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

Direct link
FKBP5 expression in human adipose tissue increases following dexamethasone exposure and is associated with insulin resistance
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical diabetology and metabolism.ORCID iD: 0000-0001-5498-3899
Show others and affiliations
2014 (English)In: Metabolism: Clinical and Experimental, ISSN 0026-0495, E-ISSN 1532-8600, Vol. 63, no 9, 1198-1208 p.Article in journal (Refereed) Published
Abstract [en]


To study effects of dexamethasone on gene expression in human adipose tissue aiming to identify potential novel mechanisms for glucocorticoid-induced insulin resistance.


Subcutaneous and omental adipose tissue, obtained from non-diabetic donors (10 M/15 F; age: 28–60 years; BMI: 20.7–30.6 kg/m2), was incubated with or without dexamethasone (0.003–3 μmol/L) for 24 h. Gene expression was assessed by microarray and real time-PCR and protein expression by immunoblotting.


FKBP5 (FK506-binding protein 5) and CNR1 (cannabinoid receptor 1) were the most responsive genes to dexamethasone in both subcutaneous and omental adipose tissue (~ 7-fold). Dexamethasone increased FKBP5 gene and protein expression in a dose-dependent manner in both depots. The gene product, FKBP51 protein, was 10-fold higher in the omental than in the subcutaneous depot, whereas the mRNA levels were similar. Higher FKBP5 gene expression in omental adipose tissue was associated with reduced insulin effects on glucose uptake in both depots. Furthermore, FKBP5 gene expression in subcutaneous adipose tissue was positively correlated with serum insulin, HOMA-IR and subcutaneous adipocyte diameter and negatively with plasma HDL-cholesterol. FKBP5 SNPs were found to be associated with type 2 diabetes and diabetes-related phenotypes in large population-based samples.


Dexamethasone exposure promotes expression of FKBP5 in adipose tissue, a gene that may be implicated in glucocorticoid-induced insulin resistance.

Place, publisher, year, edition, pages
2014. Vol. 63, no 9, 1198-1208 p.
National Category
Endocrinology and Diabetes
URN: urn:nbn:se:uu:diva-232423DOI: 10.1016/j.metabol.2014.05.015ISI: 000340864400014PubMedID: 24997500OAI: oai:DiVA.org:uu-232423DiVA: diva2:747936
Available from: 2014-09-17 Created: 2014-09-17 Last updated: 2016-02-23

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Pereira, Maria JFall, ToveSidibeh, Cherno OEriksson, Jan W
By organisation
Clinical diabetology and metabolismMolecular epidemiology
In the same journal
Metabolism: Clinical and Experimental
Endocrinology and Diabetes

Search outside of DiVA

GoogleGoogle Scholar
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

Altmetric score

Total: 169 hits
ReferencesLink to record
Permanent link

Direct link