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      ALK7 expression is specific for adipose tissue, reduced in obesity and correlates to factors implicated in metabolic disease

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          Abstract

          Human adipose tissue is a major site of expression of inhibin beta B (INHBB) which homodimerizes to form the novel adipokine activin B. Our aim was to determine if molecules needed for a local action of activin B are expressed in adipose tissue.

          Microarray analysis showed that adipose tissue expressed activin type I and II receptors and that the expression of activin receptor-like kinase 7 (ALK7) was adipose tissue specific. In obesity discordant siblings from the SOS Sib Pair study, adipose tissue ALK7 expression was higher in lean ( n = 90) compared to obese ( n = 90) subjects ( p = 4 × 10 −31). Adipose tissue ALK7 expression correlated with several measures of body fat, carbohydrate metabolism and lipids. In addition, ALK7 and INHBB expression correlated but only in lean subjects and in subjects with normal glucose tolerance.

          We conclude that activin B may have local effects in adipose tissue and thereby influence obesity and its comorbidities.

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          A large-scale analysis of tissue-specific pathology and gene expression of human disease genes and complexes.

          Patricia Donahoe, Celia N. Hansen, Francisco Roque … (2009)
          Heritable diseases are caused by germ-line mutations that, despite tissuewide presence, often lead to tissue-specific pathology. Here, we make a systematic analysis of the link between tissue-specific gene expression and pathological manifestations in many human diseases and cancers. Diseases were systematically mapped to tissues they affect from disease-relevant literature in PubMed to create a disease-tissue covariation matrix of high-confidence associations of >1,000 diseases to 73 tissues. By retrieving >2,000 known disease genes, and generating 1,500 disease-associated protein complexes, we analyzed the differential expression of a gene or complex involved in a particular disease in the tissues affected by the disease, compared with nonaffected tissues. When this analysis is scaled to all diseases in our dataset, there is a significant tendency for disease genes and complexes to be overexpressed in the normal tissues where defects cause pathology. In contrast, cancer genes and complexes were not overexpressed in the tissues from which the tumors emanate. We specifically identified a complex involved in XY sex reversal that is testis-specific and down-regulated in ovaries. We also identified complexes in Parkinson disease, cardiomyopathies, and muscular dystrophy syndromes that are similarly tissue specific. Our method represents a conceptual scaffold for organism-spanning analyses and reveals an extensive list of tissue-specific draft molecular pathways, both known and unexpected, that might be disrupted in disease.
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            Adipocytokines and the metabolic complications of obesity.

            Philip A Kern, Neda Rasouli (2008)
            Adipose tissue is increasingly recognized as an active endocrine organ with many secretory products and part of the innate immune system. With obesity, macrophages infiltrate adipose tissue, and numerous adipocytokines are released by both macrophages and adipocytes. Adipocytokines play important roles in the pathogenesis of insulin resistance and associated metabolic complications such as dyslipidemia, hypertension, and premature heart disease. Published literature was analyzed with the intent of addressing the role of the major adipose secretory proteins in human obesity, insulin resistance, and type 2 diabetes. This review analyzes the characteristics of different adipocytokines, including leptin, adiponectin, pro-inflammatory cytokines, resistin, retinol binding protein 4, visfatin, and others, and their roles in the pathogenesis of insulin resistance. Inflamed fat in obesity secretes an array of proteins implicated in the impairment of insulin signaling. Further studies are needed to understand the triggers that initiate inflammation in adipose tissue and the role of each adipokine in the pathogenesis of insulin resistance.
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              Separation of human adipocytes by size: hypertrophic fat cells display distinct gene expression.

              Margareta Jernås, Malin Lönn, Britt Gabrielsson … (2006)
              Enlarged adipocytes are associated with insulin resistance and are an independent predictor of type 2 diabetes. To understand the molecular link between these diseases and adipocyte hypertrophy, we developed a technique to separate human adipocytes from an adipose tissue sample into populations of small cells (mean 57.6+/-3.54 microm) and large cells (mean 100.1+/-3.94 microm). Microarray analysis of the cell populations separated from adipose tissue from three subjects identified 14 genes, of which five immune-related, with more than fourfold higher expression in large cells than small cells. Two of these genes were serum amyloid A (SAA) and transmembrane 4 L six family member 1 (TM4SF1). Real-time RT-PCR analysis of SAA and TM4SF1 expression in adipocytes from seven subjects revealed 19-fold and 22-fold higher expression in the large cells, respectively, and a correlation between adipocyte size and both SAA and TM4SF1 expression. The results were verified using immunohistochemistry. In comparison with 17 other human tissues and cell types by microarray, large adipocytes displayed by far the highest SAA and TM4SF1 expression. Thus, we have identified genes with markedly higher expression in large, compared with small, human adipocytes. These genes may link hypertrophic obesity to insulin resistance/type 2 diabetes.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biochem Biophys Res Commun
                Title: Biochemical and Biophysical Research Communications
                Publisher: Academic Press
                ISSN (Print): 0006-291X
                ISSN (Electronic): 1090-2104
                Publication date PMC-release: 01 May 2009
                Publication date (Print): 01 May 2009
                Volume: 382
                Issue: 2
                Pages: 309-314
                Affiliations
                [a ]Department of Molecular and Clinical Medicine and Center for Cardiovascular and Metabolic Research, The Sahlgrenska Academy, Vita Stråket 15, 41345 Göteborg, Sweden
                [b ]Section of Genomic Medicine, Hammersmith Hospital, Imperial College London, United Kingdom
                [c ]CNRS 8090-Institute of Biology, Pasteur Institute, Lille, France
                Author notes
                [* ]Corresponding author. Fax: +46 31 418527 kajsa.sjoholm@ 123456medic.gu.se
                [1]

                These authors contributed equally to this work.

                Article
                Publisher ID: YBBRC22721
                DOI: 10.1016/j.bbrc.2009.03.014
                PMC ID: 2681012
                PubMed ID: 19275893
                SO-VID: 7a7458b4-9348-4746-b13f-08925fa8f804
                Copyright © © 2009 Elsevier Inc.
                License:

                This document may be redistributed and reused, subject to certain conditions.

                History
                Date received : 27 February 2009
                Categories
                Subject: Article

                ScienceOpen disciplines: Biochemistry
                Keywords: expression,human,microarray,adipose tissue,activin receptor-like kinase,obesity
                Data availability:
                ScienceOpen disciplines: Biochemistry
                Keywords: expression, human, microarray, adipose tissue, activin receptor-like kinase, obesity

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