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Human subcutaneous adipose tissue Glut 4 mRNA expression in obesity and type 2 diabetes

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Abstract

Cellular resistance to insulin caused by reduced glucose transport and metabolism is a primary defect leading to the development of metabolic disease. While the etiology of insulin resistance is multifactorial, reduced insulin action is associated with impaired activity of the glucose transporter GLUT4 in insulin-sensitive tissues. Yet, the role of adipose tissue GLUT4 deregulation in the pathogenesis of insulin resistance, obesity, and diabetes is still unclear. In this study, we assessed the relative GLUT4 level in human subcutaneous adipose tissue from obese, diabetic, and diabetic obese versus control subjects, using a real-time PCR method. GLUT4 mRNA levels were considerably decreased among type 2 diabetic patients compared with those of the controls (P < 0.01), whereas no such difference was found between obese and normal-weight controls. Multiple linear regressions analysis in both diabetic non-obese and diabetic obese groups showed a negative correlation between GLUT4 mRNA expression and both markers of obesity or insulin resistance (P < 0.01). However, in obese group, GLUT4 was inversely associated only with HOMA-IR (P < 0.01). Our findings showed that adipose GLUT4 gene expression changes were more related to insulin resistance and type 2 diabetes rather than to obesity.

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Acknowledgments

We thank Pr. Abdeljélil Zaouche for help to subject recruitment from Chirurgic Visceral Service of Charles Nicolle Hospital. This work was supported by a PHC-Utique program/CMCU grant n°06G0910 for Soumaya Kouidhi and EU contract n°018652 “CRESCENDO.” The authors declare that there is no conflict of interest that would prejudice the impartiality of this work.

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Correspondence to Soumaya Kouidhi.

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Soumaya Kouidhi and Rym Berrhouma are contributed equally.

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Kouidhi, S., Berrhouma, R., Rouissi, K. et al. Human subcutaneous adipose tissue Glut 4 mRNA expression in obesity and type 2 diabetes. Acta Diabetol 50, 227–232 (2013). https://doi.org/10.1007/s00592-011-0295-8

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  • DOI: https://doi.org/10.1007/s00592-011-0295-8

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