ライフサイエンスコーパス: insulin treatment

1 ncluded among the considerations to initiate insulin treatment.

2 tes, 828 developed diabetes, and 237 started insulin treatment.

3 ized to the plasma membrane independently of insulin treatment.

4 ylation level of IRS-2 was down-regulated by insulin treatment.

5 rarily depriving type 1 diabetic patients of insulin treatment.

6 ogen signaling blockade but not by long-term insulin treatment.

7 Mobility was not increased by insulin treatment.

8 e not previously been shown to be altered by insulin treatment.

9 se (p70S6K) in the basal state and following insulin treatment.

10 uals with overt diabetes at this age started insulin treatment.

11 2 rose in the ISOM but was not reversed with insulin treatment.

12 Akt2(-/-) cells and did not change following insulin treatment.

13 abetic myocardium, which was reversible upon insulin treatment.

14 tic rats and fully restored within 2 h after insulin treatment.

15 y state levels of calmodulin mRNA seen after insulin treatment.

16 thioredoxin activity, which normalized with insulin treatment.

17 d C: 13.8 +/- 3.0 arbitrary intensity units) insulin treatment.

18 tivity remained inhibited after compensatory insulin treatment.

19 t was substantially restored after 6 days of insulin treatment.

20 This phase is reversible with insulin treatment.

21 n the first three months of life and require insulin treatment.

22 tin structure was compromised during chronic insulin treatment.

23 induced by platelet-derived growth factor or insulin treatment.

24 slational complexes could be attenuated with insulin treatment.

25 This interaction is enhanced with insulin treatment.

26 he SH3 domains of CAP and was independent of insulin treatment.

27 , respectively, to insufficient or excessive insulin treatment.

28 t for 2 weeks and after 10 days of intensive insulin treatment.

29 e) of the induction seen by high glucose and insulin treatment.

30 ucose uptake in vitro to the level seen with insulin treatment.

31 ding to complete beta-cell failure requiring insulin treatment.

32 thesis, we measured the recovery rates after insulin treatment.

33 e association with the IR appears to require insulin treatment.

34 abetic rats, and this effect was reversed by insulin treatment.

35 ch prolactin gene expression is increased by insulin treatment.

36 se changes can be attenuated with 2 weeks of insulin treatment.

37 and whether changes could be minimized with insulin treatment.

38 nt, 33% on oral glucose lowering, and 40% on insulin treatment.

39 reventing FAK phosphorylation in response to insulin treatment.

40 < 0.005), and the increase was prevented by insulin treatment.

41 157F)-mediated responses were potentiated by insulin treatment.

42 of GLUT4 protein similar to that elicited by insulin treatment.

43 arcuate nucleus was unaltered by diabetes or insulin treatment.

44 AgRP, mRNA levels was partially reversed by insulin treatment.

45 ic function are restored to normal levels by insulin treatment.

46 osol to the membrane fraction in response to insulin treatment.

47 mplex interacts with IR and is stimulated by insulin treatment.

48 tization of glycogen synthase due to chronic insulin treatment.

49 P labeling at sites 1 and 2 was increased by insulin treatment.

50 phosphorylated at site 2, was unaffected by insulin treatment.

51 osphorylated upon epidermal growth factor or insulin treatment.

52 achieve glycaemic targets with conventional insulin treatment.

53 acid balance was significantly improved with insulin treatment.

54 y to that of HA-RSK2 but was not affected by insulin treatment.

55 opathy initially increases with the onset of insulin treatment.

56 ion of actin membrane ruffles in response to insulin treatment.

57 (GVBD) to the same extent as progesterone or insulin treatment.

58 letely recovered to control levels following insulin treatment.

59 played regulatory T-cell features after oral insulin treatment.

60 curate calculations, particularly with acute insulin treatment.

61 and lactate secretion, an effect similar to insulin treatment.

62 on of diabetes, age at diagnosis, and use of insulin treatment.

63 cells, and the complex dissociated following insulin treatment.

64 sally, which was further amplified following insulin treatment.

65 rmanent neonatal diabetes requiring lifelong insulin treatment.

66 in treatment and nucleolar localization with Insulin treatment.

67 lood pressure treatment, lipid treatment, or insulin treatment.

68 vity were prevented by glycemic control with insulin treatment.

69 ficantly different from baseline after acute insulin treatment.

70 ed mucus layer, which could be restored with insulin treatment.

71 ore pronounced in case of tightly controlled insulin treatment.

72 high morbidity and mortality in T1D despite insulin treatment.

73 pituitary cell cultures from these mice with insulin treatment.

74 3r2) form heterodimers that are disrupted by insulin treatment.

75 induced in lipogenic tissues by feeding and insulin treatment.

76 nses to infection may be altered by postburn insulin treatments.

77 n effect that was also partially reversed by insulin treatment (1.8 +/- 0.3 ng/ml).

78 virus (FIV) infected cats, daily intranasal insulin treatment (20.0 IU/200 mul for 6 weeks) reduced

79 However, chronic insulin treatment (24 h) did not decrease IR expression

80 Chronic insulin treatment (24 h) in control cells caused an incr

81 Acute insulin treatment (3 mU, 15 min prior) also elevated thr

82 Hyperphagia was prevented by insulin treatment (32 +/- 2 g/day).

83 .67 to 5.02; p = 0.0002) or diabetes without insulin treatment (5.2% vs. 1.8%; hazard ratio: 2.96; 95

84 Insulin treatment activated the insulin receptor substra

85 Acute insulin treatment activates phosphodiesterase 3B, reduce

86 e target glycaemic control with conventional insulin treatment, advancing to a basal-bolus insulin re

87 normalization following short-term (1 week) insulin treatment after longer periods of untreated diab

88 etic mice, which could not be prevented with insulin treatment after stroke.

89 kin-6 levels, was significantly decreased by insulin treatments after injury.

90 A in gastrocnemius muscle, and refeeding and insulin treatment again reversed the effects of starvati

91 The insulin treatment also attenuated anesthesia-induced hyp

92 High dose insulin treatment also decreased the basal level of apop

93 Insulin treatment also failed to stimulate muscle cytoch

94 Insulin treatment also increased VEGF protein levels in

95 Insulin treatment also led to accumulation of Ser-412-ph

96 Insulin treatment also led to phosphatidylinositol-3 (PI

97 Intensive insulin treatment also prevented most abnormalities, des

98 Exendin-4 or GLP-1-Tf (but not insulin) treatment also improved pancreatic morphology,

99 However, insulin treatment altered the transcription of 29 additi

100 of SNAT3 on the cell surface after 0.5 h of insulin treatment, although no effect was observed after

101 1 diabetic participants (n = 7) during both insulin treatment and 8 h of insulin deprivation and in

102 antibodies against insulin receptors before insulin treatment and alpha(2)M* stimulation significant

103 irect association of cdc42 and p85, and both insulin treatment and CA-cdc42 expression stimulated PI3

104 Once diagnosed, patients require lifelong insulin treatment and can experience numerous disease-as

105 3) Insulin treatment and constitutively active G(q) express

106 d be corrected toward normal after 3 days of insulin treatment and euglycemia.

107 Five of six patients remained free of insulin treatment and maintained FPG <126 mg/dl and HbA1

108 age, duration of diabetes, SBP, PP, ACR, and insulin treatment and negatively with GFR and weight (al

109 as nuclear translocation upon EGF, VEGF and Insulin treatment and nucleolar localization with Insuli

110 rane PIP(2) in cells following the sustained insulin treatment and observed a restoration in cortical

111 e and this effect was completely reversed by insulin treatment and partially reversed by leptin treat

112 Insulin treatment and PKB overexpression resulted in pho

113 ts, and they returned to normal levels after insulin treatment and resolution of hyperglycemic crises

114 In cultured myocytes, insulin treatment and SREBP-1 overexpression decreased,

115 cholesterol biosynthetic genes is induced by insulin treatment and that this localization precedes th

116 translocation was observed within minutes of insulin treatment and was paralleled by an increase in l

117 y immunoblotting after serum deprivation and insulin treatment, and caspase-3 activation was examined

118 ber of diabetic foot ulcer hospitalizations, insulin treatment, and peripheral vascular disease; HR=1

119 Maternal obesity, insulin treatment, and suboptimal in-hospital breastfeed

120 ife and can survive well over a year with no insulin treatment, and they maintain near normal body we

121 She is reluctant to commence insulin treatment as she dislikes the idea of injections

122 gical glycated hemoglobin level (P = 0.019), insulin treatment at baseline (P = 0.001), and a lower e

123 nalysis, age, diabetes duration, being under insulin treatment, blood glucose level, having non-commu

124 dies, we observed that either adiponectin or insulin treatment (but not LPA treatment) caused phospho

125 , glycogen synthase activity is increased by insulin treatment, but at higher levels of G(L) expressi

126 ion of lipogenic enzyme genes in response to insulin treatment, but it is not sufficient for the indu

127 t due to hypoinsulinemia in T1DM mice, since insulin treatment, but not high glucose, increases ATP7A

128 pose tissue (BAT) was measured in rats after insulin treatment by positron emission tomography combin

129 X zeta-mediated stimulation was repressed by insulin treatment, by bisperoxovanadate treatment, and b

130 usion were observed as early as 15 min after insulin treatment; by 20 min, a new 5'-splice site varia

131 Intensive insulin treatment can delay the onset and progression of

132 sm for heterologous desensitization, whereby insulin treatment can impair GPCR signaling, and highlig

133 vestigated whether islet transplantation and insulin treatment can relieve diabetic neuropathy and re

134 Insulin treatment caused a change of at least 1.3-fold i

135 Long-term insulin treatment caused a sustained increase in [Ca(2+)

136 Insulin treatment caused greater ENaC activity in split-

137 Insulin treatment caused increased beta-arrestin1 Ser-41

138 Insulin treatment completely normalized glucose-induced

139 06 to -676 were deleted was not repressed by insulin treatment, confirming that this sequence is nece

140 d through the HSP by glucosamine and chronic insulin treatment correlated with increased O-GlcNAc lev

141 ubjected to ischemia and reperfusion chronic insulin treatment decreased the basal apoptotic level, a

142 In osteoblasts, continuous insulin treatment decreases the fraction of cellular GHR

143 onclusion, improvement of glycemic status by insulin treatment did not alter whole-body amino acid tu

144 iption factor FoxO1 was somewhat reduced and insulin treatment did not elicit normal translocation of

145 Our previous studies have shown that chronic insulin treatment down-regulates cellular beta-arrestin

146 Refeeding and insulin treatment effectively reversed these effects of

147 7 days beyond cessation of insulin treatment) elevation of threshold in ad libitum

148 nge, fat-free parenteral nutrition and acute insulin treatment, even in nondiabetic persons, may be v

149 l of type 1 diabetic hearts was shortened by insulin treatment ex vivo, and this effect was blocked b

150 In contrast to the shorter-duration group, insulin treatment for 1 week after 3 weeks of diabetes d

151 Inhaled insulin treatment for 3 months significantly improved gl

152 nner Sir Frederick Banting, who codiscovered insulin treatment for diabetes.

153 nner Sir Frederick Banting, who codiscovered insulin treatment for diabetes.

154 0.001), and were more likely to be receiving insulin treatment for hyperglycemia (P=0.02).

155 Insulin treatment for the last 4 of 12 weeks of diabetes

156 Insulin treatment given immediately following MI suppres

157 ality was similar in the intensive and loose insulin treatment groups (14% vs. 15%, p=.9), as was 6-m

158 As with insulin treatment, GTPgammaS stimulation of glucose tran

159 al worsening of diabetic macular edema after insulin treatment has been observed in a number of studi

160 The use of intensive insulin treatment has shown superior benefits in the tre

161 ho had severe hypoglycemia in the absence of insulin treatment (hazard ratio, 3.84; 95% CI, 2.37 to 6

162 Insulin treatment improved behavioral deficits and resto

163 Moreover, intranasal insulin treatment improved neurobehavioral performance,

164 dministration of AGP abolished the effect of insulin treatment in diabetic mice.

165 cantly increased rather than decreased after insulin treatment in diabetic patients.

166 horylation of Ser-473 by both mechanical and insulin treatment in MSC was prevented by the mTOR inhib

167 glycemia, limiting the benefits of intensive insulin treatment in patients with diabetes.

168 cotransporters 1 and 2, in combination with insulin treatment in patients with type 1 diabetes.

169 d with poor glycemic control, and effects of insulin treatment in people with type 2 diabetes.

170 rediabetes to diabetes and for initiation of insulin treatment in previously untreated patients with

171 luated by Hoechst staining, was inhibited by insulin treatment in R28 cells, but not in L6 muscle cel

172 In summary, continuous insulin treatment in rat H4 hepatoma cells reduces GH bi

173 eins were not affected by glycemic status or insulin treatment in subjects with type 2 diabetes.

174 nted suppression of glucagon secretion after insulin treatment in the presence of high glucose.

175 abolism, biochemical and clinical effects of insulin treatment in the severely burned, and the vagari

176 rgeting p110alpha block the acute effects of insulin treatment in vivo, whereas a p110beta inhibitor

177 Insulin treatments in subjects with type 2 diabetes had

178 sly known to be tyrosine phosphorylated with insulin treatment, including sites on the insulin recept

179 Three hours of insulin treatment increased Opa-1 protein levels, promot

180 f characteristic of Akt phosphorylation, and insulin treatment increased phosphorylation at five of t

181 of extracts of Akita mice demonstrated that insulin treatment increased the expression of GIRK1, SRE

182 Insulin treatment increased the number of alpha(2)M* hig

183 In control Akt2(+/+) fibroblasts, insulin treatment increased the phosphorylation of endog

184 In SOCS-1-expressing cells, insulin treatment increases the extent of interaction wi

185 Insulin treatment induced p70S6K, mTOR, and Akt phosphor

186 of the human CYP7A1 gene, whereas prolonged insulin treatment induces SREBP-1c, which inhibits human

187 We report that chronic insulin treatment induces the degradation of IRS-1, but

188 Two weeks of insulin treatment initiated after 4 weeks of diabetes in

189 Two weeks of insulin-treatment initiated after 6 weeks of diabetes at

190 that control of hyperglycemia with intensive insulin treatment is associated with improved outcomes f

191 After insulin treatment kinetic parameters of glycogen synthas

192 dFOXO is phosphorylated by dAkt upon insulin treatment, leading to cytoplasmic retention and

193 (i) Chronic insulin treatment leads to enhanced beta-arrestin-1 degr

194 Ultrafast microscopic analysis revealed that insulin treatment leads to the mobilization of GLUT4-con

195 Delaying insulin treatment led to AbetaO binding that was no long

196 We demonstrate that insulin treatment led to enhanced post-translational pro

197 rt that, in HIV-infected microglia cultures, insulin treatment led to reduced viral replication and i

198 Interestingly, insulin treatment lowered blood pressure and prevented r

199 stable diabetic phenotype and its rescue by insulin treatment make the INS(C94Y) transgenic pig an a

200 lycemia and that its inhibition by intensive insulin treatment may exacerbate paradoxically the lipid

201 fter adjusting for the duration of diabetes, insulin treatment, metabolic abnormalities, and autonomi

202 Insulin treatment minimized production of some of these

203 Here, we investigated whether insulin treatment modulates the diabetic immune system t

204 Insulin treatment must be individualized, and there are

205 uring insulin deprivation (n = 6) and during insulin treatment (n = 6) and in nondiabetic control sub

206 In contrast, insulin treatment normalized myocardial Hsp60 in the dia

207 Although insulin treatment normalized plasma glucose and many oth

208 Insulin treatment of 3T3-L1 adipocytes decreased the amo

209 Insulin treatment of 3T3-L1 adipocytes induces a rapid c

210 Insulin treatment of 3T3-L1 adipocytes stimulated associ

211 Insulin treatment of 3T3-L1 adipocytes stimulated WNK1 p

212 Insulin treatment of 3T3-L1 adipocytes stimulates both t

213 Insulin treatment of adipocytes caused AS160 to redistri

214 es connecdenn 1 interaction with Rab35 after insulin treatment of adipocytes.

215 In vitro insulin treatment of adipose tissue from fed or starved

216 Interestingly, insulin treatment of alphaXBPKD cells reduced tyrosine p

217 Insulin treatment of C2C12 muscle cells caused transcrip

218 that PI(3,5)P2 was present and increased by insulin treatment of cardiomyocytes via immunohistochemi

219 Here we show that insulin treatment of Chinese hamster ovary cells express

220 ulation of adiponectin secretion reported on insulin treatment of cultured adipocytes.

221 noprecipitates was also acutely activated by insulin treatment of cultured adipocytes.

222 Insulin treatment of cultured atrial myocytes stimulated

223 We found that insulin treatment of cultured bovine aortic endothelial

224 In summary, short-term insulin treatment of cultured, liver-derived cells selec

225 Insulin treatment of diabetic mice reduced mortality rat

226 Refeeding starved rats and insulin treatment of diabetic rats decreased pyruvate de

227 Insulin treatment of diabetic rats normalized changes in

228 Sustained systemic insulin treatment of diabetic rats prevented loss of ins

229 In addition, intranasal insulin treatment of experimentally feline immunodeficie

230 Our present studies suggest that insulin treatment of hepatoma cells results in a time-de

231 Insulin treatment of HFF GcgR(-/-) to simulate HFF-induc

232 Insulin treatment of HIV-infected primary human microgli

233 Insulin treatment of hyperglycemic B6-Ins2Akita/+ males

234 Upon insulin treatment of insulin-responsive adipocytes, O-Gl

235 Insulin treatment of mouse ATDC5 chondroprogenitors indu

236 Insulin treatment of murine myoblast cells induces the f

237 Insulin treatment of NIH-3T3(IR) fibroblasts overexpress

238 Insulin treatment of primary human neurons prevented HIV

239 lin is deficient, as occurs during exogenous insulin treatment of type 1 diabetes, or when chronic hy

240 Insulin treatment of vascular endothelial cells promoted

241 Insulin treatment or ectopic expression of the wild-type

242 etic mice was increased to control levels by insulin treatment or intracellular infusion of PI 3,4,5-

243 In the adjusted analysis being under insulin treatment (OR = 3.24; 95% CI: 1.56-6.75), diabet

244 us stroke (OR, 2.16; 95% CI, 1.12-4.16), and insulin treatment (OR, 2.99; 95% CI, 1.84-4.87).

245 d pressure (SBP) (ORper 10mmHg+ = 1.19), and insulin treatment (ORinsulin+ = 2.44).

246 Insulin treatment overcame this abnormality.

247 lower (1.15% +/- 0.33%/h) than during either insulin treatment (P = 0.01) or in nondiabetic controls

248 Insulin treatment partially corrected the hyperglycemia

249 We found that the insulin treatment prevented anesthesia-induced deficit i

250 Further, insulin treatment prevented H(2)O(2)-induced NF-kappaB a

251 immunoblotting and immunohistochemistry that insulin treatment prevented the decrease of GFAP express

252 tivation of caspase 3, and cleavage of PARP; insulin treatment prevented these changes.

253 Insulin treatment promoted an increase in levels of the

254 So far, clinical trials have indicated that insulin treatment provides no solution to this common cl

255 Insulin treatment reduced blood glucose levels and heart

256 Insulin treatment reduced intracellular ECs (2-arachidon

257 Insulin treatment reduced leucine nitrogen flux and tran

258 Insulin treatment reduced the difference in patterns bet

259 ated with automated and late fit after acute insulin treatment, reflecting the rapid early 18F-FDG up

260 Exogenous insulin treatment regenerates testes and restores fertil

261 Moreover, insulin treatment rescued the defective differentiation

262 abetes diagnosis less than 15 years, current insulin treatment, residual beta-cell function, and abse

263 Insulin treatment restored GK regulation in inhibited ce

264 Insulin treatment restored insulin receptor-beta autopho

265 Following differentiation, insulin treatment resulted in a 5-fold stimulation of gl

266 Prolonged insulin treatment resulted in decreased expression of bo

267 In this study with diabetic mice, insulin treatment resulted in increased vascular leakage

268 Using this model, we found that insulin treatment resulted in the nuclear exclusion of F

269 eased by 75% in the diabetic adipocytes, and insulin treatment reversed this effect.

270 arct size, HT, and behavior outcome, whereas insulin treatment showed a protective effect.

271 However, insulin treatment significantly normalized diabetes-indu

272 ggressive screening and early institution of insulin treatment significantly reduced this risk over t

273 Insulin treatment stimulated glycogen synthase activity

274 Insulin treatment stimulates the tyrosine phosphorylatio

275 estigated the effect of 11 days of intensive insulin treatment (T(2)D+) on whole-body amino acid kine

276 ouse retinas, which were not reversible with insulin treatment that achieved normoglycemia.

277 However, unlike insulin treatment, the peptide treatment did not increas

278 During insulin treatment, the rate of mucosal protein synthesis

279 the diabetic rats were restored to normal by insulin treatments, the AQP9 levels returned to baseline

280 VEGF mRNA levels are also increased by insulin treatment through the PI 3-kinase-dependent path

281 Here, we show that acute insulin treatment, through the downstream kinase protein

282 affected by insulin deficiency and systemic insulin treatment to determine whether they contribute t

283 to overt diabetes and from diabetes free of insulin treatment to insulin use.

284 model, with significant recovery after acute insulin treatment, using a mouse vena cava IDIF approach

285 membrane in such a way that after 30 min of insulin treatment, virtually every receptor molecule in

286 Although insulin treatment was capable of reversing all these cha

287 rm equivalent age, normoglycemia without any insulin treatment was found in both groups.

288 Insulin treatment was the strongest predictor of ADP-ind

289 he combination of maximal AICAR plus maximal insulin treatments was partially additive, suggesting th

290 Duration of diabetes, age at diagnosis, and insulin treatment were associated with increasing risk o

291 es inadequately controlled with conventional insulin treatment were randomly assigned (1:1:1), via a

292 Additionally, insulin treatments were associated with alterations in B

293 s-1 and phospho-Akt levels following in vivo insulin treatment, whereas AGN194204 increased hepatic I

294 hormone (CRH) expression were normalized by insulin treatment, whereas the expression of mRNA encodi

295 HepG2 cells are significantly attenuated by insulin treatment, whereas the phosphatidylinositol 3-ki

296 ence imaging to show for the first time that insulin treatment, which is protective in animal models

297 Insulin treatment with LG reduced the A(0.5) to 96 +/- 1

298 In hepatocytes incubated in the presence of insulin, treatment with a PKA-selective agonist mimicked

299 he cohort included 22,395 women who received insulin treatment, with 321 incident breast cancer event

300 etes with onset after 35 years of age and no insulin treatment within the first 6 months after diagno