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The expression of inhibin beta B is high in human adipocytes, reduced by weight loss, and correlates to factors implicated in metabolic disease.

Journal article
Authors Kajsa Sjöholm
Jenny Palming
Ted Lystig
Eva Jennische
Teresa K Woodruff
Björn Carlsson
Lena M S Carlsson
Published in Biochemical and biophysical research communications
Volume 344
Issue 4
Pages 1308-14
ISSN 0006-291X
Publication year 2006
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 1308-14
Language en
Links dx.doi.org/10.1016/j.bbrc.2006.04.0...
Keywords Adipocytes, chemistry, metabolism, Cells, Cultured, Female, Gene Expression Regulation, Humans, Inhibin-beta Subunits, analysis, genetics, metabolism, Male, Metabolic Syndrome X, genetics, Oligonucleotide Array Sequence Analysis, RNA, Messenger, analysis, metabolism, Weight Loss, genetics
Subject categories Medical and Health Sciences

Abstract

Adipose tissue is an endocrine organ that produces and secretes adipokines. The aim of this study was to identify genes predominantly expressed in human subcutaneous adipocytes. For this purpose, an algorithm was developed and DNA microarray expression profiles from 33 human tissues and cell types were used to select genes. Inhibin beta B (INHBB; coding for the activin betaB subunit) was identified and high expression in adipocytes was confirmed by real-time PCR and immunohistochemistry. INHBB expression in adipose tissue was down regulated by diet-induced weight loss (p<0.001). Furthermore, INHBB expression was positively correlated to total (p<0.001) and subcutaneous (p<0.01) adipose tissue areas and serum levels of fasting insulin (p<0.01) and cholesterol (p<0.05). In conclusion, INHBB expression was high in human adipocytes, reduced by weight loss and adipose tissue INHBB mRNA levels correlated to metabolic risk factors. This suggests that activin B produced in adipocytes may play a role in the metabolic syndrome.

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http://www.gu.se/english/research/publication/?publicationId=58302
Utskriftsdatum: 2020-02-22