ライフサイエンスコーパス: hyperglycemia

1 n and extracellular perturbations, including hyperglycemia.

2 eased R-Ras palmitoylation in the setting of hyperglycemia.

3 identification of novel targets for treating hyperglycemia.

4 y explained by effects beyond a reduction in hyperglycemia.

5 42% of MHS patients have hyperglycemia.

6 sis associated with experimental PH, HF, and hyperglycemia.

7 omote the control of oxidative processes and hyperglycemia.

8 ding to disturbed pancreatic development and hyperglycemia.

9 expression of IL-10 ameliorates postprandial hyperglycemia.

10 mediating LTCC potentiation during diabetic hyperglycemia.

11 loped moderate intra-insulitis and transient hyperglycemia.

12 betic rats (STZ-rats) analyzed at 8 weeks of hyperglycemia.

13 nd oxidation are reduced in diabetes despite hyperglycemia.

14 sensitivity analysis excluding patients with hyperglycemia.

15 on process in place, but had small effect on hyperglycemia.

16 ar inflammatory response under conditions of hyperglycemia.

17 tion and vascular reactivity during diabetic hyperglycemia.

18 ntly in survivors of ICU experiencing stress hyperglycemia.

19 e production and, in turn, reduce or prevent hyperglycemia.

20 um exchanger (NCX) to these responses during hyperglycemia.

21 ed metabolic demand, leading to uncontrolled hyperglycemia.

22 egy to reduce daily exposure to postprandial hyperglycemia.

23 r increases of plasma leptin and more severe hyperglycemia.

24 et-induced adiposity, hepatic steatosis, and hyperglycemia.

25 the effect of elevated ZEB1, as noted during hyperglycemia.

26 ting in severe insulin resistance and severe hyperglycemia.

27 deficiency drastically ameliorated diabetic hyperglycemia.

28 toxicity of cardiomyocytes in the context of hyperglycemia.

29 respectively, following 72 h of physiologic hyperglycemia.

30 cesses leads to beta-cell failure and severe hyperglycemia.

31 iation in the beta-cell environment, such as hyperglycemia.

32 te to vascular complications during diabetic hyperglycemia.

33 y attenuated glucose utilization and fasting hyperglycemia.

34 how EPA improved murine hyperinsulinemia and hyperglycemia.

35 alpha-cells strongly contributes to diabetic hyperglycemia.

36 1 in pancreatic beta cells in the context of hyperglycemia.

37 proving Nrf2/nNOS expression in experimental hyperglycemia.

38 tal microorganisms have been associated with hyperglycemia.

39 ly coronary heart disease, in the setting of hyperglycemia.

40 elta-deficient diabetic mice did not develop hyperglycemia.

41 ultaneously triggered insulin resistance and hyperglycemia.

42 recipients who received tacrolimus developed hyperglycemia.

43 e alterations probably cause these patients' hyperglycemia.

44 on, limits insulin secretion and exacerbates hyperglycemia.

45 The most common serious adverse events were hyperglycemia (12 patients with intervention and 7 patie

46 As such, overall postprandial hyperglycemia (24-h incremental area under the glucose c

47 to 18 months before PDAC diagnosis (phase 1, hyperglycemia), a significant proportion of patients dev

48 impair insulin action, and ultimately cause hyperglycemia, a condition known to impair recovery from

49 be a clinically relevant procedure to mimic hyperglycemia, a positive correlation between the rates

50 We previously demonstrated that hyperglycemia activates nuclear factor of activated T ce

51 streptozotocin (STZ) (35 mg/kg) resulted in hyperglycemia, activation of lens aldose reductase 2 (AL

52 1.173; 95% CI = 1.020-1.349; p = 0.026) and hyperglycemia (adjusted OR(gamma) = 1.306; 95% CI = 1.14

53 The LCBF significantly reduced postprandial hyperglycemia after breakfast (P < 0.01) and did not adv

54 onal studies on the association of admission hyperglycemia (aHG) with outcomes of patients with acute

55 nction, likely due to insulin resistance and hyperglycemia, albeit without progression over 5 years.

56 ffect DeltaGFR, but significantly attenuated hyperglycemia, albuminuria, and glomerulosclerosis and i

57 s to measure blood glucose, hypoglycemia and hyperglycemia alerts, and action prompts.

58 leukemic cell line, U937 cells, dividing in hyperglycemia also accumulate intracellular HA and that

59 dy demonstrated high prevalence of transient hyperglycemia and a significant TB/DM and TB/IGR associa

60 d DELTA LIKE-4 are up-regulated secondary to hyperglycemia and activate both canonical and rapid nonc

61 Pericytes exposed to hyperglycemia and AGEs displayed diminished expression o

62 type 1 diabetes, beta cell responsiveness to hyperglycemia and alpha cell responsiveness to hypoglyce

63 exia), patients had significant increases in hyperglycemia and decreases in serum lipids, body weight

64 ctivity and vascular reactivity during acute hyperglycemia and diabetes.

65 glycemic control, but in excess, can lead to hyperglycemia and diabetes.

66 nsufficient insulin levels and, as a result, hyperglycemia and diabetes.

67 livary gland dysfunction was associated with hyperglycemia and elevation of serum IL1beta, IL16, and

68 ing 3-HIB is elevated according to levels of hyperglycemia and established type 2 diabetes.

69 -body Galpha(z)-null mice are protected from hyperglycemia and glucose intolerance after long-term hi

70 ncreased free fatty acids (FFA) and produced hyperglycemia and glucose intolerance.

71 d female MOER mice exhibited fasting and fed hyperglycemia and glucose intolerance.

72 ute intravenous injection of glucose induced hyperglycemia and glucosuria with increased GFR in mice.

73 Grade 3 hyperglycemia and grade 4 hypophosphatemia were dose-lim

74 that loss of E47 prevents the development of hyperglycemia and hepatic steatosis in response to GCs.

75 keletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis, by enhancing muscle

76 r insulin resistance (IR) is associated with hyperglycemia and hepatic steatosis.

77 in the "STAM" model of mice, in which severe hyperglycemia and HF feeding results in rapid hepatic li

78 r progression is accelerated by hyperoxemia, hyperglycemia and hypercarbia but inhibited by hypoxemia

79 use did not interact with the HFD to worsen hyperglycemia and hyperinsulinemia during an OGTT, HFD-f

80 A similar attenuation of hyperglycemia and hyperinsulinemia in wild-type mice wit

81 irst investigated EPA's preventative role on hyperglycemia and hyperinsulinemia.

82 ment and increased BACE1 and Abeta accompany hyperglycemia and hyperlipidemia.

83 athogenic for monogenic hyperphagic obesity, hyperglycemia and hypertension.

84 Diabetes is associated with hyperglycemia and impairment of retinal microvascular fu

85 nt to lower overall exposure to postprandial hyperglycemia and improve glycemic variability.

86 n a pre-clinical study, neratinib attenuates hyperglycemia and improves beta-cell function, survival

87 Obese mice, which differ in their degree of hyperglycemia and in liver fat content.

88 f adipsin in diabetic db/db mice ameliorates hyperglycemia and increases insulin levels while preserv

89 cate that glucose activates vagal control of hyperglycemia and inflammation in fasted septic mice via

90 However the relationship between hyperglycemia and inflammation remains unknown.

91 Stress hyperglycemia and insulin resistance are evolutionarily

92 aluating cardiac effects of diabetic milieu (hyperglycemia and insulin resistance) on lipotoxic-media

93 ointestinal symptoms, hepatocellular injury, hyperglycemia and ketosis, neurologic illnesses, ocular

94 ally fatal consequences, is characterized by hyperglycemia and metabolic acidosis due to the accumula

95 sregulation of glucose homeostasis result in hyperglycemia and pigmented rice, unique combination of

96 n ideal food material to manage the cause of hyperglycemia and resultant oxidative stress.

97 Vagal stimulation attenuated hyperglycemia and serum TNF levels in sham but only hype

98 ific dopaminergic type-1 agonist, attenuated hyperglycemia and systemic inflammation in diabetic endo

99 Experimental diabetes increased hyperglycemia and systemic inflammation in experimental

100 persons with TB and the association between hyperglycemia and TB at enrollment and 3 months after TB

101 llment in newly diagnosed DM, but persistent hyperglycemia and TB/DM association in patients with HIV

102 there is a long latency between the onset of hyperglycemia and the appearance of structural microangi

103 vors of critical illness experiencing stress hyperglycemia and to explore underlying mechanisms.

104 eptozocin-induced diabetes (2 weeks, in vivo hyperglycemia) and age-matched control pigs for vasoreac

105 ing additional CGM metrics for hypoglycemia, hyperglycemia, and glucose control; hemoglobin A1c (HbA1

106 se monitor (Dexcom) to measure hypoglycemia, hyperglycemia, and glycemic variability for 5 days follo

107 y, resulting in systemic insulin resistance, hyperglycemia, and hepatic inflammation, highlighting th

108 h included whole-animal glucose intolerance, hyperglycemia, and impaired insulin secretion.

109 I-7) in iPS cell-derived ECs when exposed to hyperglycemia, and in human iPS-ECs from diabetic patien

110 sequently inhibit food consumption, obesity, hyperglycemia, and liver steatosis in HFD-treated male m

111 ral elafin overexpression inhibited obesity, hyperglycemia, and liver steatosis in high-fat diet (HFD

112 ration of modified elafin inhibited obesity, hyperglycemia, and liver steatosis in the HFD-treated mi

113 red insulin and/or leptin) slightly improves hyperglycemia, and normalizes key metabolic defects (e.g

114 ggest that inflammatory pathways linked with hyperglycemia are confounding factors for salivary gland

115 dicated that both inflammatory responses and hyperglycemia are involved in the similar pathophysiolog

116 by a mixed-meal tolerance test (MMTT) and a hyperglycemia/arginine clamp procedure.

117 Unlike absolute hyperglycemia, relative hyperglycemia, as assessed by the stress hyperglycemia r

118 Similarly, in vitro hyperglycemia augmented venular constrictions.

119 Exposure to chronic hyperglycemia because of diabetes mellitus can lead to d

120 glutamate must be tightly controlled during hyperglycemia because of the risk for neurotoxicity with

121 sumption do not really capture boy's chronic hyperglycemia, boys being more physically active than gi

122 f Ad.scIL-23 did not accelerate the onset of hyperglycemia but instead resulted in the development of

123 -products (AGEs) accumulate during prolonged hyperglycemia, but the mechanistic pathways that lead to

124 We assessed the contribution of hyperglycemia by comparing insulin sensitivity in contro

125 betes (T2D), sustained remission of diabetic hyperglycemia can be induced by a single intracerebroven

126 ype 2 diabetes (T2D), sustained remission of hyperglycemia can be induced by a single intracerebroven

127 lved in the pathogenesis of normalization of hyperglycemia caused by the tacrolimus.

128 Chronic hyperglycemia causes myocardial injury, raising the poss

129 he TSP2-deficient mice developed obesity and hyperglycemia comparable with diabetic control mice, the

130 inner retinal dysfunction after induction of hyperglycemia compared to hyperglycemic littermate contr

131 a), a significant proportion of patients had hyperglycemia compared with controls, and patients had s

132 significant proportion of patients developed hyperglycemia, compared with controls, without soft tiss

133 rated retinal dysfunction after induction of hyperglycemia, consistent with normal-appearing retinal

134 vious findings of associations among chronic hyperglycemia, cortical thinning, and depressive symptom

135 ndently associated with the dyslipidemia and hyperglycemia criteria of MS.

136 Hyperglycemia decreased APT-1 activity in human umbilica

137 hat persistent activation of IMD resulted in hyperglycemia, depleted fat reserves, and developmental

138 ls of Ak mice drastically reduces the severe hyperglycemia, diabetes incidence, hypoinsulinemia, beta

139 h late failure of insulin production, severe hyperglycemia/diabetes, lipodystrophy, hepatosteatosis,

140 We assessed the prevalence of hyperglycemia (DM and impaired glucose regulation [IGR])

141 Hyperglycemia during acute ischemic stroke is common and

142 Hyperglycemia during myocardial infarction (MI) has a st

143 upport to efforts toward optimizing maternal hyperglycemia during pregnancy.

144 T1DM is accompanied by hyperglycemia, dyslipidemia, and increased inflammation

145 that relative insulin deficiency rather than hyperglycemia elevated levels of apolipoprotein C3 (APOC

146 (2) In conclusion, both in vitro and in vivo hyperglycemia enhance retinal venular responses to endog

147 h metabolic memory in which prior periods of hyperglycemia enhance the future risk of developing DKD

148 During pregnancy, hyperglycemia exposes women to the risk of having a macr

149 the peritoneal pouch of recipients reversed hyperglycemia for >60 days.

150 sults demonstrate that sustained physiologic hyperglycemia for 72 h 1) increases absolute insulin sec

151 s, HIF-1alpha protein turnover is rapid, and hyperglycemia further destabilizes the protein.

152 Hyperglycemia further exacerbates this uncoupled mutuali

153 clinical trial included adult patients with hyperglycemia (glucose concentration of >110 mg/dL if ha

154 eight gain, inflammation, hepatic steatosis, hyperglycemia, glucose intolerance, and insulin resistan

155 tests and ex vivo analyses revealed fasting hyperglycemia, glucose intolerance, reduced sensitivity

156 We examined the effects of statins on hyperglycemia, glucose tolerance, fatty acid accumulatio

157 microbiota is involved in the regulation of hyperglycemia has not been reported.

158 ic neuromuscular tissues exposed to in-vitro hyperglycemia (HG).

159 the consequence of this hormone peptide in a hyperglycemia (high blood sugar) environment.

160 ompasses medical conditions such as obesity, hyperglycemia, high blood pressure, and dyslipidemia tha

161 novel method for therapy of hyperinsulinemic hyperglycemia, highly selectively killing beta-cells by

162 Type 2 Diabetes Mellitus (T2DM), exhibiting hyperglycemia, hyperinsulinemia, and insulin resistance

163 compromised by severe side effects including hyperglycemia, hyperlipidemia and obesity.

164 In addition to hyperglycemia, hyperlipidemia is also closely related wi

165 development of metabolic syndrome, including hyperglycemia, hyperlipidemia, and insulin resistance.

166 mal and abnormal blood conditions, including hyperglycemia/hypoglycemia, hyperoxemia/hypoxemia, and h

167 Px resulted in stable hyperglycemia, hypoinsulinemia, decreased C-peptide, and

168 O-EtOAc)-mediated attenuation of obesity and hyperglycemia in a mouse model.

169 pensity for diet-induced obesity and fasting hyperglycemia in adulthood.

170 ificantly reduced the EGP-lowering effect of hyperglycemia in both humans and rats.

171 d glucose intolerance, hyperinsulinemia, and hyperglycemia in C57BL/6J mice.

172 d glucose infusion rates were used to manage hyperglycemia in critically ill children with cardiovasc

173 hallenge the clinical concept of normalizing hyperglycemia in diabetes as a causative treatment strat

174 fer facile routes to ameliorate postprandial hyperglycemia in diabetes via control of starch digestio

175 erglucagonemia is partly responsible for the hyperglycemia in diabetes, making glucagon an attractive

176 lpha-cell mass are associated with states of hyperglycemia in diabetes.

177 bolism, and is therapeutically used to treat hyperglycemia in diabetes.

178 harmacological inhibition of DUSP26 improves hyperglycemia in diabetic mice and protects human islet

179 th factor 1 (FGF1) has been shown to reverse hyperglycemia in diabetic rodent models through peripher

180 report that Notch1 signaling is activated by hyperglycemia in diabetic skin and specifically impairs

181 ovel therapeutic strategies that counteracts hyperglycemia in disease settings.

182 a link-involving IL-17-between psoriasis and hyperglycemia in humans and mice.

183 irculating elafin levels are associated with hyperglycemia in men with T2DM.

184 al microvessels and brain tissue paralleling hyperglycemia in mice of both DM types.

185 teatosis, hepatocyte death, inflammation and hyperglycemia in mice with diet-induced steatohepatitis.

186 syngeneic pancreatic islet cells to reverse hyperglycemia in murine streptozotocin induced- or non-o

187 rated disease progression and rapid onset of hyperglycemia in NOD mice.

188 contributes to reduced insulin secretion and hyperglycemia in patients with type 2 diabetes mellitus

189 a lead FGF19 analog, NGM282, did not correct hyperglycemia in patients with type 2 diabetes.

190 cholesterol, they have propensity to induce hyperglycemia in patients.

191 activity against sugar-induced postprandial hyperglycemia in rats plausibly due to the presence of i

192 the most effective treatment for controlling hyperglycemia in severely obese patients with diabetes.

193 ycemia and serum TNF levels in sham but only hyperglycemia in splenectomized mice.

194 ligent and exclusive use of insulin to avert hyperglycemia in the face of hypercytokinemia and potent

195 f ST8Sia6 in pancreatic beta cells mitigated hyperglycemia in the multiple low-dose streptozotocin mo

196 evention and treatment of tacrolimus-induced hyperglycemia in transplant recipients.

197 hes to prevent insulin resistance and stress hyperglycemia in trauma and surgery patients and thereby

198 ly used antihyperglycemic therapies to lower hyperglycemia in type 2 diabetes mellitus the high preva

199 ta suggest EPA prevents hyperinsulinemia and hyperglycemia, in part, through RvE1's activation of ERV

200 We further found that hyperglycemia increased TSP2 expression in fibroblasts,

201 In vivo hyperglycemia increased vitreous levels of ET-1 but not

202 We therefore hypothesized that hyperglycemia increases platelet glucose utilization, wh

203 a target for sustained remission of diabetic hyperglycemia induced by FGF1.

204 Hyperglycemia -induced reactive oxygen species are key m

205 esent study investigates the role of JunD in hyperglycemia-induced and reactive oxygen species-driven

206 cardial injury, raising the possibility that hyperglycemia-induced cardiac autoimmunity could contrib

207 (alpha MHC JunD(tg)) were protected against hyperglycemia-induced cardiac dysfunction.

208 Knowledge of diabetes and hyperglycemia-induced deficits in BMSC regulation, and s

209 1D rats, suggesting that obesity exaggerates hyperglycemia-induced epigenetic modifications, accelera

210 It also prevented hyperglycemia-induced hemoglobin and insulin glycation.

211 We identified a novel mechanism of acute hyperglycemia-induced hyperfiltration wherein increases

212 istone modifications, and microRNAs mediates hyperglycemia-induced JunD downregulation and myocardial

213 distal nephron in the conditions of HS- and hyperglycemia-induced kidney injury.

214 Findings from this study suggest that hyperglycemia-induced LOX-PP overexpression may contribu

215 In mice, this is attributed in part to hyperglycemia-induced monocytosis, which increases monoc

216 The mechanism of hyperglycemia-induced oxidative stress in podocytes is n

217 Hyperglycemia-induced podocyte dysfunction is a major co

218 The findings support a model wherein hyperglycemia-induced REDD1 blunts the Nrf2 antioxidant

219 Second, in the streptozotocin model of hyperglycemia-induced renal injury ENaC activity in hype

220 and adhesion factors, a marked reduction of hyperglycemia-induced retinal leukostasis, and restorati

221 resents a novel model to study mechanisms of hyperglycemia-induced retinopathy wherein extensive proa

222 ESIGN, SETTING, AND PARTICIPANTS: The Stroke Hyperglycemia Insulin Network Effort (SHINE) randomized

223 nfer high risk for the development of NAFLD: hyperglycemia, insulin resistance, and dyslipidemia.

224 Fasting hyperglycemia is a hallmark of T2D derived largely from

225 Hyperglycemia is a potent regulator of endogenous glucos

226 Hyperglycemia is associated with protein kinase A (PKA)-

227 Persistent hyperglycemia is causally associated with pancreatic bet

228 iabetes and a body mass index of 30 to 35 if hyperglycemia is inadequately controlled despite optimal

229 that about half of the suppression of EGP by hyperglycemia is mediated by central K(ATP) channels.

230 Diabetes is primarily known but untreated, hyperglycemia is often severe, and many patients with TB

231 Lowering hyperglycemia is the typical therapeutic goal in clinica

232 Elevated blood glucose (hyperglycemia) is a hallmark metabolic abnormality in di

233 nt in the CGM group and 2 in the BGM group), hyperglycemia/ketosis (1 participant with an event in CG

234 ine vehicle was without effect, remission of hyperglycemia lasting >3 weeks was observed following bi

235 te and increased collagenolysis confirm that hyperglycemia leads to a chronic inflammation in and aro

236 Here, we investigated whether hyperglycemia leads to accentuation of oxidant and ER st

237 Population-based data suggest that hyperglycemia may be present up to three years before th

238 ry responses and the pathological process of hyperglycemia may influence each other by several comple

239 Maternal hyperglycemia may not affect placental fatty acid uptake

240 However, hyperglycemia may only be a symptom of diabetes but not

241 Following 72 h of physiologic hyperglycemia, metabolic clearance rate of insulin was m

242 ession of autoimmunity, resulting in delayed hyperglycemia, mice that received HK BF by intravenous i

243 ion (n = 7 [10.8%]), fatigue (n = 4 [6.2%]), hyperglycemia (n = 3 [4.6%]), and elevated ALT (n = 3 [4

244 o treatment was 40%, the most frequent being hyperglycemia (n = 6), nausea (n = 7) and vomiting (n =

245 ke neurological recovery in association with hyperglycemia, neuroinflammation, and atrophy of PV(+) i

246 logical mechanisms, including the effects of hyperglycemia on components of the extracellular matrix

247 nvestigation aimed to quantify the impact of hyperglycemia on host-bacterial interactions in establis

248 However, the impact of hyperglycemia on retinal venular constriction remains un

249 ation of pancreatic beta-cell function after hyperglycemia onset.

250 n risk could be identified prior to onset of hyperglycemia or albuminuria, and monitored non-invasive

251 By 6weeks, prior to development of either hyperglycemia or albuminuria, fa/fa rats were hyperinsul

252 are not associated with other biomarkers of hyperglycemia or diabetes (p > 0.2).

253 of the operative field (OR 2.98, P < 0.001), hyperglycemia (OR 2.80, P = 0.003), duration of surgery

254 ated with the central obesity (P = 0.01) and hyperglycemia (P < 0.001) criteria of MS, whereas higher

255 erolemia (p = 0.036); GGC with lower risk of hyperglycemia (p = 0.022), better sleep pattern (p = 0.0

256 Elevations in extracellular glucose (hyperglycemia) potentiate vascular L-type Ca(2+) channel

257 e analysis (odds ratio = 1.09 per 0.1 stress hyperglycemia ratio increment; p < 0.001) and after adju

258 than 6.5% (odds ratio = 1.08 per 0.1 stress hyperglycemia ratio increment; p < 0.001) and glycosylat

259 mmol/mol) (odds ratio = 1.08 per 0.1 stress hyperglycemia ratio increment; p = 0.005).

260 like admission glucose concentration, stress hyperglycemia ratio was significantly associated with mo

261 In contrast, stress hyperglycemia ratio was significantly associated with mo

262 lucose concentration to calculate the stress hyperglycemia ratio, an index of relative glycemia.

263 ive hyperglycemia, as assessed by the stress hyperglycemia ratio, independently predicts in-hospital

264 associated with reduced steroid exposure and hyperglycemia, reduced grade 2 to 3 infections, improvem

265 Unlike absolute hyperglycemia, relative hyperglycemia, as assessed by th

266 tasis and are used to treat hypoglycemia and hyperglycemia, respectively, in patients with diabetes.

267 Hyperglycemia resulted in reduced membrane thickness (by

268 elial activation induced by inflammation and hyperglycemia results in the endoplasmic reticulum (ER)

269 A state of chronic hyperglycemia seems to be a stronger mediator of inflamm

270 luconeogenesis is a major contributor to the hyperglycemia seen in T2DM.

271 and liposome administration at the onset of hyperglycemia significantly delayed diabetes progression

272 Periods of hyperglycemia significantly reduced exendin uptake in mu

273 rried by non-diabetic recipients, regardless hyperglycemia status of oocyte donors.

274 al pouch of diabetic nude mice also reversed hyperglycemia successfully.

275 He reports no symptoms of hyperglycemia, such as frequent urination, increased thi

276 nditions (studies using a pancreatic clamp), hyperglycemia suppressed EGP by ~50% in both humans with

277 ulin resistance, moderate rather than severe hyperglycemia, sustained hyperinsulinemia without late f

278 tus (PTDM), 5% (n = 118) developed transient hyperglycemia (t-HG) post-LT, and 65% (n = 1431) never d

279 growth factor 1 (FGF1) induces remission of hyperglycemia that is sustained for weeks.

280 he required instructive signal for mediating hyperglycemia through hepatic gluconeogenesis, which is

281 Metformin can improve patients' hyperglycemia through significant suppression of hepatic

282 8-HEPE itself, reversed hyperinsulinemia and hyperglycemia through the G-protein coupled receptor ERV

283 tyric acid content in the cecum and arrested hyperglycemia through the regulation of glucose-regulati

284 se variations, termed transient intermittent hyperglycemia (TIH), appear to be an independent risk fa

285 sion from the initial vascular response upon hyperglycemia to a proliferative stage with neovaculariz

286 vestigate whether using measures of relative hyperglycemia to determine individualized glycemic treat

287 es included rates of serious hypoglycemia or hyperglycemia using ICD-9-CM and ICD-10-CM diagnostic co

288 For in vitro hyperglycemia, vessels from euglycemic pigs were exposed

289 The baseline rate of serious hyperglycemia was 22.33 per 1000 person-years (95% CI, 1

290 Spontaneous hyperglycemia was developed in a colony of C57BL/6J mice

291 Hyperglycemia was observed in a tacrolimus-treated mouse

292 RvE1's effects on hyperinsulinemia and hyperglycemia were divergent in diversity outbred mice t

293 d, the stress-induced insulin resistance and hyperglycemia were largely abolished demonstrating an es

294 Enhanced vasoconstrictions during hyperglycemia were prevented by KB-R7943, while mRNA exp

295 l hypertension, fat metabolism disorder, and hyperglycemia) were not associated with worse kidney fun

296 not exhibit beta cell secretory responses to hyperglycemia, whereas the high C-peptide group showed i

297 tus is a metabolic disorder characterized by hyperglycemia, which can be counteracted by inhibition o

298 ain mechanisms underlying the association of hyperglycemia with depressive symptoms are unknown.

299 We aim to evaluate the associations of hyperglycemia with inflammation and neutrophil to lympho

300 As such, we induced hyperglycemia with streptozotocin in mice with monoallel

301 n receptor pathogenic variants, INSR) causes hyperglycemia without steatosis.