ライフサイエンスコーパス: C-peptide

1 for glucose, 0.8% for triglyceride, 0.2% for C-peptide).

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

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

4 lular domains and the corresponding secreted C-peptide.

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

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

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

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

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

10 e was associated with subsequently decreased C-peptide.

11 y albumin/creatinine ratio (ACR) and fasting C-peptide.

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

13 of beta-coefficients in Models 1-4: 19-21%), C-peptides (23-25%), fat masses (0.48-0.60 kg), and fat-

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

15 fference in the primary endpoint (stimulated C-peptide 75 +/- 5 days after the first transplant) betw

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

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

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

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

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

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

22 e, analyzed by ANCOVA adjusting for baseline C-peptide, age, and sex (n = 82) with significance defin

23 After adjustment for baseline C-peptide, age, BMI, and sex, baseline levels of miR-318

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

25 ean mixed-meal tolerance test-stimulated AUC C-peptide, analyzed by ANCOVA adjusting for baseline C-p

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

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

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

29 HIP2.5 epitope, which is a fusion of insulin C-peptide and chromogranin A (ChgA) fragments, and compa

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

31 In hiPSCs, BET inhibitors strongly repressed C-peptide and glucagon during endocrine differentiation.

32 Acetate and early-phase insulin, C-peptide and glucagon-like peptide-1 (GLP-1) secretion

33 we report 2-year area under the curve (AUC) C-peptide and HbA(1c), prespecified secondary end points

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

35 Area under the curve (AUC) C-peptide and peak C-peptide were stratified by quartile

36 igh C-peptide group showed increases in both C-peptide and proinsulin (P <= 0.01).

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

38 detectable MMTT C-peptide demonstrated acute C-peptide and proinsulin responses to arginine that were

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

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

41 ent at baseline identifies associations with C-peptide and stratifies subjects for future severity of

42 -1 levels, explaining, together with fasting C-peptide and waist circumference, 21% of the variance i

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

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

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

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

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

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

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

50 le hyperglycemia, hypoinsulinemia, decreased C-peptide, and increased glycated hemoglobin (HbA1c) com

51 alculated as responses for glucose, insulin, C-peptide, and incretin hormones; glucagon-like peptide-

52 No differences in triglyceride, C-peptide, and insulin AUCs were observed after the KE d

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

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

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

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

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

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

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

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

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

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

63 ied by peak mixed-meal tolerance test (MMTT) C-peptide as negative (<0.007 pmol/mL; n = 15), low (0.0

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

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

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

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

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

69 The mean (+/-SD) 4-hour C-peptide AUC at week 52 differed significantly between

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

71 o a 4-hour mixed-meal tolerance test (4-hour C-peptide AUC) at week 52.

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

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

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

75 3p/miR-103a-3p predicted differences in MMTT C-peptide AUC/peak levels at the 12-month visit; the com

76 At 1 year, the AUC C-peptide/AUC glucose (AUC Ratio) was significantly high

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

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

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

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

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

82 e used to demonstrate saturable and specific C-peptide binding to RBCs when delivered as part of a co

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

84 reported DR4-restricted epitopes within the C-peptide (C25-35) or A-chain (A1-15) of proinsulin.

85 hin both the B-chain (B16-27 and B22-C3) and C-peptide (C25-35).

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

87 uppressed in the low, intermediate, and high C-peptide compared with the negative group (P <= 0.0001)

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

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

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

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

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

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

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

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

96 Human C-peptide concentrations and in vivo glucose responsiven

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

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

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

100 Insulin and C-peptide concentrations were significantly higher durin

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

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

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

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

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

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

107 at miRNAs may be useful in predicting future C-peptide decline for improved subject stratification in

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

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

110 As C-peptide decreased to nonmeasurable concentrations, the

111 Moreover, the secretion of insulin and C-peptide decreased.

112 All groups with detectable MMTT C-peptide demonstrated acute C-peptide and proinsulin re

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

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

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

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

117 In hiPSCs, the outcome was different because C-peptide expression remained lower than in controls, bu

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

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

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

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

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

123 in peptide (2.5HIP) consisting of an insulin C-peptide fragment fused to a peptide from chromogranin

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

125 reast cancer with regard to plasma levels of c-peptide, gastric inhibitory polypeptide, insulin, lept

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

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

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

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

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

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

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

133 Insulin secretion (assessed by C-peptide/glucose ratio) was reduced by 37 +/- 16% (A),

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

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

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

137 n increased from EU to HYPO only in the high C-peptide group compared with negative (P = 0.01).

138 responses to hyperglycemia, whereas the high C-peptide group showed increases in both C-peptide and p

139 glucose and more time in range for the high C-peptide group.CONCLUSIONThese results indicate that in

140 HYPO) clamp.RESULTSLow and intermediate MMTT C-peptide groups did not exhibit beta cell secretory res

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

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

143 cessful in >50% of eligible candidates, with C-peptide >252 pmol/L emerging as the best prognostic fa

144 l cells cultured >=96 hours exhibited longer C-peptide >=0.5 ng/mL (103 versus 48 mo; P = 0.006), and

145 bgroups were compared by numbers with plasma C-peptide >=0.5 ng/mL, low glycemic variability associat

146 mL, low glycemic variability associated with C-peptide >=1.0 ng/mL, and with insulin independence.

147 e patients with low glycemic variability and C-peptide >=1.0 ng/mL, at month 12 (9/10 versus 12/30; P

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

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

150 c markers including glucose, HbA1c, insulin, C-peptide, HOMA-IR, triglycerides, and blood pressure.

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

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

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

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

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

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

157 jects with T1D who experienced rapid loss of C-peptide; in contrast, slow disease progression was ass

158 TRS] >=6.75), the area under the curve (AUC) C-peptide increased significantly from baseline to 1 yea

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

160 Measurement of human C-peptide indicated that higher engrafted islet mass res

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

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

163 C-peptide, insulin, leptin, and other metabolic hormones

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

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

166 BACKGROUNDResidual C-peptide is detected in many people for years following

167 gic significance of low levels of detectable C-peptide is not known.METHODSWe studied 63 adults with

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

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

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

171 area under the concentration-time curve for C-peptide level in response to a 4-hour mixed-meal toler

172 .3%) versus 6.1% (5.9%-6.8%) (P=0.16); basal C-peptide level was 460 rhomol/L (350-510 rhomol/L) vers

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

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

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

176 he 1019 Medalists, 32.4% retained detectable C-peptide levels (>0.05 ng/mL, median: 0.21 ng/mL).

177 High c-peptide levels (>= the median level of controls) were

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

179 by age, the significant association between c-peptide levels and breast cancer risk was evident in o

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

181 , as shown by measurable posttransplantation C-peptide levels and histopathological evidence of insul

182 Serum C-peptide levels demonstrated significant glucose respon

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

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

185 ngrafted islet mass resulted in higher human C-peptide levels in post-transplantation.

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

187 L-10(+) cluster had a significant decline in C-peptide levels in the period preceding the IL-10 respo

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

189 Longitudinally (n = 181, median: 4 years), C-peptide levels increased in 12.2% (n = 22) and decreas

190 Thirty Medalists with baseline C-peptide levels of 0.1 ng/mL or higher underwent the cl

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

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

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

194 During the EU-HYPO clamp, C-peptide levels were proportionately suppressed in the

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

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

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

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

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

200 , 5.8% responded with a doubling of baseline C-peptide levels.

201 an insulin levels and a trend towards higher C-peptide levels.

202 s the peptide precursor to (biomimetic) N-to-C peptide ligation.

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

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

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

206 d stratifies subjects for future severity of C-peptide loss after 1 year.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 c events, the ratio of fasting proinsulin to C-peptide over time, and response profile.

237 at were positively correlated with peak MMTT C-peptide (P < 0.0001 for both analytes).

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

239 ponses except for an increase in early phase C-peptide (P = 0.04).

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

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

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

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

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

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

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

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

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

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

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

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

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

253 Results: C-peptide release was not detectable in any T1DM individ

254 inical measures of beta-cell function (e.g., C-peptide release) may not reflect BCM.

255 ts, autoantibody status, beta cell function, C-peptide release, and monogenetic diabetes genes in a c

256 14 days, respectively (P < 0.01); the plasma C-peptide response remained unchanged in subjects with N

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

258 Mean acute C-peptide response to arginine at maximal glycemic poten

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

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

261 C-peptide response was measured with a mixed meal tolera

262 ta-cell function as steady-state and maximal C-peptide responses adjusted for insulin sensitivity.

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

264 = 0.027) insulin secretion assessed by acute C-peptide responses improved after ivacaftor treatment.

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

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

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

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

269 glucose tolerance testing (IPGTT), and human C-peptide secretion for 517 days.

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

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

272 the islets viability, apoptosis, insulin and C-peptide secretion, and apoptosis markers were evaluate

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

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

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

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

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

278 are observed only at high levels of residual C-peptide that likely contribute to glycemic control.FUN

279 ted epitopes within the C-terminal region of C-peptide that partially overlap with previously reporte

280 Here, we report that C-peptide, the 31-amino acid peptide secreted in equal a

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

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

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

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

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

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

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

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

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

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

291 Human C-peptide was measured to evaluate human islet function

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 Overall, only c-peptide was observed significantly associated with bre

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

297 erential correlations of insulin and HbA(1c) C-peptide was the most highly connected node in the earl

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

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

300 rea under the curve (AUC) C-peptide and peak C-peptide were stratified by quartiles of expression of

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