You are here

Article Text

Article menu

Download PDFPDF

Metabolism
Pregnancy induces pancreatic insulin secretion in women with long-standing type 1 diabetes
  1. Daniel Espes1,2,
  2. Louise Magnusson3,4,
  3. José Caballero-Corbalan3,
  4. Erik Schwarcz5,
  5. Rosaura Casas4,
  6. Per-Ola Carlsson3,6
  1. 1Science for Life Laboratory, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
  2. 2Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Uppsala, Sweden
  3. 3Department of Medical Sciences, Uppsala University, Uppsala, Sweden
  4. 4Department of Biomedical and Clinical Sciences, Linköping University, Linkoping, Sweden
  5. 5Department of Internal Medicine, Örebro University Hospital, Orebro, Sweden
  6. 6Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
  1. Correspondence to Professor Per-Ola Carlsson; per-ola.carlsson{at}mcb.uu.se

Abstract

Introduction Pregnancy entails both pancreatic adaptations with increasing β-cell mass and immunological alterations in healthy women. In this study, we have examined the effects of pregnancy on β-cell function and immunological processes in long-standing type 1 diabetes (L-T1D).

Research design and methods Fasting and stimulated C-peptide were measured after an oral glucose tolerance test in pregnant women with L-T1D (n=17) during the first trimester, third trimester, and 5–8 weeks post partum. Two 92-plex Olink panels were used to measure proteins in plasma. Non-pregnant women with L-T1D (n=30) were included for comparison.

Results Fasting C-peptide was detected to a higher degree in women with L-T1D during gestation and after parturition (first trimester: 64.7%, third trimester: 76.5%, and post partum: 64.7% vs 26.7% in non-pregnant women). Also, total insulin secretion and peak C-peptide increased during pregnancy. The plasma protein levels in pregnant women with L-T1D was dynamic, but few analytes were functionally related. Specifically, peripheral levels of prolactin (PRL), prokineticin (PROK)-1, and glucagon (GCG) were elevated during gestation whereas levels of proteins related to leukocyte migration (CCL11), T cell activation (CD28), and antigen presentation (such as CD83) were reduced.

Conclusions In summary, we have found that some C-peptide secretion, that is, an indirect measurement of endogenous insulin production, is regained in women with L-T1D during pregnancy, which might be attributed to elevated peripheral levels of PRL, PROK-1, or GCG.

  • pregnancy
  • C-peptide
  • immunomodulation
  • diabetes mellitus, type 1

Data availability statement

Data are available on reasonable request. Data will be made available on reasonable request.

http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/bmjdrc-2022-002948

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Data availability statement

    Data are available on reasonable request. Data will be made available on reasonable request.

    View Full Text

    Footnotes

    • DE and LM are joint first authors.

    • Contributors DE and P-OC were responsible for study conception, patient recruitment and clinical data collection. JC-C and ES recruited patients and collected clinical data. DE acquired clinical and proteomic data. DE calculated the total insulin secretion. LM calculated the insulin resistance, analyzed clinical and proteomic data, made the network analyses, and interpreted data. LM wrote the manuscript, which was revised by DE and P-OC. Manuscript submission was approved by all authors. P-OC is the guarantor of this manuscript.

    • Funding This study was supported by the Swedish Research Council, Barndiabetesfonden, Diabetesfonden, the Novo Nordisk Foundation, the Swedish Society for Medical Research, and the Regional research council in Uppsala-Örebro.

    • Disclaimer Funders were not involved in the study design, acquisition, analysis, and interpretation of data, or writing of this article.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.