ライフサイエンスコーパス: insulin-dependent

1 to 1.14 mg . kg(-1) . day(-1)) and remained insulin dependent.

2 ly (0.83+/-0.05) or completely (1.00+/-0.07) insulin dependent.

3 tor of triacylglycerol synthesis, and 3) was insulin-dependent.

4 Myo1c also contributed to insulin-dependent actin filament remodeling.

5 In addition, insulin-dependent activation of Akt, important in mediat

6 PDK-1 binding motif significantly decreases insulin-dependent activation of Akt.

7 tophosphorylation, but both proteins inhibit insulin-dependent activation of ERK1/2 and protein kinas

8 ckdown markedly and specifically potentiates insulin-dependent activation of kinase Akt, likely refle

9 phosphate as the sole in vivo product of the insulin-dependent activation of PI3K-C2alpha, confirming

10 any differences between the two strains; the insulin-dependent activation of PKB/cAKT was not differe

11 Like insulin-dependent activation, IR-TM requires that IR hav

12 Caco-2/TC7 enterocytes, ceramide effects on insulin-dependent AKT phosphorylation are mediated by pr

13 t not restricting media methionine, enhanced insulin-dependent Akt phosphorylation in 3T3-L1 adipocyt

14 ich was associated with a failure to undergo insulin-dependent Akt phosphorylation in the hypothalamu

15 atic glucose production by insulin, enhanced insulin-dependent Akt phosphorylation in the liver, and

16 vation of the gene coding for FoxO3 enhances insulin-dependent Akt phosphorylation.

17 ike-structures were increased with decreased insulin-dependent Akt phosphorylation.

18 a ubiquitously expressed kinase inhibited by insulin-dependent Akt/PKB/SGK.

19 dingly, loss of PI3K-C2gamma does not affect insulin-dependent Akt1 activation as well as S6K and Fox

20 that can lower blood glucose levels via both insulin-dependent and -independent mechanisms, and propo

21 GTT depends on a complex interaction of both insulin-dependent and -independent mechanisms.

22 in synthesis in skeletal muscle through both insulin-dependent and -independent mechanisms.

23 ue to whole body glucose homeostasis through insulin-dependent and independent mechanisms.

24 t LCN13 regulates glucose metabolism by both insulin-dependent and insulin-independent mechanisms.

25 ession of Cyp7a1, a BA synthesis enzyme, was insulin-dependent and was markedly decreased in Insr(P11

26 ation, and CHD risks associated with type 1 (insulin-dependent) and type 2 (insulin-independent) diab

27 e efficacy of new treatments in both type 1 (insulin-dependent) and type 2 (non-insulin-dependent) di

28 e effects of knocking down these genes in an insulin-dependent, anti-lipolysis assay in 3T3-L1 adipoc

29 PIP4K II beta expression did not impair insulin-dependent association of PI3K with insulin recep

30 The mutant was capable of insulin-dependent autophosphorylation and phosphorylatio

31 The amount of insulin-dependent autophosphorylation of the mutant rece

32 er (FRET) cell-based assay that measures the insulin-dependent colocalization of Akt2 fused with eith

33 lly, expression of MICAL-L2-CT abrogated the insulin-dependent colocalization of Rab13 with ACTN4 or

34 Rab13, MICAL-L2, and ACTN4 formed an insulin-dependent complex assessed by pull down and conf

35 The insulin dependent diabetes (Idd)22 locus was identified

36 l recessive genetic disease characterized by insulin dependent diabetes and vision, hearing and brain

37 dependent diabetes mellitus (type 1) and non-insulin dependent diabetes mellitus (type 2) after liver

38 t congenic mice having protective alleles at insulin-dependent diabetes (Idd) 3, Idd5.1, and Idd5.2 (

39 D) because of protective alleles at multiple insulin-dependent diabetes (Idd) genes, but develops aut

40 Several genetic insulin-dependent diabetes (Idd) intervals that confer r

41 In the NOD mouse model of type 1 diabetes, insulin-dependent diabetes (Idd) loci control the develo

42 Although more than 20 insulin-dependent diabetes (Idd) loci have been implicat

43 At least 20 insulin-dependent diabetes (Idd) loci modify the progres

44 s (T1D) is a polygenic disease with multiple insulin-dependent diabetes (Idd) loci predisposing human

45 ograft survival in congenic NOD mice bearing insulin-dependent diabetes (Idd) loci that reduce the fr

46 NOD.Idd3/5 congenic mice have insulin-dependent diabetes (Idd) regions on chromosomes

47 n the NOD mouse model has been linked to >30 insulin-dependent diabetes (Idd) susceptibility loci.

48 iabetes (T1D) protection associated with the insulin-dependent diabetes (Idd)10 locus on chromosome 3

49 r beta cell-specific Th2 cells in regulating insulin-dependent diabetes (IDDM).

50 nt, 1.29; 95% CI, 1.28 to 1.30), presence of insulin-dependent diabetes (odds ratio, 2.14; 95% CI, 2.

51 se (n = 96), rheumatoid arthritis (n = 346), insulin-dependent diabetes (presumed to be type 1) (n =

52 lar mechanism involved in the development of insulin-dependent diabetes (type 1 diabetes).

53 s of interest are the acute treatment of non-insulin-dependent diabetes (type 2), the management of c

54 aving the NOD diabetes susceptibility region insulin-dependent diabetes 3 (Idd3).

55 se have been mapped to chromosome 1, Idd5.1 (insulin-dependent diabetes 5.1) and Idd5.2.

56 In conclusion, insulin-dependent diabetes altered the normal rhythmicit

57 The average percentage of insulin-dependent diabetes among patients with NODM afte

58 the therapy of choice for patients suffering insulin-dependent diabetes and end stage renal failure.

59 scle protein catabolism present in rats with insulin-dependent diabetes and other catabolic condition

60 alpha-cell is not intrinsically abnormal in insulin-dependent diabetes because of STZ-induced destru

61 um levels in clear lenses from subjects with insulin-dependent diabetes did not differ from that in l

62 l maintenance of islets, eventually leads to insulin-dependent diabetes in most patients.

63 y receptor on myeloid cells as a gene in the insulin-dependent diabetes locus 13.2 (Idd13.2) that dri

64 s enhanced engraftment potential maps to the insulin-dependent diabetes locus 9 (Idd9) locus, and as

65 2.0 versus 1.0 or lower: 1.37 [1.32-1.43]), insulin-dependent diabetes mellitus (1.45 [1.39-1.51]),

66 ratio, 11.2; P = 0.04), and 6 of 43 with non-insulin-dependent diabetes mellitus (14%; odds ratio, 11

67 e Finland-United States Investigation of Non-Insulin-Dependent Diabetes Mellitus (FUSION) Genetics st

68 bese diabetic (NOD) mice before the onset of insulin-dependent diabetes mellitus (IDDM) and may be cr

69 n effective therapy that enables people with insulin-dependent diabetes mellitus (IDDM) and renal fai

70 lar attention has been focused on autoimmune insulin-dependent diabetes mellitus (IDDM) because nonob

71 Insulin-dependent diabetes mellitus (IDDM) can lead to v

72 s long been implicated in the development of insulin-dependent diabetes mellitus (IDDM) caused by vir

73 roiditis (AIT), multiple sclerosis (MS), and insulin-dependent diabetes mellitus (IDDM) during 1990-1

74 Also, after risk adjustment, patients with insulin-dependent diabetes mellitus (IDDM) had higher ri

75 Genetic analysis of autoimmune insulin-dependent diabetes mellitus (IDDM) has focused o

76 sulted in delay or transient protection from insulin-dependent diabetes mellitus (IDDM) in NOD mice.

77 in an Ag-specific manner and in turn prevent insulin-dependent diabetes mellitus (IDDM) in nonobese d

78 nduces GAD65-specific Th2 cells and prevents insulin-dependent diabetes mellitus (IDDM) in nonobese d

79 Insulin-dependent diabetes mellitus (IDDM) is characteri

80 In mice, coxsackievirus B4 (CB4) induces insulin-dependent diabetes mellitus (IDDM) resembling th

81 ated microenvironment in the pathogenesis of insulin-dependent diabetes mellitus (IDDM), an LTbeta re

82 acceleration in the kinetics and severity of insulin-dependent diabetes mellitus (IDDM).

83 ical calcific pancreatitis (n = 15), and non-insulin-dependent diabetes mellitus (n = 43) and control

84 We investigated whether risk for non-insulin-dependent diabetes mellitus (NIDDM) and metaboli

85 Patients with non-insulin-dependent diabetes mellitus (NIDDM) exhibit poor

86 Non-insulin-dependent diabetes mellitus (NIDDM) is a multifa

87 d the role of MIF in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) using MIF(-/

88 sposition factors for the development of non-insulin-dependent diabetes mellitus (NIDDM).

89 insulin sensitizers in rodent models of non-insulin-dependent diabetes mellitus (NIDDM).

90 from adipose tissue in animal models of non-insulin-dependent diabetes mellitus (NIDDM).

91 from adipose tissue in animal models of non-insulin-dependent diabetes mellitus (NIDDM).

92 proved to be caused by mtDNA mutations; non-insulin-dependent diabetes mellitus (NIDDM); and hyperte

93 imic events and molecules involved in type 1 insulin-dependent diabetes mellitus (T1D), we previously

94 he presence of autoimmune conditions such as insulin-dependent diabetes mellitus (T1DM) or a family h

95 opathy (DR) in African Americans with type 1 insulin-dependent diabetes mellitus (T1DM).

96 er there was a difference in outcome between insulin-dependent diabetes mellitus (type 1) and non-ins

97 uccessful in correcting the hyperglycemia of insulin-dependent diabetes mellitus (type 1), the result

98 regions of HLA-DRB1 and HLA-DQB1 within the insulin-dependent diabetes mellitus 1 locus in T1D monoc

99 H3K4me3, H3K9me2, H3K9Ac, and H4K16Ac at the insulin-dependent diabetes mellitus 1 region in monocyte

100 wn linkage of both HLA-DQ2.3 and -DQ3.2 with insulin-dependent diabetes mellitus and celiac disease,

101 All patients had long-standing insulin-dependent diabetes mellitus and subsequent renal

102 associated with end-stage renal disease and insulin-dependent diabetes mellitus and the prolonged, v

103 Insulin resistance and non-insulin-dependent diabetes mellitus are major causes of

104 sity, hypertension, hyperlipidaemia, and non-insulin-dependent diabetes mellitus are set against asso

105 DM in HLA-DR4-restricted presentation of an insulin-dependent diabetes mellitus autoantigen, glutama

106 ansfer into young NOD mice and could inhibit insulin-dependent diabetes mellitus development, althoug

107 e Finland-United States Investigation of Non-Insulin-Dependent Diabetes Mellitus Genetics study and p

108 induced beta cell destruction and subsequent insulin-dependent diabetes mellitus in RIP-mCD80(+) mice

109 Insulin-dependent diabetes mellitus is associated with a

110 One of the major complicating factors in insulin-dependent diabetes mellitus is nephropathy.

111 The development of spontaneous insulin-dependent diabetes mellitus is preceded by the o

112 Insulin-dependent diabetes mellitus is usually caused by

113 stantial negative effect similar to that for insulin-dependent diabetes mellitus or smoking in adults

114 ith a reduced dementia risk in initially non-insulin-dependent diabetes mellitus patients.

115 nsplantation for patients with long-standing insulin-dependent diabetes mellitus that progresses to r

116 of pancreas transplantation in patients with insulin-dependent diabetes mellitus who have received a

117 is is an uncommon but severe complication of insulin-dependent diabetes mellitus with unclear pathoph

118 ctors (eg, dialysis-dependent renal failure, insulin-dependent diabetes mellitus) continued to increa

119 diseases, including dilated cardiomyopathy, insulin-dependent diabetes mellitus, and chronic inflamm

120 utosomal-recessive disorder characterized by insulin-dependent diabetes mellitus, caused by nonautoim

121 diabetic (NOD) mice, a spontaneous model for insulin-dependent diabetes mellitus, exhibit elevated le

122 Nonobese diabetic (NOD) mice, a model of insulin-dependent diabetes mellitus, have a defect in na

123 in patients with a history of long-standing insulin-dependent diabetes mellitus, have been reported

124 ry of peptides bound by the type I diabetes (insulin-dependent diabetes mellitus, IDDM)-associated HL

125 th increased risk of type 2 diabetes, or non-insulin-dependent diabetes mellitus, in Mexican American

126 tis, Graves' disease, Hashimoto thyroiditis, insulin-dependent diabetes mellitus, inflammatory bowel

127 ene are linked to an early onset form of non-insulin-dependent diabetes mellitus, MODY-4.

128 by mutations in WFS1 and is characterized by insulin-dependent diabetes mellitus, optic atrophy, and

129 e mutation was diagnosed at age 3 years with insulin-dependent diabetes mellitus, the central feature

130 We report that in a model of insulin-dependent diabetes mellitus, the generation of r

131 IPEX manifests most commonly with diarrhea, insulin-dependent diabetes mellitus, thyroid disorders,

132 reatic diseases in Bangladesh, including non-insulin-dependent diabetes mellitus, was undertaken.

133 li had less N-sulfation of HS as a result of insulin-dependent diabetes mellitus.

134 th for any MPS result than patients with non-insulin-dependent diabetes mellitus.

135 imal-medial thickness (IMT) in children with insulin-dependent diabetes mellitus.

136 tes, tropical calcific pancreatitis, and non-insulin-dependent diabetes mellitus.

137 ing protection from cyclophosphamide-induced insulin-dependent diabetes mellitus.

138 nued to destroy their beta cells and develop insulin-dependent diabetes mellitus.

139 notype and correlate with the progression of insulin-dependent diabetes mellitus.

140 who, at baseline, were free of dementia and insulin-dependent diabetes mellitus.

141 ng (BB) DRlyp/lyp rat develops an autoimmune insulin-dependent diabetes similar to human type 1 diabe

142 The mouse T1D susceptibility locus insulin-dependent diabetes susceptibility 3 (Idd3), whic

143 iabetes susceptibility regions, particularly insulin-dependent diabetes susceptibility genes (Idd)9/1

144 ll number and function might lie within Idd (insulin-dependent diabetes susceptibility locus) regions

145 type 1 diabetes-protective haplotypes at the insulin-dependent diabetes susceptibility region 10 (Idd

146 es, pigmented hypertrichotic dermatosis with insulin-dependent diabetes syndrome, characterized by au

147 and pigmented hypertrichotic dermatosis with insulin-dependent diabetes syndromes due to either mistr

148 n is a promising alternative to conventional insulin-dependent diabetes treatment but is not yet a pr

149 litazone (TRO) was used for treatment of non-insulin-dependent diabetes until its removal from the ma

150 or both E2F1 and E2F2 develop nonautoimmune, insulin-dependent diabetes with high penetrance.

151 or epistasis between alleles of several Idd (insulin-dependent diabetes) loci.

152 endent predictors of LOS were increased age, insulin-dependent diabetes, and decreased HRV.

153 processes (acute graft-versus-host disease, insulin-dependent diabetes, and sepsis), where it appear

154 with high-fat diet (HFD) that developed non-insulin-dependent diabetes, two episodes of systemic MSC

155 ter propensity to insulin resistance and non-insulin-dependent diabetes, whereas slow growth as a con

156 e 1 diabetes results in non-obesity-related, insulin-dependent diabetes, which presents throughout th

157 hyperglycemic drugs for the treatment of non-insulin-dependent diabetes.

158 provides a genetically amenable model of non-insulin-dependent diabetes.

159 defense against hypoglycemia and is lost in insulin-dependent diabetes.

160 as a novel insulin therapy for patients with insulin-dependent diabetes.

161 ewable source of tissue for the treatment of insulin-dependent diabetes.

162 induce islet neogenesis for the treatment of insulin-dependent diabetes.

163 ld be the basis of a new type of therapy for insulin-dependent diabetes.

164 t could become beneficial in controlling non-insulin-dependent diabetes.

165 al and enteric innervation in a patient with insulin-dependent diabetes.

166 tly needed for successful stable reversal of insulin-dependent diabetes.

167 estoring endocrine function in patients with insulin-dependent diabetes.

168 abetic people; halving the prevalence of non-insulin-dependent diabetes; and complete cessation of ci

169 betes in adults (LADA) and classical type 1 (insulin dependent) diabetes remains unclear.

170 y of subjects with diabetes have type 2 (non-insulin dependent) diabetes.

171 As our knowledge of type 1 (insulin-dependent) diabetes increases, so does our appre

172 cular morphology and function in type 2 (non-insulin-dependent) diabetes mellitus (type 2D), small ar

173 h type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes mellitus, including islet tr

174 t JNK2 may play an important role in type 1 (insulin-dependent) diabetes that is caused by autoimmune

175 ardium samples were harvested from 5 type II insulin-dependent diabetic and 5 matched nondiabetic pat

176 eatic islet transplantation (PIT) now offers insulin-dependent diabetic patients metabolic stability.

177 ansplant (SPK) is now a common treatment for insulin-dependent diabetic patients with end-stage renal

178 n potentially improve glycemic regulation in insulin-dependent diabetic patients.

179 mple of 60 adults, including healthy and non-insulin-dependent diabetic subjects of either gender, wi

180 junal biopsy was obtained from a 38-year-old insulin-dependent diabetic with evidence for diabetic ga

181 regions of the autoantigen IA-2 in type one (insulin-dependent) diabetic patients with autoantibodies

182 hway is responsible for hyperglycemia in non-insulin-dependent diabetics.

183 lycemics was diagnosed in 7 (15%) donors and insulin-dependent DM in 5 (11%) donors.

184 gh pressure liquid chromatography-measurable insulin-dependent elevation in total [(3)H]inositol-PtdI

185 studies show that MARCKS plays a key role in insulin-dependent endothelial signaling to PIP(2) and is

186 dinately regulated in those tissues that use insulin-dependent energy metabolism (skeletal muscle, he

187 r (EGF)-stimulated chemotactic migration and insulin-dependent entry into S-phase of mammary epitheli

188 3 bind to the insulin receptor in vivo in an insulin-dependent fashion.

189 insulin receptor and act as agonists in the insulin-dependent fat cell assay, suggesting that Site 1

190 a proximal cause of Type II diabetes [a non-insulin dependent form of diabetes mellitus (NIDDM)], is

191 thers with dietetically treated GDM, 98 with insulin-dependent GDM, and 65 without GDM.

192 mality of insulin signaling is a decrease of insulin-dependent glucose disposal followed by an increa

193 Impaired insulin-dependent glucose disposal in muscle and fat is

194 ensitivity (euglycemic clamp measurements of insulin-dependent glucose disposal rate), blood pressure

195 Insulin-dependent glucose homeostasis is highly sensitiv

196 The combination of impaired insulin-dependent glucose metabolism in skeletal muscle

197 detection of insulin resistance, we measured insulin-dependent glucose uptake by hAT from nondiabetic

198 armacological treatment with rFGF1 increases insulin-dependent glucose uptake in skeletal muscle and

199 tive feedback loops that ultimately shut off insulin-dependent glucose uptake in vivo.

200 unilocular lipid droplets exhibited impaired insulin-dependent glucose uptake, associated with defect

201 T4 facilitative glucose transporter mediates insulin-dependent glucose uptake.

202 te insulin signaling in tissues that display insulin-dependent glucose uptake.

203 ters that determine the insulin influence on insulin-dependent glucose utilization and reflect the ef

204 gh-fat (HF) diet blunts the enhanced in vivo insulin-dependent glucose utilization for de novo lipoge

205 ow-fat diet, glucose tolerance is normal but insulin-dependent glucose utilization is decreased in sk

206 Because Akt and Rac1 have been implicated in insulin dependent Glut4 membrane translocation, we hypot

207 enhanced, whereas its knockdown suppressed, insulin-dependent Glut4 membrane translocation in both 3

208 Moreover, inactivation of DHHC7 suppressed insulin-dependent Glut4 membrane translocation in both 3

209 demonstrate that Elmo2 is a new regulator of insulin-dependent Glut4 membrane translocation through m

210 pothesize here that Elmo2 may play a role in insulin-dependent Glut4 membrane translocation.

211 ClipR-59 on the plasma membrane and impaired insulin-dependent Glut4 membrane translocation.

212 le network has been shown to be required for insulin-dependent GLUT4 redistribution; however, the pre

213 on-regulating GTPase, Rac1, is necessary for insulin-dependent GLUT4 translocation.

214 toskeleton has been shown to be required for insulin-dependent GLUT4 translocation; however, the role

215 However, it is unclear whether insulin-dependent growth is merely a result of its metab

216 that reaching critical weight depends on the insulin-dependent growth of the prothoracic glands (PGs)

217 ovide insight into the physiological role of insulin-dependent H(2)O(2) generation, which is not only

218 biobreeding diabetes-prone (BBDP) rats mimic insulin-dependent human autoimmune T1D, whereas nondiabe

219 d using terms such as diabetes mellitus, non-insulin-dependent, hyperglycemia, prevalence, epidemiolo

220 kinase B/Akt using an antibody that exhibits insulin-dependent immunoreactivity with a phosphospecifi

221 In IRKO cells, the insulin-dependent increase in phospho-Akt was completely

222 expression using targeted siRNA blunted the insulin-dependent induction of cholesterol genes.

223 Likewise, we determined that insulin-dependent insulin receptor and IRS1 tyrosine pho

224 SOCS-1 and SOCS-6 do not inhibit insulin-dependent IR autophosphorylation, but both prote

225 Purified plasma membranes exhibited insulin-dependent kinase activity in assays using substr

226 reated cells had higher specific activity of insulin-dependent kinase relative to controls.

227 s significantly, albeit partially, decreased insulin-dependent leptin mRNA and protein expression, wh

228 recombinant FGF1 (rFGF1) results in potent, insulin-dependent lowering of glucose levels in diabetic

229 of endocytosis, cytochalasin D, also blocked insulin-dependent MAPK phosphorylation.

230 using small interfering RNA markedly reduced insulin-dependent MAPK regulation in HepG2 cells.

231 Injection of pde3a mRNA potentiates insulin-dependent maturation of Xenopus oocytes and resc

232 nduced maturation and completely blocked the insulin-dependent maturation, indicating that the associ

233 The insulin-dependent mechanism is associated with increased

234 of the mutant KSR1 in HIRcB cells inhibited insulin-dependent MEK and ERK phosphorylation.

235 reduction of PTP1B is sufficient to increase insulin-dependent metabolic signaling and improve insuli

236 increases insulin sensitivity and decreases insulin-dependent mitogenesis in vivo.

237 is that coordination is achieved through an insulin-dependent negative feedback action of the liver

238 eptor substrate-1 in cardiomyocytes, causing insulin-dependent negative signaling feedback, including

239 s study was to determine whether deficits in insulin-dependent neurotrophic support contributed to de

240 The results demonstrate that loss of insulin-dependent neurotrophic support may contribute to

241 IT prevented NHE3 trafficking to the BBM and insulin-dependent NHE3 activation.

242 Maintenance of ICC requires insulin-dependent or insulin-like growth factor I (IGF-I

243 This recruitment is activated by an insulin-dependent pathway and therefore responds to fed/

244 Here we report an insulin-dependent pathway that specifically targets coll

245 PG acts as a size-assessing tissue by using insulin-dependent PG cell growth to determine when criti

246 We find that homeostasis is achieved by insulin-dependent phosphorylation changes in GSase sensi

247 ession of PFKFB3 in HEK293 cells potentiated insulin-dependent phosphorylation of Akt and Akt substra

248 Central resistin treatment inhibited insulin-dependent phosphorylation of insulin receptor (I

249 Cholesterol depletion also blocked insulin-dependent phosphorylation of MEK and mitogen-act

250 us PLCgamma1 binding to the IR and inhibited insulin-dependent phosphorylation of mitogen-activated p

251 el, we have examined mutant mice lacking the insulin-dependent phosphorylation site of CBP.

252 results indicate that Akt signaling mediates insulin-dependent physiological heart growth during post

253 , better glucose tolerance, stronger hepatic insulin-dependent PKB/Akt phosphorylation, lower serum i

254 gnificantly increasing the risk of long-term insulin-dependent posttransplant diabetes mellitus.

255 we demonstrate that de novo lipogenesis, an insulin-dependent process driven by the multifunctional

256 A number of insulin-dependent processes were found to be sensitive t

257 uptake in neuronal tissues is primarily non-insulin dependent, proteins involved in insulin signalin

258 rane cholesterol delocalized Ras and blocked insulin-dependent Ras traffic.

259 is was associated with inhibition of hepatic insulin-dependent receptor autophosphorylation and IRS-1

260 We measured insulin receptor amount and insulin-dependent receptor autophosphorylation as well a

261 SOCS-3 associated with the IR and suppressed insulin-dependent receptor autophosphorylation, insulin

262 it of PI 3-kinase is required to mediate the insulin-dependent recruitment of PI 3-kinase to the plas

263 ncentration sufficient to completely inhibit insulin-dependent redistribution of the GLUT4 reporter t

264 to intracellular storage sites and undergoes insulin-dependent redistribution to the cell surface.

265 Insulin-dependent reformation of large LDs involves two

266 Insulin-dependent regulation of glucose metabolism is im

267 tudied the mechanism by which FoxO1 mediates insulin-dependent regulation of IL-1beta expression in c

268 d FoxO1 binding and resulted in abolition of insulin-dependent regulation of MTP expression.

269 Adipocytes play an important role in the insulin-dependent regulation of organismal fuel metaboli

270 ranscription factor Runx2 and modulates IGF1/insulin-dependent regulation of osteocalcin expression i

271 We also found that an insulin-dependent response to fasting in intestinal cell

272 Na-expressing A7 cells were unable to elicit insulin-dependent Shc tyrosine phosphorylation and p42/4

273 tivity by wortmannin was sufficient to block insulin-dependent signalling but did not prevent the ear

274 hesized in neurons, and represses endogenous insulin-dependent signalling in peripheral fat body.

275 We independently confirmed insulin-dependent spatial regulation by using static spa

276 endosomal signaling lipid, is implicated in insulin-dependent stimulation of TORC1 activity in adipo

277 othalamic lesions and subsequent obesity are insulin-dependent, suggesting that responses to GTG may

278 e autonomic regulation of metabolism undergo insulin-dependent synaptic plasticity involving TRPV1 re

279 ohort study, 20 patients with long-standing, insulin-dependent T2DM and a body mass index (BMI) betwe

280 and DPN in non-severely obese patients with insulin-dependent T2DM.

281 ivity is important for maintaining basal and insulin-dependent transepithelial Na+ transport and ENaC

282 Insulin-dependent translocation of glucose transporter 4

283 Insulin-dependent translocation of glucose transporter 4

284 tingly, the NIH-PPAR gamma cells show normal insulin-dependent translocation of IRAP and form an insu

285 Insulin-dependent translocation of Shc, SOS1, and MAPK t

286 Here, we demonstrate that GIP increases insulin-dependent translocation of the Glut4 glucose tra

287 t in the NIH-PPAR gamma cells results in its insulin-dependent translocation to the plasma membrane a

288 Insulin-dependent type 1 diabetes is an autoimmune disea

289 Ninety-eight adult participants with non-insulin-dependent type 2 diabetes who were diagnosed for

290 Insulin-dependent (type 1) diabetes mellitus (T1D) onset

291 Although it is known that insulin-dependent (type 1) diabetes results in depressed

292 When subjects with non-insulin-dependent (type 2) diabetes mellitus (n = 11) we

293 In prospective studies on non-insulin-dependent (type 2) diabetes mellitus patients, a

294 Its deficiency leads to insulin-dependent (type I) diabetes whereas resistance t

295 Non-insulin-dependent (type II) diabetes mellitus (NIDDM) is

296 nists for evaluation in the treatment of non-insulin-dependent (type II) diabetes mellitus (NIDDM).

297 In addition, insulin-dependent tyrosine phosphorylation of insulin re

298 nd that latrunculin treatment did not affect insulin-dependent tyrosine phosphorylation of the insuli

299 ome a widely accepted therapeutic option for insulin-dependent uremic patients.

300 nsulin independent (II>or=2 weeks), 29% were insulin dependent with detectable C-peptide, 26% had los