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

Direct link
Soluble CD93 Is Involved in Metabolic Dysregulation but Does Not Influence Carotid Intima-Media Thickness
Karolinska Inst, Dept Med Solna, Cardiovasc Med Unit, Stockholm, Sweden..
Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden..
Karolinska Inst, Dept Med Solna, Cardiovasc Med Unit, Stockholm, Sweden..
Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.;Nova Southeastern Univ, Cell Therapy Inst, Ft Lauderdale, FL USA..
Show others and affiliations
2016 (English)In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 65, no 10, 2888-2899 p.Article in journal (Refereed) Published
Abstract [en]

Type 2 diabetes and cardiovascular disease are complex disorders involving metabolic and inflammatory mechanisms. Here we investigated whether sCD93, a group XIV c-type lectin of the endosialin family, plays a role in metabolic dysregulation or carotid intima-media thickness (IMT). Although no association was observed between sCD93 and IMT, sCD93 levels were significantly lower in subjects with type 2 diabetes (n = 901, mean 6 SD 156.6 +/- 40.0 ng/mL) compared with subjects without diabetes (n = 2,470, 164.1 +/- 44.8 ng/mL, P < 0.0001). Genetic variants associated with diabetes risk (DIAGRAM Consortium) did not influence sCD93 levels (individually or combined in a single nucleotide polymorphism score). In a prospective cohort, lower sCD93 levels preceded the development of diabetes. Consistent with this, a cd93-deficient mouse model (in addition to apoe deficiency) demonstrated no difference in atherosclerotic lesion development compared with apoe(-/-) cd93-sufficient littermates. However, cd93-deficient mice showed impaired glucose clearance and insulin sensitivity (compared with littermate controls) after eating a high-fat diet. The expression of cd93 was observed in pancreatic islets, and leaky vessels were apparent in cd93-deficient pancreases. We further demonstrated that stress-induced release of sCD93 is impaired by hyperglycemia. Therefore, we propose CD93 as an important component in glucometabolic regulation.

Place, publisher, year, edition, pages
2016. Vol. 65, no 10, 2888-2899 p.
National Category
Endocrinology and Diabetes
URN: urn:nbn:se:uu:diva-311222DOI: 10.2337/db15-1333ISI: 000388372900010PubMedID: 27659228OAI: oai:DiVA.org:uu-311222DiVA: diva2:1059611
Swedish Heart Lung Foundation, 20120615, 20130664, 20140186Swedish Research Council, 8691, 0593Knut and Alice Wallenberg FoundationSwedish Foundation for Strategic Research Stockholm County CouncilEU, FP7, Seventh Framework Programme, IMI/115006Swedish Diabetes AssociationForte, Swedish Research Council for Health, Working Life and WelfareNovo NordiskMagnus Bergvall FoundationStiftelsen Gamla Tjänarinnor
Available from: 2016-12-22 Created: 2016-12-22 Last updated: 2016-12-22Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Syvänen, Ann-Christine
By organisation
Molecular MedicineScience for Life Laboratory, SciLifeLab
In the same journal
Endocrinology and Diabetes

Search outside of DiVA

GoogleGoogle Scholar

Altmetric score

Total: 34 hits
ReferencesLink to record
Permanent link

Direct link