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Acquired Obesity Increases CD68 and Tumor Necrosis Factor-α and Decreases Adiponectin Gene Expression in Adipose Tissue: A Study in Monozygotic Twins

Authors :
Kirsi H. Pietiläinen
Ewa Ehrenborg
Elena Korsheninnikova
Katja Kannisto
Jaakko Kaprio
Hannele Yki-Järvinen
Anders Hamsten
Aila Rissanen
Source :
The Journal of Clinical Endocrinology & Metabolism. 91:2776-2781
Publication Year :
2006
Publisher :
The Endocrine Society, 2006.

Abstract

Both acquired and genetic factors regulate adipose tissue function.We determined whether adipose tissue mRNA expression is regulated by obesity, independently of genetic effects, by studying monozygotic (MZ) twins.Seventeen healthy pairs of MZ twins aged 24-27 yr (body mass index 20.0-33.9 kg/m(2), intrapair differences in body weight 0.1-24.7 kg), were identified from the population-based FinnTwin16 cohort. Body fat percent was determined by dual-energy x-ray absorptiometry, sc and intraabdominal fat by magnetic resonance imaging, liver fat by proton spectroscopy, and insulin sensitivity by using the euglycemic insulin clamp technique. Adipocyte cell size and expression of 10 genes (real-time PCR) were determined in sc adipose tissue biopsies. Serum levels of some of the genes were measured using ELISA.Within MZ twin pairs, acquired obesity was significantly related to increased adipocyte size and increased adipose tissue mRNA expressions of leptin, TNFalpha and the macrophage marker CD68, and decreased mRNA expressions of adiponectin and peroxisome proliferator-activated receptor-gamma. Intrapair differences in liver fat correlated directly with those in leptin and CD68 expression. CD68 expression and serum TNFalpha concentrations were correlated with insulin resistance.Acquired obesity independent of genetic influences is able to increase expression of macrophage and inflammatory markers and decrease adiponectin expression in adipose tissue.

Details

ISSN :
19457197 and 0021972X
Volume :
91
Database :
OpenAIRE
Journal :
The Journal of Clinical Endocrinology & Metabolism
Accession number :
edsair.doi.dedup.....37d10481594883b7657f69ff4e5359ef