Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Aug 25:13:876470.
doi: 10.3389/fendo.2022.876470. eCollection 2022.

The etiology and pathogenesis of type 1 diabetes - A personal, non-systematic review of possible causes, and interventions

Affiliations
Review

The etiology and pathogenesis of type 1 diabetes - A personal, non-systematic review of possible causes, and interventions

Karsten Buschard. Front Endocrinol (Lausanne). .

Abstract

In this review after a lifelong research career, my personal opinion on the development of type 1 diabetes (T1D) from its very start to clinical manifestation will be described. T1D is a disease of an increased intestinal permeability and a reduced pancreas volume. I am convinced that virus might be the initiator and that this virus could persist on strategically significant locations. Furthermore, intake of gluten is important both in foetal life and at later ages. Disturbances in sphingolipid metabolism may also be of crucial importance. During certain stages of T1D, T cells take over resulting in the ultimate destruction of beta cells, which manifests T1D as an autoimmune disease. Several preventive and early treatment strategies are mentioned. All together this review has more new theories than usually, and it might also be more speculative than ordinarily. But without new ideas and theories advancement is difficult, even though everything might not hold true during the continuous discovery of the etiology and pathogenesis of T1D.

Keywords: beta-cell activity; etiology; gluten; pathogenesis; sphingolipids; sulfatide; type 1 diabetes; virus.

PubMed Disclaimer

Conflict of interest statement

The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Schematic drawing of various factors involved in development of Type 1 Diabetes.

Similar articles

Cited by

References

    1. Anderson AM, Landry LG, Alkanani AA, Pyle L, Powers AC, Atkinson MA, et al. . Human islet T cells are highly reactive to preproinsulin in type 1 diabetes. Proc Natl Acad Sci USA (2021) 118(41):1–12. doi: 10.1073/pnas.2107208118 - DOI - PMC - PubMed
    1. Ziegler AG, Rewers M, Simell O, Simell T, Lempainen J, Steck A, et al. . Seroconversion to multiple islet autoantibodies and risk of progression to diabetes in children. Jama (2013) 309(23):2473–9. doi: 10.1001/jama.2013.6285 - DOI - PMC - PubMed
    1. Xia CQ, Liu YT, Guan QB, Clare-Salzler M. Anti-lymphocyte antibody-based immunotherapy in type 1 diabetes. Chin Med J (Engl) (2013) 126(5):957–64. - PubMed
    1. Pescovitz MD, Greenbaum CJ, Krause-Steinrauf H, Becker DJ, Gitelman SE, Goland R, et al. . Rituximab, b-lymphocyte depletion, and preservation of beta-cell function. N Engl J Med (2009) 361(22):2143–52. doi: 10.1056/NEJMoa0904452 - DOI - PMC - PubMed
    1. Barcenilla H, Pihl M, Wahlberg J, Ludvigsson J, Casas R. Intralymphatic GAD-alum injection modulates b cell response and induces follicular helper T cells and PD-1+ CD8+ T cells in patients with recent-onset type 1 diabetes. Front Immunol (2021) 12:797172. doi: 10.3389/fimmu.2021.797172 - DOI - PMC - PubMed

MeSH terms