Acquired obesity increases CD68 and tumor necrosis factor-alpha and decreases adiponectin gene expression in adipose tissue: a study in monozygotic twins.
BACKGROUND
Both acquired and genetic factors regulate adipose tissue function.


OBJECTIVE
We determined whether adipose tissue mRNA expression is regulated by obesity, independently of genetic effects, by studying monozygotic (MZ) twins.


METHODS
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.


RESULTS
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.


CONCLUSIONS
Acquired obesity independent of genetic influences is able to increase expression of macrophage and inflammatory markers and decrease adiponectin expression in adipose tissue.
Pietiläinen
Kirsi H
KH
M.Sc., Obesity Research Unit, Biomedicum Helsinki, C428a, P.O. Box 700, FIN-00029 HUS, Finland. kirsi.pietilainen@helsinki.fi
Kannisto
Katja
K
Korsheninnikova
Elena
E
Rissanen
Aila
A
Kaprio
Jaakko
J
Ehrenborg
Ewa
E
Hamsten
Anders
A
Yki-Järvinen
Hannele
H
D015502:Absorptiometry, Photon; D017667:Adipocytes / Q000166:cytology; D052242:Adiponectin / Q000235:genetics*; D000273:Adipose Tissue / Q000737:chemistry*; D000328:Adult; D015703:Antigens, CD / Q000235:genetics*; D015214:Antigens, Differentiation, Myelomonocytic / Q000235:genetics*; D001823:Body Composition; D048429:Cell Size; D005260:Female; D015870:Gene Expression; D015309:Glucose Clamp Technique; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D009765:Obesity / Q000378:metabolism*; D047495:PPAR gamma / Q000235:genetics; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000235:genetics*; D014430:Twins, Monozygotic / Q000235:genetics*; D000097382:CD68 Molecule
D052242:Adiponectin; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D047495:PPAR gamma; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C067980:CD68 antigen, human; D000097382:CD68 Molecule