Metallothionein 2a Gene Expression is Increased in Subcutaneous Adipose Tissue of Type 2 Diabetic PatientsVanessa Haynes1, Timothy Connor1, Andre Tchernof2, Hubert Vidal3 and Severine Dubois1,3*
- *Corresponding Author:
- Séverine Dubois
Inserm U872, Centre de Recherche des Cordeliers-équipe 6
15, rue de l’école de médecine, Paris, France
E-mail: [email protected]
Received date April 04, 2012; Accepted date July 20, 2012; Published date July 25, 2012
Citation: Haynes V, Connor T, Tchernof A, Vidal H, Dubois S (2012) Metallothionein 2a Gene Expression is Increased in Subcutaneous Adipose Tissue of Type 2 Diabetic Patients. J Diabetes Metab 3: 206 doi:10.4172/2155-6156.1000206
Copyright: © 2012 Haynes V, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Study background: Insulin resistance plays an important role in the pathogenesis of type2 diabetes and the metabolic syndrome. Many of the genes and pathways involved have been identified but some remain to be defined. Metallothioneins (Mts) are a family of anti-oxidant proteins and metallothionein 2a (Mt2a) polymorphims have been recently associated with type 2 diabetes and related complications. Our objective was to determine Mt2a gene expression levels in adipose tissues from diabetic patients and determine the effect of Mt treatment on adipocyte insulin sensitivity.
Methods: Samples of subcutaneous and visceral adipose tissues from lean, type 2 diabetic and non-diabetic obese patients were analysed using RT-qPCR for Mt2a mRNA abundance. The regulation of Mt2a expression was further studied in 3T3-L1 adipocytes treated or not with TNFα (10 ng/ml, 72ôÂÂÂh) to induce insulin resistance. The effects of Mt on glucose uptake were investigated in cultured adipocytes treated with recombinant Mt protein.
Results: We found that Mt2a gene expression was significantly higher in adipose tissue of type 2 diabetic patients in comparison to lean (p=0.003) subjects. In 3T3-L1 adipocytes, insulin resistance induced by TNFα increased Mt2a mRNA levels (p=3×10-4) and insulin-stimulated glucose uptake was significantly inhibited by 53% (p=8×10-4) compared to vehicle, when 3T3-L1 adipocytes were treated with Mt protein.
Conclusions: These data suggest that Mt2a might be involved in insulin resistance through the up-regulation of Mt gene expression, which may lead to the modulation of insulin action in fat cells. These results suggest the concept of considering Mt proteins as markers and potential targets in type 2 diabetes.