Limitations of the fasting proinsulin to insulin ratio as a measure of β-cell health in people with and without impaired glucose tolerance.


Journal

European journal of clinical investigation
ISSN: 1365-2362
Titre abrégé: Eur J Clin Invest
Pays: England
ID NLM: 0245331

Informations de publication

Date de publication:
Jun 2021
Historique:
revised: 02 12 2020
received: 27 10 2020
accepted: 04 12 2020
pubmed: 9 12 2020
medline: 31 12 2021
entrez: 8 12 2020
Statut: ppublish

Résumé

The fasting proinsulin to insulin ratio is elevated in people with type 2 diabetes and has been suggested as a marker of β-cell health. However, its utility in discriminating between individuals with varying degrees of β-cell dysfunction is unclear. Proinsulin has a very different half-life to insulin and unlike insulin does not undergo hepatic extraction prior to reaching the systemic circulation. Given these limitations, we sought to examine the relationship between fasting and postprandial concentrations of β-cell polypeptides (proinsulin, insulin and C-peptide) in people with normal and impaired glucose tolerance in differing metabolic environments. Subjects were studied on two occasions in random order while undergoing an oral challenge. During one study day, free fatty acids were elevated (to induce insulin resistance) by infusion of Intralipid with heparin. Proinsulin to insulin and proinsulin to C-peptide ratios were calculated for the 0-, 30-, 60- and 240-minute time points. Insulin action (Si) and β-cell responsivity (Φ) indices were calculated using the oral minimal model. The fasting proinsulin to c-peptide or fasting proinsulin to insulin ratios did not differ between groups and did not predict subsequent β-cell responsivity to glucose during the glycerol or Intralipid study days in either group. Among nondiabetic individuals, the fasting proinsulin to insulin ratio is not a useful marker of β-cell function.

Sections du résumé

BACKGROUND BACKGROUND
The fasting proinsulin to insulin ratio is elevated in people with type 2 diabetes and has been suggested as a marker of β-cell health. However, its utility in discriminating between individuals with varying degrees of β-cell dysfunction is unclear. Proinsulin has a very different half-life to insulin and unlike insulin does not undergo hepatic extraction prior to reaching the systemic circulation. Given these limitations, we sought to examine the relationship between fasting and postprandial concentrations of β-cell polypeptides (proinsulin, insulin and C-peptide) in people with normal and impaired glucose tolerance in differing metabolic environments.
DESIGN METHODS
Subjects were studied on two occasions in random order while undergoing an oral challenge. During one study day, free fatty acids were elevated (to induce insulin resistance) by infusion of Intralipid with heparin. Proinsulin to insulin and proinsulin to C-peptide ratios were calculated for the 0-, 30-, 60- and 240-minute time points. Insulin action (Si) and β-cell responsivity (Φ) indices were calculated using the oral minimal model.
RESULTS RESULTS
The fasting proinsulin to c-peptide or fasting proinsulin to insulin ratios did not differ between groups and did not predict subsequent β-cell responsivity to glucose during the glycerol or Intralipid study days in either group.
CONCLUSIONS CONCLUSIONS
Among nondiabetic individuals, the fasting proinsulin to insulin ratio is not a useful marker of β-cell function.

Identifiants

pubmed: 33289929
doi: 10.1111/eci.13469
pmc: PMC8169515
mid: NIHMS1654141
doi:

Substances chimiques

Biomarkers 0
Blood Glucose 0
C-Peptide 0
Insulin 0
Proinsulin 9035-68-1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e13469

Subventions

Organisme : NCATS NIH HHS
ID : UL1 TR000135
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK082396
Pays : United States
Organisme : NIH HHS
ID : DK82396
Pays : United States
Organisme : Università degli Studi di Padova
ID : CPDA145405
Organisme : NIDDK NIH HHS
ID : R01 DK126206
Pays : United States
Organisme : NIH HHS
ID : DK116231
Pays : United States
Organisme : NIH HHS
ID : DK78646
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK116231
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK078646
Pays : United States

Informations de copyright

© 2020 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.

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Auteurs

Aoife M Egan (AM)

Division of Endocrinology, Diabetes and Metabolism, Mayo Clinic, Rochester, MN, USA.

Marcello C Laurenti (MC)

Division of Endocrinology, Diabetes and Metabolism, Mayo Clinic, Rochester, MN, USA.

Maria Daniela Hurtado Andrade (MD)

Division of Endocrinology, Diabetes and Metabolism, Mayo Clinic, Rochester, MN, USA.

Chiara Dalla Man (C)

Department of Information Engineering, Università degli Studi di Padova, Padova, Italy.

Claudio Cobelli (C)

Department of Information Engineering, Università degli Studi di Padova, Padova, Italy.

Kent R Bailey (KR)

Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, MN, USA.

Adrian Vella (A)

Division of Endocrinology, Diabetes and Metabolism, Mayo Clinic, Rochester, MN, USA.

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Classifications MeSH