Format

Send to

Choose Destination
Atherosclerosis. 2007 Nov;195(1):e150-8. Epub 2007 Jun 5.

Fatty acid binding protein 4 is increased in metabolic syndrome and with thiazolidinedione treatment in diabetic patients.

Author information

1
Research Unit on Lipids and Atherosclerosis, Faculty of Medicine and Health Sciences, IRCIS, Department of Internal Medicine, Sant Joan University Hospital, Reus, Spain. anna.cabre@urv.cat

Abstract

OBJECTIVE:

To study the role of FABP4 in the plasma of type 2 diabetic (T2D) subjects with and without metabolic syndrome (MS) and the impact of thiazolidinedione (TZD) treatment.

METHODS AND RESULTS:

FABP4 was analyzed in 274 individuals (169 T2D subjects and 105 controls). MS-T2D subjects had higher FABP4 levels than non-MS-T2D subjects and controls (53% and 76% increase, respectively, p<0.005). FABP4 levels in T2D subjects were positively correlated to the number of MS elements, obesity degree, adiponectin, triglycerides, lipoperoxides, C-reactive protein, age, systolic blood pressure and diabetes duration (p<0.05). Neither clinical or subclinical atherosclerosis, nor plasma levels of insulin, glucose or RBP4 were associated to FABP4. TZD-treated T2D subjects showed >30% higher FABP4 levels (p<0.05) than non-TZD-treated T2D. A subgroup study confirmed that TZD treatment prospectively increased FABP4 levels (p<0.05) along with an increase of peripheral blood mononuclear cell PPARgamma activity (p<0.05). Furthermore, in vitro studies showed that TZD treatment increased FABP4 mRNA, intracellular protein levels and extracellular secretion from human adipocytes.

CONCLUSIONS/INTERPRETATION:

FABP4 plasma concentrations are increased with the early presence of MS components, as well as inflammation and oxidation markers in T2D subjects. TZD increases FABP4 plasma concentrations, reflecting PPARgamma activation. FABP4 plasma measurements could be useful in the management of T2D subjects.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center