The Prevalence of Polyneuropathy in Type 2 Diabetes Subgroups Based on HOMA2 Indices of β-Cell Function and Insulin Sensitivity
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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.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Diabetes Care |
| Vol/bind | 46 |
| Udgave nummer | 8 |
| Sider (fra-til) | 1546-1555 |
| Antal sider | 10 |
| ISSN | 0149-5992 |
| DOI | |
| Status | Udgivet - 2023 |
Bibliografisk note
Funding Information:
Acknowledgments. The authors are grateful to all participants and staff members in the DD2. The authors thank biostatistician Helene M. L. Svane (Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark) for excellent statistical advice on the project. Funding. F.P.B.K. is supported by a PhD grant from Aarhus University. The DD2 study was supported by the Danish Agency for Science and Higher Education (grant nos. 09-067009 and 09-075724), the Danish Health and Medicines Authority, the Danish Diabetes Association, Region of Southern Denmark, and the Novo Nordisk Fonden (grant nos. NNF17SA0030962-2, NNF2000063292 and NNF17SA0030364). The DD2 biobank was supported by an unrestricted donation from Novo Nordisk A/S. Project partners are listed on the website www.DD2.dk. Duality of Interest. The Department of Clinical Epidemiology, Aarhus University Hospital, receives funding for other studies from companies in the form of research grants to (and administered by) Aarhus University. None of these studies have any relation to the current study. B.C.C. has received grants from the American Academy of Neurology Research, contract and personal fees from the American Academy of Neurology editorial board, and personal fees from Dynamed and from medical legal work, including the Vaccine Injury Compensation Program. J.V.S., K.H., M.H.O., P.V., N.J., C.B., and A.V. are all affiliated with the Danish Steno Diabetes Centers. The Steno Diabetes Centers are funded partly by a donation from the Novo Nordisk Foundation. No other potential conflicts of interest relevant to this article were reported. Author Contributions. F.P.B.K., D.H.C., and R.W.T. conceived the study idea. F.P.B.K., D.H.C., and R.W.T. designed the study. F.P.B.K. did data management and statistical analysis. J.S.N. is the principal manager of the DD2. H.T.S. provided expert knowledge of clinical epidemiology, while B.C.C., T.S.J., and H.A. provided expert knowledge of neuropathy. J.V.S., K.H., H.B.-N., P.V., N.J., M.H.O., T.H., C.B., and A.V. contributed with expert knowledge of type 2 diabetes and pathophysiological subgroups. F.P.B.K., D.H.C., B.C.C., H.T.S., and R.W.T. prepared the first draft of the manuscript. All authors contributed to the interpretation of data and the drafting of the manuscript, as well as critically revising the manuscript draft. All authors approved the final version of the manuscript. F.P.B.K. and R.W.T. are the guarantors of this work and, as such, had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Prior Presentation. Preliminary results from this study were presented as a poster at the 38th International Conference on Pharmacoepidemiology and Therapeutic Risk Management, Copenhagen, Denmark, 27 August 2022 (abstract no. 1183387), and as an oral presentation at the 58th Annual Meeting of European Association for the Study of Diabetes, Stockholm, Sweden, 22 September 2022 (abstract no. A-22-312-EASD).
Funding Information:
The authors are grateful to all participants and staff members in the DD2. The authors thank biostatistician Helene M. L. Svane (Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark) for excellent statistical advice on the project. Funding. F.P.B.K. is supported by a PhD grant from Aarhus University. The DD2 study was supported by the Danish Agency for Science and Higher Education (grant nos. 09-067009 and 09-075724), the Danish Health and Medi-cines Authority, the Danish Diabetes Association, Region of Southern Denmark, and the Novo Nordisk Fonden (grant nos. NNF17SA0030962-2, NNF2000063292 and NNF17SA0030364). The DD2 biobank was supported by an unrestricted donation from Novo Nordisk A/S. Project part-ners are listed on the website www.DD2.dk.
Publisher Copyright:
© 2023 by the American Diabetes Association.
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