Hypoxia increases leptin expression in human PAZ6 adipose cells
Leptin, an adipose tissue-derived cytokine involved in the control of body weight, also participates in a variety of biological functions, including angiogenesis. Because reduced oxygen availability is a major inducer of angiogenesis, we hypothesized that low cellular oxygen tension could regulate l...
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description | Leptin, an adipose tissue-derived cytokine involved in the control of body weight, also participates in a variety of biological functions, including angiogenesis. Because reduced oxygen availability is a major inducer of angiogenesis, we hypothesized that low cellular oxygen tension could regulate leptin expression in adipose cells.
Differentiated PAZ6 adipocytes were cultured for 48 h in the presence of chemical inducers of cellular hypoxia (cobalt chloride or desferrioxamine) or in an atmosphere containing only 6% oxygen. The effect of hypoxia on the expression of leptin and several adipose genes was assessed by semi-quantitative RT-PCR. The effect of hypoxia on leptin promoter activity was tested in PAZ6 cells transiently transfected with a luciferase reporter construct, containing 1.87 kb of the human leptin promoter. Leptin secretion in the culture medium was determined by radioimmunoassay.
Hypoxia increased leptin mRNA expression, leptin promoter activity and leptin secretion in the culture medium by two- to threefold ( p |
doi_str_mv | 10.1007/s00125-002-0804-y |
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Differentiated PAZ6 adipocytes were cultured for 48 h in the presence of chemical inducers of cellular hypoxia (cobalt chloride or desferrioxamine) or in an atmosphere containing only 6% oxygen. The effect of hypoxia on the expression of leptin and several adipose genes was assessed by semi-quantitative RT-PCR. The effect of hypoxia on leptin promoter activity was tested in PAZ6 cells transiently transfected with a luciferase reporter construct, containing 1.87 kb of the human leptin promoter. Leptin secretion in the culture medium was determined by radioimmunoassay.
Hypoxia increased leptin mRNA expression, leptin promoter activity and leptin secretion in the culture medium by two- to threefold ( p<0.05). The expression of the glucose transporter isoform 1 (GLUT-1) mRNA, a well known hypoxia inducible gene, was also increased. In contrast, glucose transporter isoform 4 (GLUT-4), hormone sensitive lipase (HSL), fatty acid binding protein (aP2) and uncoupling protein 2 (UCP2) mRNAs were markedly reduced by hypoxia. In addition, a similar hypoxia-induced increase in leptin mRNA and secretion was observed in primary rat adipose cells.
Hypoxia markedly and specifically increased leptin gene expression through activation of the leptin gene promoter, and this resulted in an increased leptin production by human PAZ6 adipocytes.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-002-0804-y</identifier><identifier>PMID: 12032628</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Adipose Tissue - metabolism ; Biological and medical sciences ; Cell Hypoxia - physiology ; Cell Line ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation ; Glucose Transporter Type 1 ; Humans ; Leptin - genetics ; Life Sciences ; Monosaccharide Transport Proteins - genetics ; Protein Isoforms - genetics ; RNA, Messenger - genetics ; Transcription, Genetic ; Vertebrates: skin, associated glands, phaneres, light organs, various exocrine glands (salt gland, uropygial gland...), adipose tissue, connective tissue</subject><ispartof>Diabetologia, 2002-04, Vol.45 (4), p.527-530</ispartof><rights>2002 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-6a1df0c96af705826456089694eb0d08cac1c197ca8305cee94c48c55f142c4f3</citedby><orcidid>0000-0002-9508-036X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13654066$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12032628$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-03972875$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>GROSFELD, A</creatorcontrib><creatorcontrib>ZILBERFARB, V</creatorcontrib><creatorcontrib>TURBAN, S</creatorcontrib><creatorcontrib>ANDRE, J</creatorcontrib><creatorcontrib>GUERRE-MILLO, M</creatorcontrib><creatorcontrib>ISSAD, T</creatorcontrib><title>Hypoxia increases leptin expression in human PAZ6 adipose cells</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><description>Leptin, an adipose tissue-derived cytokine involved in the control of body weight, also participates in a variety of biological functions, including angiogenesis. Because reduced oxygen availability is a major inducer of angiogenesis, we hypothesized that low cellular oxygen tension could regulate leptin expression in adipose cells.
Differentiated PAZ6 adipocytes were cultured for 48 h in the presence of chemical inducers of cellular hypoxia (cobalt chloride or desferrioxamine) or in an atmosphere containing only 6% oxygen. The effect of hypoxia on the expression of leptin and several adipose genes was assessed by semi-quantitative RT-PCR. The effect of hypoxia on leptin promoter activity was tested in PAZ6 cells transiently transfected with a luciferase reporter construct, containing 1.87 kb of the human leptin promoter. Leptin secretion in the culture medium was determined by radioimmunoassay.
Hypoxia increased leptin mRNA expression, leptin promoter activity and leptin secretion in the culture medium by two- to threefold ( p<0.05). The expression of the glucose transporter isoform 1 (GLUT-1) mRNA, a well known hypoxia inducible gene, was also increased. In contrast, glucose transporter isoform 4 (GLUT-4), hormone sensitive lipase (HSL), fatty acid binding protein (aP2) and uncoupling protein 2 (UCP2) mRNAs were markedly reduced by hypoxia. In addition, a similar hypoxia-induced increase in leptin mRNA and secretion was observed in primary rat adipose cells.
Hypoxia markedly and specifically increased leptin gene expression through activation of the leptin gene promoter, and this resulted in an increased leptin production by human PAZ6 adipocytes.</description><subject>Adipose Tissue - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell Hypoxia - physiology</subject><subject>Cell Line</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation</subject><subject>Glucose Transporter Type 1</subject><subject>Humans</subject><subject>Leptin - genetics</subject><subject>Life Sciences</subject><subject>Monosaccharide Transport Proteins - genetics</subject><subject>Protein Isoforms - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>Transcription, Genetic</subject><subject>Vertebrates: skin, associated glands, phaneres, light organs, various exocrine glands (salt gland, uropygial gland...), adipose tissue, connective tissue</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFFLwzAQx4Mobk4_gC_SFwUfqpc0SdMnGUOdMNAHBfElZGnKIl1be6us396WFsc9hMv97s_xI-SSwh0FiO8RgDIRArAQFPCwPSJTyqOu40wdk2k_DqmSnxNyhvgNAJHg8pRMKIOISaam5GHZVuXem8AXtnYGHQa5q3a-CNy-qh2iL4tuFmyarSmCt_mXDEzqqxJdYF2e4zk5yUyO7mJ8Z-Tj6fF9sQxXr88vi_kqtDyGXSgNTTOwiTRZDEIxyYUElciEuzWkoKyx1NIktkZFIKxzCbdcWSEyypnlWTQjt0PuxuS6qv3W1K0ujdfL-Ur3fxAlMVOx-KUdezOwVV3-NA53euuxv9YUrmxQx7QrFvcgHUBbl4i1y_6TKejesB4M686w7g3rttu5GsOb9dalh41RaQdcj4BBa_KsNoX1eOAiKThIGf0Bc6qB1Q</recordid><startdate>20020401</startdate><enddate>20020401</enddate><creator>GROSFELD, A</creator><creator>ZILBERFARB, V</creator><creator>TURBAN, S</creator><creator>ANDRE, J</creator><creator>GUERRE-MILLO, M</creator><creator>ISSAD, T</creator><general>Springer</general><general>Springer Verlag</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-9508-036X</orcidid></search><sort><creationdate>20020401</creationdate><title>Hypoxia increases leptin expression in human PAZ6 adipose cells</title><author>GROSFELD, A ; ZILBERFARB, V ; TURBAN, S ; ANDRE, J ; GUERRE-MILLO, M ; ISSAD, T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-6a1df0c96af705826456089694eb0d08cac1c197ca8305cee94c48c55f142c4f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adipose Tissue - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cell Hypoxia - physiology</topic><topic>Cell Line</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation</topic><topic>Glucose Transporter Type 1</topic><topic>Humans</topic><topic>Leptin - genetics</topic><topic>Life Sciences</topic><topic>Monosaccharide Transport Proteins - genetics</topic><topic>Protein Isoforms - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>Transcription, Genetic</topic><topic>Vertebrates: skin, associated glands, phaneres, light organs, various exocrine glands (salt gland, uropygial gland...), adipose tissue, connective tissue</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GROSFELD, A</creatorcontrib><creatorcontrib>ZILBERFARB, V</creatorcontrib><creatorcontrib>TURBAN, S</creatorcontrib><creatorcontrib>ANDRE, J</creatorcontrib><creatorcontrib>GUERRE-MILLO, M</creatorcontrib><creatorcontrib>ISSAD, T</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GROSFELD, A</au><au>ZILBERFARB, V</au><au>TURBAN, S</au><au>ANDRE, J</au><au>GUERRE-MILLO, M</au><au>ISSAD, T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypoxia increases leptin expression in human PAZ6 adipose cells</atitle><jtitle>Diabetologia</jtitle><addtitle>Diabetologia</addtitle><date>2002-04-01</date><risdate>2002</risdate><volume>45</volume><issue>4</issue><spage>527</spage><epage>530</epage><pages>527-530</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Leptin, an adipose tissue-derived cytokine involved in the control of body weight, also participates in a variety of biological functions, including angiogenesis. Because reduced oxygen availability is a major inducer of angiogenesis, we hypothesized that low cellular oxygen tension could regulate leptin expression in adipose cells.
Differentiated PAZ6 adipocytes were cultured for 48 h in the presence of chemical inducers of cellular hypoxia (cobalt chloride or desferrioxamine) or in an atmosphere containing only 6% oxygen. The effect of hypoxia on the expression of leptin and several adipose genes was assessed by semi-quantitative RT-PCR. The effect of hypoxia on leptin promoter activity was tested in PAZ6 cells transiently transfected with a luciferase reporter construct, containing 1.87 kb of the human leptin promoter. Leptin secretion in the culture medium was determined by radioimmunoassay.
Hypoxia increased leptin mRNA expression, leptin promoter activity and leptin secretion in the culture medium by two- to threefold ( p<0.05). The expression of the glucose transporter isoform 1 (GLUT-1) mRNA, a well known hypoxia inducible gene, was also increased. In contrast, glucose transporter isoform 4 (GLUT-4), hormone sensitive lipase (HSL), fatty acid binding protein (aP2) and uncoupling protein 2 (UCP2) mRNAs were markedly reduced by hypoxia. In addition, a similar hypoxia-induced increase in leptin mRNA and secretion was observed in primary rat adipose cells.
Hypoxia markedly and specifically increased leptin gene expression through activation of the leptin gene promoter, and this resulted in an increased leptin production by human PAZ6 adipocytes.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>12032628</pmid><doi>10.1007/s00125-002-0804-y</doi><tpages>4</tpages><orcidid>https://orcid.org/0000-0002-9508-036X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adipose Tissue - metabolism Biological and medical sciences Cell Hypoxia - physiology Cell Line Fundamental and applied biological sciences. Psychology Gene Expression Regulation Glucose Transporter Type 1 Humans Leptin - genetics Life Sciences Monosaccharide Transport Proteins - genetics Protein Isoforms - genetics RNA, Messenger - genetics Transcription, Genetic Vertebrates: skin, associated glands, phaneres, light organs, various exocrine glands (salt gland, uropygial gland...), adipose tissue, connective tissue |
title | Hypoxia increases leptin expression in human PAZ6 adipose cells |
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