ライフサイエンスコーパス: C-peptide

1 s corresponding to the native CHR sequence ("C-peptides").

2 idly in response to local application of KV1-C peptide.

3 ype 1 diabetes as measured by 2-h-stimulated C-peptide.

4 on, glycosylated hemoglobin A1c, and fasting C-peptide.

5 n normal subjects, with similar findings for C-peptide.

6 nously administered insulin, which lacks the C-peptide.

7 eta-Cell function was monitored by measuring C-peptide.

8 l islets secreting glucose-regulatable human C-peptide.

9 point-of-care determinations of insulin and C-peptide.

10 (FRET) signal in the presence of insulin or C-peptide.

11 compared within individuals for glucose and C-peptide.

12 lular domains and the corresponding secreted C-peptide.

13 mmol/L restored normoglycemia and normalized C-peptide.

14 the specific orientation of tryptic and Lys-C peptides.

15 ound that 93% of individuals have detectable C-peptide 2 years from diagnosis.

16 ns of leptin (28%), triglycerides (19%), and C-peptide (4%) (all P-trend </= 0.04); 2) the aMED was a

17 changes in circulating glucose, insulin and c-peptide (a marker of endogenous insulin).

18 inaemia status using serum concentrations of C-peptide, a marker of insulin secretion.

19 In response to insulin-induced hypoglycemia, C-peptide (absent before transplant) was appropriately s

20 lso does an increase in the concentration of C-peptide across the range of values.

21 , body mass index, physical activity, plasma C-peptide, adiponectin, and 25-hydroxyvitamin D.

22 , we evaluate our definition (no decrease in C-peptide) against published alternatives and determine

23 and HLA-DR molecules, one T cell recognized C-peptide amino acids 19-35, and two clones from separat

24 of glycosylated insulin-B chain and insulin-C peptide and BigLEN.

25 with structural data showing that its gamma-C peptide and eptifibatide exhibit comparable electrosta

26 plasma glucose concentrations while reducing C-peptide and attenuating endogenous insulin levels.

27 s: 2-h plasma glucose and HKDC1, and fasting C-peptide and BACE2.

28 ic sorting after intracellular staining with c-peptide and glucagon antibody.

29 ically healthy if below the first tertile of C-peptide and metabolically unhealthy if above the first

30 clinical islet transplantation because serum C-peptide and proinsulin levels are difficult to interpr

31 Fasting proinsulin-to-C-peptide and proinsulin secretory ratios during glucose

32 Rapid release of C-peptide and proinsulin was observed 3 hr after mixing

33 -1 levels, explaining, together with fasting C-peptide and waist circumference, 21% of the variance i

34 a decline in beta-cell function (measured by C-peptide) and provision of glycaemic control at reduced

35 Serum was used to monitor glucose, C-peptide, and alloreactive antibodies.

36 The 90-min glucose, time-to-peak C-peptide, and area under the curve for glucose were con

37 Plasma glucose, insulin, C-peptide, and glucagon concentrations were measured eve

38 Plasma glucose, insulin, C-peptide, and glucagon levels and insulin secretion rat

39 PI-CF subjects had lower acute insulin, C-peptide, and glucagon responses compared with PS-CF an

40 The GLP-1, glucose, C-peptide, and glucagon responses to a standardized test

41 enous arginine with measurements of insulin, C-peptide, and glucagon to examine beta-cell and alpha-c

42 Blood glucose, insulin, C-peptide, and glucose-dependent insulinotropic polypept

43 sting insulin, Homeostasis Model Assessment, C-peptide, and glucose.

44 h PUFA significantly lowered glucose, HbA1c, C-peptide, and HOMA.

45 classification index was 0.63 for CRP, IL-6, C-peptide, and non-HMW adiponectin and 0.46 for GLDH, in

46 easures, higher concentrations of CRP, IL-6, C-peptide, and non-HMW adiponectin were associated with

47 ission tomography [FDG-PET]), fasting plasma C-peptide, and phosphorylated ribosomal protein S6 (pS6)

48 o demonstrate specific staining for insulin, C-peptide, and proinsulin together with insulin secretor

49 increased fasting serum leptin, insulin, and C-peptide, and reduced high-molecular-weight ADN at embr

50 Glucose, insulin, C-peptide, and the amended insulin-glucose ratio were me

51 The difference in C peptide area under curve between the canakinumab and p

52 At 12 months, the mean change in C-peptide area under curve was -229 pmol/L (95% CI -316

53 int was the change from baseline in mean 2 h C-peptide area under the curve (AUC) at 12 months.

54 Primary outcomes included C-peptide area under the curve (AUC) following a mixed-m

55 ipants in the ATG group had a mean change in C-peptide area under the curve of -0.195 pmol/mL (95% CI

56 This work has identified the insulin C-peptide as an abundant source of CD8(+) T cell epitope

57 hyperinsulinemia, but metabolic clearance of C-peptide, assessed by infusion of stable isotope-labele

58 While preservation of stimulated C-peptide at >/=0.2 nmol/L has clinically beneficial out

59 ted with teplizumab had a reduced decline in C-peptide at 2 years (mean -0.28 nmol/L [95% CI -0.36 to

60 for Model 2 covariates, maternal glucose and C-peptide at OGTT.

61 Patch-clamp recordings confirmed that KV1-C peptide attenuates KV1 channel blocker (5-(4-phenylalk

62 The mean 2 h C-peptide AUC at 12 months increased by 0.015 nmol/L (95

63 Adjusted C-peptide AUC was 59% (95% CI 6.1-112) higher at 2 years

64 y secondary endpoints were met: the mean 4 h C-peptide AUC was significantly higher (mean increase of

65 ed at 24 months and included meal-stimulated C-peptide AUC, insulin use, hypoglycemic events, and imm

66 ths were the change from baseline in the 4 h C-peptide AUC, insulin use, major hypoglycaemic events,

67 t, at 12 months, alefacept preserved the 4 h C-peptide AUC, lowered insulin use, and reduced hypoglyc

68 not leucine-5g, increased plasma insulin and C-peptide AUCs (P < 0.01 for both), but neither dose aff

69 of alefacept, both the 4-hour and the 2-hour C-peptide AUCs were significantly greater in the treatme

70 nger effect on peak insulin response than on C-peptide-based insulin secretion rate, suggesting a pos

71 Human proinsulin with C-peptide-bearing Superfolder Green Fluorescent Protein

72 The mean difference in MMTT-stimulated AUC C-peptide between treated and placebo subjects was 0.28

73 N) is homodimeric in the absence of the FliF(C) peptide but forms a heterodimeric complex with the pe

74 fasted adult DKO pigs and blood glucose and C-peptide changes after intravenous glucose or insulin a

75 Insulin and C-peptide clearance were evaluated to understand the imp

76 In addition, hyperinsulinemia increases C-peptide clearance, which may lead to modest underestim

77 wed high level of cortisol, but low level of C-peptide, compared with the control group (p < 0.05).

78 ications Trial established that a stimulated C-peptide concentration >/=0.2 nmol/L at study entry amo

79 ion (254 pmol/L [88-797 pmol/L]), and median C-peptide concentration (2.4 nmol/L [0.9-5.7 nmol/L]) re

80 ic mean 2-h area-under-the-curve (AUC) serum C-peptide concentration after a mixed-meal tolerance tes

81 d into tertiles based on the distribution of C-peptide concentration amongst the control population,

82 00), respectively, for glucose, insulin, and C-peptide concentration criteria.

83 The incremental area under the plasma C-peptide concentration curve during the first 12 min of

84 The incremental area under the plasma C-peptide concentration curve during the hyperglycemic c

85 ISR derived from C-peptide concentration is an example of nonparametric B

86 um treatment significantly decreased fasting C-peptide concentrations (change: -0.4 ng/mL after magne

87 Human C-peptide concentrations and in vivo glucose responsiven

88 calculated from plasma glucose, insulin, and C-peptide concentrations during oral glucose tolerance t

89 Residual beta-cell function was analyzed as C-peptide concentrations in blood in response to a mixed

90 augmented the early increases in insulin and C-peptide concentrations in response to the glucose chal

91 Similarly, with diazoxide, C-peptide concentrations were decreased (P = 0.0015) and

92 Insulin and C-peptide concentrations were significantly higher durin

93 shed criteria that use glucose, insulin, and C-peptide concentrations.

94 r NRG4, with markedly reduced plasma insulin C-peptide concentrations; and at SLC9A3R1, with mediator

95 acellular concentration, we prepared an EboV C-peptide conjugated to the arginine-rich sequence from

96 A membrane-permeable peptide (KV1-C peptide) corresponding to the postsynaptic density-95,

97 Stressed rats presented high levels of C-peptide, corticosterone, and glucose (P <0.05).

98 To determine whether the activity of a C-peptide could be improved by increasing its intracellu

99 ls can provide a surrogate immune marker for C-peptide decline after the diagnosis of type 1 diabetes

100 ding visit was significantly associated with C-peptide decline at the subsequent visit.

101 ociation with a significantly slower rate of C-peptide decline.

102 Endogenous insulin secretion (calculated by C-peptide deconvolution) and insulin infusion rates were

103 As C-peptide decreased to nonmeasurable concentrations, the

104 l time points) in the DYSOGTTs, 30- to 0-min C-peptide difference values changed little.

105 at every time point, n = 207), 30- to 0-min C-peptide difference values decreased (P < 0.001).

106 Likewise, 30- to 0-min C-peptide difference values did not differ between TDOGT

107 Instead, the metabolome varied along a C-peptide-driven continuum from type 1 diabetes via LADA

108 These clones recognized C-peptide epitopes presented by HLA-DQ8 and, notably, HL

109 ted in synthetic beta-amyloid and cytochrome c peptides, even though both were initially assumed to b

110 ulin bearing "superfolder" green fluorescent C-peptide expressed in pancreatic beta cells where it is

111 s in their competence to mature into insulin/c-peptide-expressing cells in vivo.

112 codynamic effects on [(18)F]FDG-PET, fasting C-peptide, fasting blood glucose, and pS6.

113 en of these markers of brain amyloid burden--c-peptide, fibrinogen, alpha-1-antitrypsin, pancreatic p

114 For C-peptide FIs (clinically represented by enfuvirtide), s

115 primary outcome was the 1-year change in AUC C-peptide following a 2-hour mixed-meal tolerance test (

116 ieved some therapeutic benefit in preserving C-peptide for a period of approximately nine months in p

117 pid, and uncomplicated nature of insulin and C-peptide FRET sensors allows rapid assessment of beta-c

118 arameters showed that fasting blood glucose, C-peptide, fructosamine, triglyceride and free fatty aci

119 ility to prevent vaginal HIV transmission: a C-peptide fusion inhibitor (C52L), a membrane-disrupting

120 Mean plasma concentrations of insulin, C-peptide, glucagon, and glucose-dependent insulinotropi

121 mpling for measurements of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP.

122 Neither load affected insulin, C-peptide, glucagon, GLP-1, or GIP.

123 ath test) and blood glucose, plasma insulin, C-peptide, glucagon, glucagon-like peptide-1 (GLP-1), gl

124 sessed plasma responses of glucose, insulin, C-peptide, glucagon, glucagon-like peptides 1 and 2, gas

125 Fasting metabolic hormone (insulin, C-peptide, glucagon, incretin, and adipokine) concentrat

126 ed no difference in decreased insulin needs, C-peptide glucose ratios, beta-scores, and transplant es

127 assessed by decrease in daily insulin needs, C-peptide/glucose ratios, beta-scores, and transplant es

128 inogenic index), and beta-cell mass (fasting C-peptide: glucose ratio) were calculated, from glucose,

129 howed similar reductions in insulin, insulin C-peptide, glycated hemoglobin, and homeostasis model as

130 Over half of the Medalists with fasting C-peptide > 0.17 nmol/l responded in MMTT by a twofold o

131 "Responders" (12-month C-peptide >/= baseline), "super responders" (24-month C-

132 >/= baseline), "super responders" (24-month C-peptide >/= baseline), and "nonresponders" (12-month C

133 The fasting C-peptide had weaker associations with outcomes.

134 ls of insulin-like growth factor (IGF)-1 and C-peptide have been implicated in colorectal carcinogene

135 However, previously reported EboV C-peptides have shown weak or insignificant antiviral ac

136 ere not significantly associated with plasma C-peptide, Hb A(1c), LDL cholesterol, CRP, or IL-6.

137 lesterol, triacylglycerol, glucose, insulin, C-peptide, homeostasis model assessment of insulin resis

138 ed beta-chain specific for pigeon cytochrome c peptide I-Ek.

139 an proinsulin bearing emerald-GFP within the C-peptide), impairing the trafficking of these "bystande

140 nsulin B-chain, and eight amino acids of the C-peptide in addition to 138 amino acids from the IGF2 g

141 contain beta-like cells that secrete insulin/C-peptide in response to D-glucose and theophylline.

142 lls and secrete bioactive insulin as well as C-peptide in response to glucose and sulfonylureas.

143 ers of mature pancreatic beta-cells, release C-peptide in response to secretagogues and survive in vi

144 ons of alpha-helix formation in the isolated C-peptide in ribonuclease A, there is growing evidence t

145 rporating glucose (in millimoles per liter), C-peptide (in nanomoles per liter), hemoglobin A1c (as a

146 ycosylated hemoglobin (HbA1c), serum porcine C peptide, in vivo glucose tolerance tests, and histolog

147 sessed by infusion of stable isotope-labeled C-peptide, increased modestly during hyperinsulinemic cl

148 At baseline, a greater C-peptide index and 90-min postprandial C-peptide level

149 ver, when we used quartiles or the median of C-peptide, instead of tertiles, as the cut-point of hype

150 ules without islets were monitored for human C-peptide (insulin) secretion during a period of 55 days

151 ucose, lactate, lipid, cholesterol, insulin, C-peptide, insulin secretion, and clearance responses to

152 ormone-binding globulin, estrone, estradiol, C-peptide, insulin-like growth factor-binding proteins 1

153 increased insulin clearance, as assessed by c-peptide/insulin ratio.

154 rescent protein [GFP] within the connecting [C]-peptide) is folded in the ER, exported, converted to

155 bility could be improved by using changes in C-peptide later than 6 months beyond baseline.

156 tcome was the change in the stimulated serum C-peptide level (after a mixed-meal tolerance test) betw

157 sally accepted clinical definition for using C-peptide level as an indication of hyperinsulinaemia.

158 t failure, hemoglobin A1c (HbA1c) or fasting C-peptide level at retransplant and subsequent pancreati

159 The stimulated C-peptide level declined to a similar degree in all stud

160 ean area under the curve (AUC) for the serum C-peptide level during the first 2 hours of a mixed-meal

161 ody mass index, physical activity, or plasma C-peptide level in this study.

162 .3%) versus 6.1% (5.9%-6.8%) (P=0.16); basal C-peptide level was 460 rhomol/L (350-510 rhomol/L) vers

163 surgery, duration of T2DM, and preoperative C-peptide level were independent predictors of remission

164 ater C-peptide index and 90-min postprandial C-peptide level were predictive of lower HbA1c at 1 year

165 ls as being hyperinsulinaemic-based on their C-peptide level-was arbitrary.

166 )D and low molar IGF-1/IGFBP-3 ratio and low C-peptide levels (reference group), participants with a

167 Plasma C-peptide levels also did not modify the aspirin-colon c

168 Associations between C-peptide levels and death as a result of breast cancer

169 y as shown by measurable posttransplantation C-peptide levels and histopathological evidence of insul

170 Insulin and C-peptide levels determined with the FRET sensors showed

171 ower (P = 0.035) for patients who maintained C-peptide levels during the first year of follow-up in b

172 in D (25(OH)D) and IGF-1, IGFBP-3 as well as C-peptide levels in 499 cases and 992 matched controls.

173 he NHS and HPFS and with fasting insulin and C-peptide levels in a nationally representative US compa

174 -instantaneous determinations of insulin and C-peptide levels in biological samples.

175 Treatment strategies to reduce C-peptide levels in patients with breast cancer, includi

176 monoclonal antibody, reduces the decline in C-peptide levels in patients with T1D 2 years after dise

177 challenge, and variably elevated insulin and C-peptide levels in the nonfasted state.

178 educed glucose-responsive plasma insulin and C-peptide levels in whole body Map4k4-depleted mice (M4K

179 Whether plasma C-peptide levels modified the association was examined b

180 ined insulin release was achieved with human C-peptide levels of 19.1 pmol/L +/- 0.9 (standard deviat

181 years of age, with type 1 diabetes, fasting C-peptide levels of more than 0.3 ng per milliliter (0.1

182 ponses to disease-associated target Ags, and C-peptide levels of participants who did (responders) or

183 lower glucose levels and higher insulin and C-peptide levels overall than did control patients at th

184 Random serum C-peptide levels showed that more than 67.4% of the part

185 Among women without type 2 diabetes, fasting C-peptide levels were associated with an increased risk

186 Postoperative random insulin C-peptide levels were detectable in 19 patients (95%) at

187 Glucose, insulin, and C-peptide levels were measured to derive surrogate measu

188 ulin resistant based on glucose, insulin and C-peptide levels, and glucose and insulin tolerance test

189 tion of exogenous insulin requirement (EIR), C-peptide levels, changes in peripheral blood T regulato

190 eatment with DM199 also resulted in elevated C-peptide levels, elevated glucagon like peptide-1 level

191 ective pain measurements, opioid use, random C-peptide levels, insulin requirements, and glycated hem

192 ssociated with higher IGF-1/IGFBP-3 ratio or C-peptide levels.

193 glycemia, and fasting and maximum stimulated C-peptide levels.

194 nt cleavage and nuclear movement of the EIN2-C' peptide, linking hormone perception and signaling com

195 tprandial changes in blood glucose, insulin, C-peptide, lipids, and gut hormones and on the resistant

196 In summary, anti-CD3 therapy reduced C-peptide loss 2 years after diagnosis using a tolerable

197 nal anti-CD20 B lymphocyte Ab, can attenuate C-peptide loss over the first year of disease.

198 -cell receptor later reappeared with further C-peptide loss over the next 2 years.

199 >/= baseline), and "nonresponders" (12-month C-peptide < baseline) were evaluated for biomarkers of o

200 e, the B-chain, and eight amino acids of the C-peptide may be an autoantigen in type 1 diabetes.

201 measures with metabolic parameters, such as C-peptide, may be useful for defining strata of the popu

202 zumab (14-day full-dose) reduced the loss of C-peptide mean area under the curve (AUC), a prespecifie

203 sets at entry, U.S. residents, patients with C-peptide mean AUC >0.2 nmol/L, those randomized </=6 we

204 ventions for 4 wk with glucose, insulin, and C-peptide measured by using oral-glucose-tolerance tests

205 nce of the insulin secretion rate (ISR) from C-peptide measurements as a quantification of pancreatic

206 ped mathematical model that uses insulin and C-peptide measurements from the insulin-modified, freque

207 d, we calculate the ISR from actual clinical C-peptide measurements in human subjects with varying de

208 nd were associated with decreased stimulated C-peptide (median [interquartile range]) at 3 months pos

209 lly, phosphatase inhibitors blunted both KV1-C peptide-mediated and protein kinase A inhibitor peptid

210 nsivity indices were estimated with the oral C-peptide minimal model.

211 elevation on fasting and glucose-stimulated C-peptide-modeled insulin secretion in prepubertal norma

212 days with measurable levels of serum porcine C peptide, near normal in vivo glucose tolerance tests a

213 Twenty islet recipients with C-peptide negative type 1 diabetes and recurrent severe

214 Ten male subjects with T1DM (C-peptide negative, age [mean +/- SEM] 26 +/- 1 years, B

215 C-peptide-negative (i.e., insulin-deficient) T1D subject

216 type 1 diabetes, we studied 19 subjects with C-peptide-negative diabetes (HbA1c 7.1 +/- 0.6%) on insu

217 rived GP2(+) cells generate beta-like cells (C-PEPTIDE(+)/NKX6-1(+)) more efficiently compared to GP2

218 ration formed by dimerization of two matured C peptides non-covalently linked with the N terminal pro

219 regression model measuring age, BMI, fasting C-peptide, number of circulating CD3(+)CD16(+)CD56(+) ce

220 e association of both fasting and stimulated C-peptide numerical values with outcomes.

221 The robust data on the C-peptide obtained under clinical trial conditions shoul

222 tes and mixed-meal-tolerance-test-stimulated C peptide of at least 0.2 nM.

223 diabetes, aged 12-35 years, and with a peak C-peptide of 0.4 nM or greater on mixed meal tolerance t

224 ulin in which the function of the 35 residue C-peptide of proinsulin is replaced by a single covalent

225 d 6 distinct but overlapping epitopes in the C-peptide of proinsulin.

226 treatment group, for a 50% higher stimulated C-peptide on entry, such as from 0.10 to 0.15 nmol/L, Hb

227 significantly reduce the loss of stimulated C peptide or improve clinical outcomes over a 15-month p

228 ropriately elevated (nonsuppressed) insulin, C-peptide, or proinsulin, but these criteria may overlap

229 Rituximab decreased the loss of C-peptide over the first year of follow-up and markedly

230 This pattern of fall in C-peptide over time has implications for understanding t

231 the plasma responses of insulin (P = 0.012), C-peptide (P = 0.004), and the insulin secretory rate (P

232 ide administration, insulin (P = 0.0016) and C-peptide (P = 0.0287) concentrations were decreased and

233 in the control arm, who showed loss in both C-peptide peak values and C-peptide when calculated as a

234 allenge, while slightly blunting insulin and C-peptide peaks.

235 ad 56% to 78% increased serum insulin, serum C-peptide, plasma GLP-1, and plasma GIP responses (P=0.0

236 At 12 months posttransplant 9 of 10 were C-peptide positive, (5 insulin independent).

237 vitro with an average efficiency of 55% into C-peptide-positive cells, expressing markers of mature b

238 arized islet-like structures containing MAFA/C-peptide-positive cells.

239 rituximab-treated subjects with significant C-peptide preservation at 6 mo (58%), the proliferative

240 d investigate factors that may be related to C-peptide preservation or loss.

241 f age each had greater teplizumab-associated C-peptide preservation than their counterparts.

242 pplication of an anti-PrP(C) antibody or PrP(C) peptide prevents Abeta oligomer-induced neurotoxicity

243 assays of proinsulin export and insulin and C-peptide production to examine the earliest events of i

244 c insulin clearance using plasma insulin and C-peptide profiles obtained from the insulin-modified fr

245 okines and chemokines), clinical parameters (C-peptide, proinsulin, glucose), and cortisol, as an ind

246 time points and used for the measurement of C-peptide, proinsulin, thrombin-antithrombin (TAT) compl

247 e curve of insulin (R = 0.59, P = 0.009) and C-peptide (R = 0.81, P < 0.0001) during the clamp.

248 with these differential effects, the insulin:C-peptide ratio and lipid composition differ between EVs

249 ated 9.6 months' delay (95% CI 3.47-15.6) in C-peptide reduction with abatacept.

250 C-peptide response also increased, although not to the l

251 As glucose levels increase, the early C-peptide response declines.

252 14 days, respectively (P < 0.01); the plasma C-peptide response remained unchanged in subjects with N

253 The primary endpoint was C-peptide response to a mixed meal challenge at 12 month

254 -adjusted change in 2-h area under the curve C-peptide response to mixed meal tolerance test from bas

255 those fluctuations are related to the early C-peptide response to oral glucose.

256 t was baseline-adjusted 2-h area under curve C-peptide response to the mixed meal tolerance test at 1

257 se fluctuations are not related to the early C-peptide response.

258 Insulin and C-peptide responses correlated robustly with the number

259 transplanted, we normalized the insulin and C-peptide responses to the number of islets transplanted

260 Improvement in C-peptide responses with immune intervention is associat

261 l amino-terminal EVH1 domain bound to a CENP-C peptide reveals a new target-recognition mode for the

262 d and accurate determinations of insulin and C-peptide secreted from human or rodent islets, verifyin

263 on exchanger-2-AE2 and CFTR), or regulatable C-peptide secreting neoislet-like clusters (expressing g

264 te hypothyroidism transiently impaired human C-peptide secretion at 16 weeks posttransplant.

265 Glucose-stimulated islet insulin or C-peptide secretion experiments are a fundamental tool f

266 lly depleted T-cells and was associated with C-peptide secretion for >1 year.

267 h nondiabetic controls even though no active c-peptide secretion was detected in plasma and almost no

268 were weaned from exogenous insulin and human C-peptide secretion was eventually regulated by meal and

269 ism resulted in severely blunted basal human C-peptide secretion, impaired glucose-stimulated insulin

270 , two 12-week courses of alefacept preserved C-peptide secretion, reduced insulin use and hypoglycemi

271 were assessed in vitro, and in vivo insulin (C-peptide) secretion was monitored for 6 weeks in (strep

272 vealed that cerebral arteries exposed to KV1-C peptide showed markedly less phosphorylation of KV1.2a

273 ere was a biphasic decline in C-peptide; the C-peptide slope was -0.0245 pmol/mL/month (95% CI -0.027

274 ncrease, despite equivalent hypoglycemia and C-peptide suppression.

275 Addition of the V(C) peptide synaptobrevin-2 (syb(57-92)) increases the do

276 a cyclic Arg-Gly-Asp-D-Phe-Lys(Cys) (cRGDfK(C)) peptide tethered to the terminus of a polyethylene g

277 ntation probes, indicate that in tryptic/Lys-C peptides the C-terminal carboxyl group appears to be i

278 In the presence of V(C) peptide, the fusion step occurs on a timescale of app

279 Blood glucose, insulin, C-peptide, the insulin-to-glucagon ratio, and HOMA-insul

280 e had substantially reduced plasma levels of C-peptide, the product of proinsulin processing to insul

281 There was a biphasic decline in C-peptide; the C-peptide slope was -0.0245 pmol/mL/month

282 Application of KV1-C peptide to cannulated, pressurized cerebral arteries r

283 the pre- to 28-day posttransplant change in C-peptide to glucose and creatinine ratio (DeltaCP/GCr).

284 eactive protein (CRP), interleukin-6 (IL-6), C-peptide, total high-molecular-weight (HMW) adiponectin

285 locally isolated islets [12 month stimulated C-peptide: transported 788 (114-1764) pmol/L (n = 9); lo

286 d newborn metabolic traits (cord glucose and C-peptide) under three models.

287 were calculated, from glucose, insulin, and c-peptide values measured during OGTT.

288 icant difference in creatinine, proteinuria, c-peptide, viral infections, lymphoproliferative disorde

289 At 1 year, the mean AUC for the level of C peptide was significantly higher in the rituximab grou

290 At the last follow-up visit, median fasting C-peptide was 0.43 (0.19-0.93) ng/mL; median insulin req

291 A 1-ng/mL increase in C-peptide was associated with a 31% increased risk of an

292 C-peptide was not different between diets.

293 While C-peptide was not significantly associated with the inci

294 At 24 months, MMTT-stimulated AUC C-peptide was not significantly different in ATG+G-CSF (

295 tolerance testing with glucose, insulin, and C-peptide was sampled at 0, 10, 30, 60, 90, and 120 minu

296 n of either high IGF-1/IGFBP-3 ratio or high C-peptide were at elevated risk for colorectal cancer wh

297 No changes in insulin or c-peptide were detected.

298 Parameters associated with higher random C-peptide were lower hemoglobin A1C, older age of onset,

299 howed loss in both C-peptide peak values and C-peptide when calculated as area under the curve during

300 ensors were capable of detecting insulin and C-peptide with high specificity and with picomolar conce