Associations of HbA1c with the timing of C-peptide responses during the oral glucose tolerance test at the diagnosis of type 1 diabetes.


Journal

Pediatric diabetes
ISSN: 1399-5448
Titre abrégé: Pediatr Diabetes
Pays: Denmark
ID NLM: 100939345

Informations de publication

Date de publication:
06 2019
Historique:
received: 16 10 2018
revised: 23 01 2019
accepted: 04 03 2019
pubmed: 21 3 2019
medline: 24 3 2020
entrez: 21 3 2019
Statut: ppublish

Résumé

In new onset type 1 diabetes (T1D), overall C-peptide measures such as area under the curve (AUC) C-peptide and peak C-peptide are useful for estimating the extent of β-cell dysfunction, and for assessing responses to intervention therapy. However, measures of the timing of C-peptide responsiveness could have additional value. We assessed the contribution of the timing of C-peptide responsiveness during oral glucose tolerance tests (OGTTs) to hemoglobin A1c (HbA1c) variation at T1D diagnosis. We analyzed data from 85 individuals <18 years with OGTTs and HbA1c measurements at diagnosis. Overall [AUC and peak C-peptide] and timing measures [30-0 minute C-peptide (early); 60 to 120 minute C-peptide sum-30 minutes (late); 120/30 C-peptide; time to peak C-peptide] were utilized. At diagnosis, the mean (±SD) age was 11.2 ± 3.3 years, body mass index (BMI)-z was 0.4 ± 1.1, 51.0% were male. The average HbA1c was 43.54 ± 8.46 mmol/mol (6.1 ± 0.8%). HbA1c correlated inversely with the AUC C-peptide (P < 0.001), peak C-peptide (P < 0.001), early and late C-peptide responses (P < 0.001 each), and 120/30 C-peptide (P < 0.001). Those with a peak C-peptide occurring at ≤60 minutes had higher HbA1c values than those with peaks later (P = 0.003). HbA1c variance was better explained with timing measures added to regression models (R These findings show that the addition of timing measures of C-peptide responsiveness better explains HbA1c variation at diagnosis than standard measures alone.

Sections du résumé

BACKGROUND
In new onset type 1 diabetes (T1D), overall C-peptide measures such as area under the curve (AUC) C-peptide and peak C-peptide are useful for estimating the extent of β-cell dysfunction, and for assessing responses to intervention therapy. However, measures of the timing of C-peptide responsiveness could have additional value.
OBJECTIVES
We assessed the contribution of the timing of C-peptide responsiveness during oral glucose tolerance tests (OGTTs) to hemoglobin A1c (HbA1c) variation at T1D diagnosis.
METHODS
We analyzed data from 85 individuals <18 years with OGTTs and HbA1c measurements at diagnosis. Overall [AUC and peak C-peptide] and timing measures [30-0 minute C-peptide (early); 60 to 120 minute C-peptide sum-30 minutes (late); 120/30 C-peptide; time to peak C-peptide] were utilized.
RESULTS
At diagnosis, the mean (±SD) age was 11.2 ± 3.3 years, body mass index (BMI)-z was 0.4 ± 1.1, 51.0% were male. The average HbA1c was 43.54 ± 8.46 mmol/mol (6.1 ± 0.8%). HbA1c correlated inversely with the AUC C-peptide (P < 0.001), peak C-peptide (P < 0.001), early and late C-peptide responses (P < 0.001 each), and 120/30 C-peptide (P < 0.001). Those with a peak C-peptide occurring at ≤60 minutes had higher HbA1c values than those with peaks later (P = 0.003). HbA1c variance was better explained with timing measures added to regression models (R
CONCLUSIONS
These findings show that the addition of timing measures of C-peptide responsiveness better explains HbA1c variation at diagnosis than standard measures alone.

Identifiants

pubmed: 30891858
doi: 10.1111/pedi.12845
pmc: PMC6655420
mid: NIHMS1041777
doi:

Substances chimiques

Blood Glucose 0
C-Peptide 0
Glycated Hemoglobin A 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

408-413

Subventions

Organisme : NIDDK NIH HHS
ID : U01 DK085476
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061010
Pays : United States
Organisme : NIAID NIH HHS
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : BLRD VA
ID : I01 BX001733
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK097512
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA076292
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103282
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061042
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085509
Pays : United States
Organisme : NIDDK NIH HHS
ID : UC4 DK117009
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK093954
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK017047
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085466
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103153
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061058
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK106984
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085499
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK107013
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103266
Pays : United States
Organisme : NIDDK NIH HHS
ID : UC4 DK106993
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK045735
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK107014
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK106994
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061034
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085461
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103180
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK085465
Pays : United States

Informations de copyright

© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Références

Pediatr Diabetes. 2017 Dec;18(8):794-802
pubmed: 28127835
Diabetes. 2012 Jun;61(6):1331-7
pubmed: 22618768
Diabetes Technol Ther. 2015 Sep;17(9):649-56
pubmed: 26317880
Diabetes Care. 2015 Jan;38 Suppl:S8-S16
pubmed: 25537714
Diabetes Care. 2009 Feb;32(2):301-5
pubmed: 19017769
Diabetologia. 1987 Apr;30(4):208-13
pubmed: 3297896
Diabetes Care. 2003 Mar;26(3):832-6
pubmed: 12610045
N Engl J Med. 2002 May 30;346(22):1685-91
pubmed: 12037147
Transplantation. 2009 Mar 15;87(5):689-97
pubmed: 19295313
Pediatr Diabetes. 2018 May;19(3):403-409
pubmed: 29171129

Auteurs

Heba M Ismail (HM)

Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana.

Carmella Evans-Molina (C)

Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.

Linda A DiMeglio (LA)

Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana.

Dorothy J Becker (DJ)

Division of Endocrinology and Metabolism, University of Pittsburgh and Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania.

Ingrid Libman (I)

Division of Endocrinology and Metabolism, University of Pittsburgh and Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania.

Emily K Sims (EK)

Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana.

David Boulware (D)

Department of Bio-statistics, H. Lee Moffitt Cancer Center, Tampa, Florida.

Kevan C Herold (KC)

Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut.

Lisa Rafkin (L)

Division of Endocrinology, Diabetes, and Metabolism, University of Miami, Miami, Florida.

Jay Skyler (J)

Division of Endocrinology, Diabetes, and Metabolism, University of Miami, Miami, Florida.

Mario A Cleves (MA)

Department of Pediatrics, Morsani College of Medicine, University of South Florida, Tampa, Florida.

Jerry Palmer (J)

Department of Medicine, VA Puget Sound Health Care System, Seattle, Washington.
Department of Medicine, University of Washington, Seattle, Washington.

Jay M Sosenko (JM)

Division of Endocrinology, Diabetes, and Metabolism, University of Miami, Miami, Florida.

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