnal hypoglycemic events occurred 31.8% less frequently in th

190 to 16 years) showed no progressively severe hypoglycemic events or diagnoses of insulinoma.

191 23.9%, and 8.1%; respective mean numbers of hypoglycemic events per patient per year were 5.7, 12.0,

192 The mean AUC for nocturnal hypoglycemic events was 37.5% lower in the threshold-sus

193 ts were lower (P = 0.002) and rates of major hypoglycemic events were about 50% reduced (P < 0.001) i

194 e group vs 27 (18%) in the placebo group and hypoglycemic events were infrequent (2 [1%] vs 4 [3%], r

195 Patients with one or more hypoglycemic events were matched with patients not exper

196 type 2 (T2DM) is the increased occurrence of hypoglycemic events which, if left untreated, may cause

197 meal-stimulated C-peptide AUC, insulin use, hypoglycemic events, and immunologic responses.

198 C-peptide secretion, reduced insulin use and hypoglycemic events, and induced favorable immunologic p

199 n hemoglobin A(1c) levels (primary outcome), hypoglycemic events, depression, quality of life, fear o

200 exogenous insulin administration, and fewer hypoglycemic events.

201 e potential to reduce the incidence of major hypoglycemic events.

202 the area under the curve (AUC) for nocturnal hypoglycemic events.

203 level of serum glucose, and the incidence of hypoglycemic events.

204 ses, thereby increasing the risk for further hypoglycemic events.

205 lpha-cell UCP2 deletion perturbs the fasting/hypoglycemic glucagon response and shows that UCP2 is ne

206 VMH were assessed during a hyperinsulinemic-hypoglycemic glucose clamp study in chronically catheter

207 his purpose, hyperinsulinemic euglycemic and hypoglycemic glucose clamps were performed on separate d

208 were equally excited or inhibited by 5-HT at hypoglycemic glucose levels in vitro.

209 glycemic- (glucose approximately 5.5 mmol/l) hypoglycemic (glucose approximately 2.8 mmol/l) clamp st

210 ti-inflammatory, antioxidant, antimicrobial, hypoglycemic, healing-promoting, and immune-boosting pro

211 when arterial blood perfusing it is hypoxic, hypoglycemic, hypercapnic, or acidic.

212 f the young type II (MODY-II) and persistent hypoglycemic hyperinsulinemia of infancy (PHHI).

213 d Oxford method before the initiation of the hypoglycemic-hyperinsulinemic clamp protocol and during

214 uding anti-cancer, anti-viral, anti-oxidant, hypoglycemic, hypo-lipidemic, and anti-inflammatory acti

215 Txnip-null mice were hypoglycemic, hypoinsulinemic, and had blunted glucose p

216 gnificant differences were observed for oral hypoglycemics in adjusted analyses.

217 cose level less than 3.9 mmol/L (<70 mg/dL) (hypoglycemic) in the previous 24 hours were identified u

218 All 1943 normoglycemic and transiently hypoglycemic infants (23-42 weeks' gestation) were eligi

219 lter, deep vein thrombosis prophylaxis, oral hypoglycemic intensification, cholesterol medication int

220 agon deficiency, plasma glucose decreased to hypoglycemic levels and was 55 +/- 2 mg/dl at 240 min (P

221 , HbA1c was normalized, and time spent while hypoglycemic (<70 mg/dL) was nearly abolished as indicat

222 Although 83% of first hypoglycemic meals were preceded by 5 min dips in VMH (b

223 min(-1))-hypoglycemic (means +/- SE 2.9 +/- 0.1 mmol/l) clamp stu

224 bin concentration of at least 6.5% or use of hypoglycemic medication (with or without insulin).

225 nd followed longitudinally for initiation of hypoglycemic medication over 1 year after beginning cort

226 ng normal fasting glucose (<100 mg/dl and no hypoglycemic medication use) or abnormal fasting glucose

227 bnormal fasting glucose (>/=100 mg/dl and/or hypoglycemic medication use).

228 Diabetes by self-report of diagnosis or hypoglycemic medication use.

229 NODAT was defined as the use of hypoglycemic medication, a random plasma glucose level m

230 abetes was defined as patients not requiring hypoglycemic medication, fasting glucose below 7 mmol/L,

231 t initially were neither diabetic nor taking hypoglycemic medications.

232 common antihypertensive, lipid-lowering, and hypoglycemic medications.

233 on and treatment algorithms with concomitant hypoglycemic medications.

234 grafts were less sensitive to gemcitabine in hypoglycemic mice compared with hyperglycemic mice.

235 creatinine, hyperglycemia managed with oral hypoglycemics, minor wound infection, and hyperuricemia

236 ecretion were not affected by glucose level, hypoglycemic MPCCs upregulated CYP3A4 enzyme activity as

237 insulinemic-hypoglycemic clamps in which the hypoglycemic nadir, 2.48 +/- 0.06 mmol/l, was reached at

238 HbA1c, mean glucose and median percent time hypoglycemic on CGM were unchanged with CSII, SD glucose

239 d autonomic failure in response to recurrent hypoglycemic or glucopenic events.

240 horter for long-term diabetics who used oral hypoglycemics or insulin.

241 re, and mortality than burn patients without hypoglycemic (p < 0.05).

242 9.1% (223/225) concordance in characterizing hypoglycemic patients.

243 Clear evidence of hypoglycemic physiological counterregulation was first d

244 xty-three percent of LQT2 patients developed hypoglycemic plasma glucose levels (<70 mg/dL) versus 36

245 The GIR required to maintain the hypoglycemic plateau was higher in nNOS knockout than wi

246 The hypoglycemic potential of blueberry and pomegranate juic

247 The hypoglycemic proportion in the vGMS period was 36% lower

248 ons larger than 50mg/dl and about 12% in the hypoglycemic range (<50mg/dl).

249 duced blood glucose levels into the markedly hypoglycemic range in overnight-fasted, streptozotocin-t

250 erstitial glucose concentrations (IG) in the hypoglycemic range or with a previous fall in IG.

251 M, average percent time in hyperglycemic and hypoglycemic range was larger in RYGBP (respectively, 4.

252 t associated with an IG concentration in the hypoglycemic range.

253 9+/-6) per brain section were present in P14 hypoglycemic rats (p<0.01, each).

254 During hypoglycemia, recurrently hypoglycemic rats exhibited a 49-63% reduction in glucag

255 that high-intensity exercise in recurrently hypoglycemic rats increases levels of a number of protei

256 recent hypothesis based on in vivo data from hypoglycemic rats is that it is the decrease in zinc cos

257 (GAD), in the VMH of control and recurrently hypoglycemic rats.

258 the fall was not significant in recurrently hypoglycemic rats.

259 vented the sucrose-induced late postprandial hypoglycemic response and the compensatory free fatty ac

260 ecreased, glucose tolerance improved and the hypoglycemic response to insulin was enhanced in CeA LV-

261 Both insulin signaling and the hypoglycemic response to insulin were similar between HK

262 ken to assess the impact of interrupting the hypoglycemic response to PH on liver regeneration in mic

263 oral insulin delivery, leading to a notable hypoglycemic response.

264 to counterregulatory failure in recurrently hypoglycemic (RH) and diabetic rats.

265 Hypoglycemic risk was similar to that of other agents.

266 w approaches for designing GKAs with reduced hypoglycemic risk.

267 ticulata (SNR) among other structures in the hypoglycemic seizure control.

268 utcome was the combined incidence of severe (hypoglycemic seizure or coma) and moderate hypoglycemia

269 Affected children present in infancy with hypoglycemic seizures after brief periods of fasting or

270 Here we studied mechanisms of control of hypoglycemic seizures induced by insulin injection in fa

271 in the function of the SNR, leading thus to hypoglycemic seizures.

272 to more rapid and consistent development of hypoglycemic seizures.

273 icipate in the failure of the SNR to control hypoglycemic seizures.

274 ith otherwise sublethal doses of LPS induced hypoglycemic shock in mice within 1-2 h.

275 njected into fish, the venom insulin elicits hypoglycemic shock, a condition characterized by dangero

276 re school of fish simultaneously experiences hypoglycemic shock, this should directly facilitate capt

277 his hypothesis, we treated SKO mice with the hypoglycemic sodium-glucose cotransporter 2 (SGLT2) inhi

278 the patients spent 77 +/- 18 min per 24 h in hypoglycemic states (<3.9 mmol/L glucose) with 36 +/- 10

279 s patients experience both hyperglycemic and hypoglycemic states.

280 creatic beta cells to prevent both hyper-and hypoglycemic states.

281 Percentage of patients taking oral hypoglycemics, statins, and angiotensin-converting enzym

282 ter repolarization abnormalities for a given hypoglycemic stimulus despite comparable sympathoadrenal

283 counterregulation in response to a standard hypoglycemic stimulus.

284 ounterregulatory responses to a standardized hypoglycemic stimulus.

285 nephrine response when given 24 h before the hypoglycemic study.

286 rowth hormone, and noradrenaline, as well as hypoglycemic symptoms and cognitive function, were simil

287 ay contribute to increased susceptibility to hypoglycemic symptoms in RYGB surgery subjects.

288 upon oral glucose stimulation and increased hypoglycemic symptoms.

289 production (EGP, using 6,6-D2-glucose), and hypoglycemic symptoms.

290 h oral corticosteroids, 25 (1.21%) initiated hypoglycemic therapy compared with 5 of 2666 patients (0

291 erglycemia that is detected and treated with hypoglycemic therapy in the tertiary ocular inflammation

292 Other risk factors for the initiation of hypoglycemic therapy included older age (RR [per each ad

293 Gender-matched patients with oral hypoglycemic-treated (T2OH) and insulin-treated type 2 d

294 ) for at least 5 years and be receiving oral hypoglycemic treatment or insulin.

295 e recipients, 87% had previously experienced hypoglycemic unawareness and 23% experienced coma and/or

296 Ten patients with type 1 diabetes with hypoglycemic unawareness received intraportal allogeneic

297 Postdonation, DM requiring oral hypoglycemics was diagnosed in 7 (15%) donors and insuli

298 Because RLIP76(-/-) mice are hypoglycemic, we studied the role of RLIP76 in insulin r

299 the human condition, the SUR-1(-/-) mouse is hypoglycemic when fasted and hyperglycemic when glucose-

300 ease in growth hormone and become profoundly hypoglycemic when fasted for 18-23 h.