The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity

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The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity. / Kristensen, Frederik Pagh Bredahl; Christensen, Diana Hedevang; Callaghan, Brian Christopher; Stidsen, Jacob Volmer; Nielsen, Jens Steen; Højlund, Kurt; Beck-Nielsen, Henning; Jensen, Troels Staehelin; Andersen, Henning; Vestergaard, Peter; Jessen, Niels; Olsen, Michael Hecht; Hansen, Torben; Brøns, Charlotte; Vaag, Allan; Sørensen, Henrik Toft; Thomsen, Reimar Wernich.

In: Diabetes Care, Vol. 46, No. 8, 2023, p. 1546-1555.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Kristensen, FPB, Christensen, DH, Callaghan, BC, Stidsen, JV, Nielsen, JS, Højlund, K, Beck-Nielsen, H, Jensen, TS, Andersen, H, Vestergaard, P, Jessen, N, Olsen, MH, Hansen, T, Brøns, C, Vaag, A, Sørensen, HT & Thomsen, RW 2023, 'The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity', Diabetes Care, vol. 46, no. 8, pp. 1546-1555. https://doi.org/10.2337/dc23-0079

APA

Kristensen, F. P. B., Christensen, D. H., Callaghan, B. C., Stidsen, J. V., Nielsen, J. S., Højlund, K., Beck-Nielsen, H., Jensen, T. S., Andersen, H., Vestergaard, P., Jessen, N., Olsen, M. H., Hansen, T., Brøns, C., Vaag, A., Sørensen, H. T., & Thomsen, R. W. (2023). The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity. Diabetes Care, 46(8), 1546-1555. https://doi.org/10.2337/dc23-0079

Vancouver

Kristensen FPB, Christensen DH, Callaghan BC, Stidsen JV, Nielsen JS, Højlund K et al. The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity. Diabetes Care. 2023;46(8):1546-1555. https://doi.org/10.2337/dc23-0079

Author

Kristensen, Frederik Pagh Bredahl ; Christensen, Diana Hedevang ; Callaghan, Brian Christopher ; Stidsen, Jacob Volmer ; Nielsen, Jens Steen ; Højlund, Kurt ; Beck-Nielsen, Henning ; Jensen, Troels Staehelin ; Andersen, Henning ; Vestergaard, Peter ; Jessen, Niels ; Olsen, Michael Hecht ; Hansen, Torben ; Brøns, Charlotte ; Vaag, Allan ; Sørensen, Henrik Toft ; Thomsen, Reimar Wernich. / The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity. In: Diabetes Care. 2023 ; Vol. 46, No. 8. pp. 1546-1555.

Bibtex

@article{925d0c7eaae64ae6bd3cffee2d52312a,
title = "The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity",
abstract = "OBJECTIVE Metabolic syndrome components may cumulatively increase the risk of diabetic polyneuropathy (DPN) in type 2 diabetes mellitus (T2DM) patients, driven by insulin resistance and hyperinsulinemia. We investigated the prevalence of DPN in three T2DM subgroups based on indices of b-cell function and insulin sensitivity. RESEARCH DESIGN AND METHODS We estimated b-cell function (HOMA2-B) and insulin sensitivity (HOMA2-S) in 4,388 Danish patients with newly diagnosed T2DM. Patients were categorized into subgroups of hyperinsulinemic (high HOMA2-B, low HOMA2-S), classical (low HOMA2-B, low HOMA2-S), and insulinopenic (low HOMA2-B, high HOMA2-S) T2DM. After a median follow-up of 3 years, patients filled the Michigan Neuropathy Screening Instrument questionnaire (MNSIq) to identify DPN (score ‡ 4). We used Poisson regression to calculate adjusted prevalence ratios (PRs) for DPN, and spline models to examine the association with HOMA2-B and HOMA2-S. RESULTS A total of 3,397 (77%) patients filled in the MNSIq. The prevalence of DPN was 23% among hyperinsulinemic, 16% among classical, and 14% among insulinopenic pa-tients. After adjusting for demographics, diabetes duration and therapy, lifestyle behaviors, and metabolic syndrome components (waist circumference, triglycer-ides, HDL cholesterol, hypertension, and HbA1c), the PR of DPN was 1.35 (95% CI 1.15–1.57) for the hyperinsulinemic compared with the classical patients. In spline analyses, we observed a linear relation of higher DPN prevalence with increasing HOMA2-B, independent of both metabolic syndrome components and HOMA2-S. CONCLUSIONS Hyperinsulinemia marked by high HOMA2-B is likely an important risk factor for DPN beyond metabolic syndrome components and insulin resistance. This should be considered when developing interventions to prevent DPN.",
author = "Kristensen, {Frederik Pagh Bredahl} and Christensen, {Diana Hedevang} and Callaghan, {Brian Christopher} and Stidsen, {Jacob Volmer} and Nielsen, {Jens Steen} and Kurt H{\o}jlund and Henning Beck-Nielsen and Jensen, {Troels Staehelin} and Henning Andersen and Peter Vestergaard and Niels Jessen and Olsen, {Michael Hecht} and Torben Hansen and Charlotte Br{\o}ns and Allan Vaag and S{\o}rensen, {Henrik Toft} and Thomsen, {Reimar Wernich}",
note = "Publisher Copyright: {\textcopyright} 2023 by the American Diabetes Association.",
year = "2023",
doi = "10.2337/dc23-0079",
language = "English",
volume = "46",
pages = "1546--1555",
journal = "Diabetes Care",
issn = "1935-5548",
publisher = "American Diabetes Association",
number = "8",

}

RIS

TY - JOUR

T1 - The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity

AU - Kristensen, Frederik Pagh Bredahl

AU - Christensen, Diana Hedevang

AU - Callaghan, Brian Christopher

AU - Stidsen, Jacob Volmer

AU - Nielsen, Jens Steen

AU - Højlund, Kurt

AU - Beck-Nielsen, Henning

AU - Jensen, Troels Staehelin

AU - Andersen, Henning

AU - Vestergaard, Peter

AU - Jessen, Niels

AU - Olsen, Michael Hecht

AU - Hansen, Torben

AU - Brøns, Charlotte

AU - Vaag, Allan

AU - Sørensen, Henrik Toft

AU - Thomsen, Reimar Wernich

N1 - Publisher Copyright: © 2023 by the American Diabetes Association.

PY - 2023

Y1 - 2023

N2 - OBJECTIVE Metabolic syndrome components may cumulatively increase the risk of diabetic polyneuropathy (DPN) in type 2 diabetes mellitus (T2DM) patients, driven by insulin resistance and hyperinsulinemia. We investigated the prevalence of DPN in three T2DM subgroups based on indices of b-cell function and insulin sensitivity. RESEARCH DESIGN AND METHODS We estimated b-cell function (HOMA2-B) and insulin sensitivity (HOMA2-S) in 4,388 Danish patients with newly diagnosed T2DM. Patients were categorized into subgroups of hyperinsulinemic (high HOMA2-B, low HOMA2-S), classical (low HOMA2-B, low HOMA2-S), and insulinopenic (low HOMA2-B, high HOMA2-S) T2DM. After a median follow-up of 3 years, patients filled the Michigan Neuropathy Screening Instrument questionnaire (MNSIq) to identify DPN (score ‡ 4). We used Poisson regression to calculate adjusted prevalence ratios (PRs) for DPN, and spline models to examine the association with HOMA2-B and HOMA2-S. RESULTS A total of 3,397 (77%) patients filled in the MNSIq. The prevalence of DPN was 23% among hyperinsulinemic, 16% among classical, and 14% among insulinopenic pa-tients. After adjusting for demographics, diabetes duration and therapy, lifestyle behaviors, and metabolic syndrome components (waist circumference, triglycer-ides, HDL cholesterol, hypertension, and HbA1c), the PR of DPN was 1.35 (95% CI 1.15–1.57) for the hyperinsulinemic compared with the classical patients. In spline analyses, we observed a linear relation of higher DPN prevalence with increasing HOMA2-B, independent of both metabolic syndrome components and HOMA2-S. CONCLUSIONS Hyperinsulinemia marked by high HOMA2-B is likely an important risk factor for DPN beyond metabolic syndrome components and insulin resistance. This should be considered when developing interventions to prevent DPN.

AB - OBJECTIVE Metabolic syndrome components may cumulatively increase the risk of diabetic polyneuropathy (DPN) in type 2 diabetes mellitus (T2DM) patients, driven by insulin resistance and hyperinsulinemia. We investigated the prevalence of DPN in three T2DM subgroups based on indices of b-cell function and insulin sensitivity. RESEARCH DESIGN AND METHODS We estimated b-cell function (HOMA2-B) and insulin sensitivity (HOMA2-S) in 4,388 Danish patients with newly diagnosed T2DM. Patients were categorized into subgroups of hyperinsulinemic (high HOMA2-B, low HOMA2-S), classical (low HOMA2-B, low HOMA2-S), and insulinopenic (low HOMA2-B, high HOMA2-S) T2DM. After a median follow-up of 3 years, patients filled the Michigan Neuropathy Screening Instrument questionnaire (MNSIq) to identify DPN (score ‡ 4). We used Poisson regression to calculate adjusted prevalence ratios (PRs) for DPN, and spline models to examine the association with HOMA2-B and HOMA2-S. RESULTS A total of 3,397 (77%) patients filled in the MNSIq. The prevalence of DPN was 23% among hyperinsulinemic, 16% among classical, and 14% among insulinopenic pa-tients. After adjusting for demographics, diabetes duration and therapy, lifestyle behaviors, and metabolic syndrome components (waist circumference, triglycer-ides, HDL cholesterol, hypertension, and HbA1c), the PR of DPN was 1.35 (95% CI 1.15–1.57) for the hyperinsulinemic compared with the classical patients. In spline analyses, we observed a linear relation of higher DPN prevalence with increasing HOMA2-B, independent of both metabolic syndrome components and HOMA2-S. CONCLUSIONS Hyperinsulinemia marked by high HOMA2-B is likely an important risk factor for DPN beyond metabolic syndrome components and insulin resistance. This should be considered when developing interventions to prevent DPN.

U2 - 10.2337/dc23-0079

DO - 10.2337/dc23-0079

M3 - Journal article

C2 - 37335990

AN - SCOPUS:85165521717

VL - 46

SP - 1546

EP - 1555

JO - Diabetes Care

JF - Diabetes Care

SN - 1935-5548

IS - 8

ER -

ID: 361392719