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Regulation of human aldoketoreductase 1C3 (AKR1C3) gene expression in the adipose tissue.

Journal article
Authors Per-Arne Svensson
Britt G. Gabrielsson
Margareta Jernås
Anders Gummesson
Kajsa Sjöholm
Published in Cellular & Molecular Biology Letters
Volume 13
Issue 4
Pages 599-613
ISSN 1425-8153
Publication year 2008
Published at Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 599-613
Language en
Keywords body-fat distribution, weight-loss, androgen inactivation, insulin-resistance, metabolic syndrome, obese subjects, men, adipogenesis, adipocytes, receptor, 3-Hydroxysteroid Dehydrogenases, genetics, metabolism, Adipose Tissue, cytology, enzymology, physiology, Adult, Diet, Reducing, Female, Gene Expression Profiling, Gene Expression Regulation, Enzymologic, Humans, Hydroxyprostaglandin Dehydrogenases, genetics, metabolism, Leptin, blood, Male, Metabolic Syndrome X, metabolism, Middle Aged, Molecular Sequence Data, Obesity, metabolism, therapy, Oligonucleotide Array Sequence Analysis, Tissue Distribution, Weight Loss
Subject categories Cell and molecular biology, Cell biology


Aldoketoreductase 1C3 (AKR1C3) is a functional prostaglandin F synthase and a negative modulator of the availability of ligands for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma). AKR1C3 expression is known to be associated with adiposity, one of the components of the metabolic syndrome. The aim of this study was to characterize the expression of AKR1C3 in the adipose tissue and adipocytes and to investigate its potential role in the metabolic syndrome. Using microarray analysis and realtime PCR, we studied the expression of AKR1C3 in adipose tissue samples from obese subjects with or without metabolic complications, during very low calorie diet-induced weight loss, and its expression in isolated human adipocytes of different sizes. The adipose tissue AKR1C3 expression levels were marginally lower in obese subjects with the metabolic syndrome compared with the levels in healthy obese subjects when analyzed using microarray (p = 0.078) and realtime PCR (p < 0.05), suggesting a secondary or compensatory effect. The adipose tissue mRNA levels of AKR1C3 were reduced during and after dietinduced weight-loss compared to the levels before the start of the diet (p < 0.001 at all time-points). The gene expression of AKR1C3 correlated with both adipose tissue mRNA levels and serum levels of leptin before the start of the diet (p < 0.05 and p < 0.01, respectively). Furthermore, large adipocytes displayed a higher expression of AKR1C3 than small adipocytes (1.5-fold, p < 0.01). In conclusion, adipose tissue AKR1C3 expression may be affected by metabolic disease, and its levels are significantly reduced in response to dietinduced weight loss and correlate with leptin levels.

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