uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Heterogeneity of Metabolic Defects in Type 2 Diabetes and Its Relation to Reactive Oxygen Species and Alterations in Beta-Cell Mass
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.ORCID iD: 0000-0003-0353-326x
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine.ORCID iD: 0000-0002-6060-6229
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Medicinal Chemistry, Theranostics. Uppsala University, Science for Life Laboratory, SciLifeLab.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.ORCID iD: 0000-0001-8843-7941
2019 (English)In: Frontiers in Physiology, ISSN 1664-042X, E-ISSN 1664-042X, Vol. 10, article id 107Article, review/survey (Refereed) Published
Abstract [en]

Type 2 diabetes (T2D) is a complex and heterogeneous disease which affects millions of people worldwide. The classification of diabetes is at an interesting turning point and there have been several recent reports on sub-classification of T2D based on phenotypical and metabolic characteristics. An important, and perhaps so far underestimated, factor in the pathophysiology of T2D is the role of oxidative stress and reactive oxygen species (ROS). There are multiple pathways for excessive ROS formation in T2D and in addition, beta-cells have an inherent deficit in the capacity to cope with oxidative stress. ROS formation could be causal, but also contribute to a large number of the metabolic defects in T2D, including beta-cell dysfunction and loss. Currently, our knowledge on beta-cell mass is limited to autopsy studies and based on comparisons with healthy controls. The combined evidence suggests that beta-cell mass is unaltered at onset of T2D but that it declines progressively. In order to better understand the pathophysiology of T2D, to identify and evaluate novel treatments, there is a need for in vivo techniques able to quantify beta-cell mass. Positron emission tomography holds great potential for this purpose and can in addition map metabolic defects, including ROS activity, in specific tissue compartments. In this review, we highlight the different phenotypical features of T2D and how metabolic defects impact oxidative stress and ROS formation. In addition, we review the literature on alterations of beta-cell mass in T2D and discuss potential techniques to assess beta-cell mass and metabolic defects in vivo.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2019. Vol. 10, article id 107
Keywords [en]
type 2 diabetes, diabetes classification, oxygen stress, reactive oxygen species, beta-cell, beta-cell mass, imaging, positron emission tomography
National Category
Biochemistry and Molecular Biology
Identifiers
URN: urn:nbn:se:uu:diva-378233DOI: 10.3389/fphys.2019.00107ISI: 000458732800001OAI: oai:DiVA.org:uu-378233DiVA, id: diva2:1296574
Funder
Swedish Child Diabetes FoundationSwedish Society for Medical Research (SSMF)Science for Life Laboratory - a national resource center for high-throughput molecular bioscienceErnfors FoundationSwedish Diabetes AssociationGöran Gustafsson Foundation for promotion of scientific research at Uppala University and Royal Institute of TechnologyAvailable from: 2019-03-15 Created: 2019-03-15 Last updated: 2019-03-15Bibliographically approved

Open Access in DiVA

fulltext(893 kB)66 downloads
File information
File name FULLTEXT01.pdfFile size 893 kBChecksum SHA-512
6185600a4572ab79cc0cde30b0016f38607dab3429acc36c266cd768a942922da2591280943c4b0ea03c9aee47700745913632841552bc38f8395dace5100640
Type fulltextMimetype application/pdf

Other links

Publisher's full text

Authority records BETA

Elksnis, AndrisMartinell, MatsEriksson, OlofEspes, Daniel

Search in DiVA

By author/editor
Elksnis, AndrisMartinell, MatsEriksson, OlofEspes, Daniel
By organisation
Department of Medical Cell BiologyFamily Medicine and Preventive MedicineTheranosticsScience for Life Laboratory, SciLifeLabDepartment of Medical Sciences
In the same journal
Frontiers in Physiology
Biochemistry and Molecular Biology

Search outside of DiVA

GoogleGoogle Scholar
Total: 66 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

doi
urn-nbn

Altmetric score

doi
urn-nbn
Total: 2227 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf