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Metabolic and Adipose Tissue Signatures in Adults With Prader-Willi Syndrome: A Model of Extreme Adiposity
Context: Prader-Willi syndrome (PWS), the most frequent syndrome of obesity, is a model of early fat mass (FM) development, but scarce data exist on adipose tissue characteristics. Objective: The objective of the study was to compare metabolic, fat distribution, and transcriptomic signatures of sc a...
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Published in: | The journal of clinical endocrinology and metabolism 2015-03, Vol.100 (3), p.850-859 |
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creator | Lacroix, Delphine Moutel, Sandrine Coupaye, Muriel Huvenne, Hélène Faucher, Pauline Pelloux, Véronique Rouault, Christine Bastard, Jean-Philippe Cagnard, Nicolas Dubern, Béatrice Clément, Karine Poitou, Christine |
description | Context:
Prader-Willi syndrome (PWS), the most frequent syndrome of obesity, is a model of early fat mass (FM) development, but scarce data exist on adipose tissue characteristics.
Objective:
The objective of the study was to compare metabolic, fat distribution, and transcriptomic signatures of sc adipose tissue (scAT) in PWS adults, with matched obese adults with primary obesities.
Main Outcomes and Measures:
Hormonal and metabolic assessments, systemic inflammation, and gene expression in scAT were compared between PWS patients and obese controls (OCs). Each 42nd PWS patient was matched with one randomly paired control with primary obesity. Matching factors were age, gender, fat mass (percentage), and diabetic status.
Results:
Compared with OCs, the PWS group had a decreased percentage of trunk FM and a better metabolic profile with decreased insulin and homeostasis model assessment, an index of insulin-resistance, and increased concentrations of serum adiponectin and ghrelin. Adipocyte size relative to body fat was significantly higher in PWS vs OCs. scAT in PWS patients was characterized by a transcriptomic functional signature with enrichment of themes related to immunoinflammation, the extracellular matrix, and angiogenesis. A RT-PCR targeted study revealed that candidate genes encoding proinflammatory markers and remodeling molecules, CD68, CD3e, IL-1β, chemokine (C-C motif) ligand 5, collagen type 4-α, and lysyl oxidase, were down-regulated.
Conclusion:
Matched for FM, PWS subjects have a better metabolic profile, a phenotype that could be linked to changes in scAT remodeling and promotion of adipocyte growth. |
doi_str_mv | 10.1210/jc.2014-3127 |
format | article |
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Prader-Willi syndrome (PWS), the most frequent syndrome of obesity, is a model of early fat mass (FM) development, but scarce data exist on adipose tissue characteristics.
Objective:
The objective of the study was to compare metabolic, fat distribution, and transcriptomic signatures of sc adipose tissue (scAT) in PWS adults, with matched obese adults with primary obesities.
Main Outcomes and Measures:
Hormonal and metabolic assessments, systemic inflammation, and gene expression in scAT were compared between PWS patients and obese controls (OCs). Each 42nd PWS patient was matched with one randomly paired control with primary obesity. Matching factors were age, gender, fat mass (percentage), and diabetic status.
Results:
Compared with OCs, the PWS group had a decreased percentage of trunk FM and a better metabolic profile with decreased insulin and homeostasis model assessment, an index of insulin-resistance, and increased concentrations of serum adiponectin and ghrelin. Adipocyte size relative to body fat was significantly higher in PWS vs OCs. scAT in PWS patients was characterized by a transcriptomic functional signature with enrichment of themes related to immunoinflammation, the extracellular matrix, and angiogenesis. A RT-PCR targeted study revealed that candidate genes encoding proinflammatory markers and remodeling molecules, CD68, CD3e, IL-1β, chemokine (C-C motif) ligand 5, collagen type 4-α, and lysyl oxidase, were down-regulated.
Conclusion:
Matched for FM, PWS subjects have a better metabolic profile, a phenotype that could be linked to changes in scAT remodeling and promotion of adipocyte growth.</description><identifier>ISSN: 0021-972X</identifier><identifier>EISSN: 1945-7197</identifier><identifier>DOI: 10.1210/jc.2014-3127</identifier><identifier>PMID: 25478934</identifier><language>eng</language><publisher>United States: Endocrine Society</publisher><subject>Adiposity - genetics ; Adolescent ; Adult ; Body Fat Distribution ; Case-Control Studies ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Female ; Gene Expression Profiling ; Humans ; Male ; Microarray Analysis ; Obesity - complications ; Obesity - genetics ; Obesity - metabolism ; Prader-Willi Syndrome - complications ; Prader-Willi Syndrome - genetics ; Prader-Willi Syndrome - metabolism ; Subcutaneous Fat - metabolism ; Transcriptome ; Young Adult</subject><ispartof>The journal of clinical endocrinology and metabolism, 2015-03, Vol.100 (3), p.850-859</ispartof><rights>Copyright © 2015 by the Endocrine Society</rights><rights>Copyright © 2015 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4181-3cf7b127f9a04d2baa7145d82d6f9b4e06f15017c760950c64312abb223ac7fc3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25478934$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lacroix, Delphine</creatorcontrib><creatorcontrib>Moutel, Sandrine</creatorcontrib><creatorcontrib>Coupaye, Muriel</creatorcontrib><creatorcontrib>Huvenne, Hélène</creatorcontrib><creatorcontrib>Faucher, Pauline</creatorcontrib><creatorcontrib>Pelloux, Véronique</creatorcontrib><creatorcontrib>Rouault, Christine</creatorcontrib><creatorcontrib>Bastard, Jean-Philippe</creatorcontrib><creatorcontrib>Cagnard, Nicolas</creatorcontrib><creatorcontrib>Dubern, Béatrice</creatorcontrib><creatorcontrib>Clément, Karine</creatorcontrib><creatorcontrib>Poitou, Christine</creatorcontrib><title>Metabolic and Adipose Tissue Signatures in Adults With Prader-Willi Syndrome: A Model of Extreme Adiposity</title><title>The journal of clinical endocrinology and metabolism</title><addtitle>J Clin Endocrinol Metab</addtitle><description>Context:
Prader-Willi syndrome (PWS), the most frequent syndrome of obesity, is a model of early fat mass (FM) development, but scarce data exist on adipose tissue characteristics.
Objective:
The objective of the study was to compare metabolic, fat distribution, and transcriptomic signatures of sc adipose tissue (scAT) in PWS adults, with matched obese adults with primary obesities.
Main Outcomes and Measures:
Hormonal and metabolic assessments, systemic inflammation, and gene expression in scAT were compared between PWS patients and obese controls (OCs). Each 42nd PWS patient was matched with one randomly paired control with primary obesity. Matching factors were age, gender, fat mass (percentage), and diabetic status.
Results:
Compared with OCs, the PWS group had a decreased percentage of trunk FM and a better metabolic profile with decreased insulin and homeostasis model assessment, an index of insulin-resistance, and increased concentrations of serum adiponectin and ghrelin. Adipocyte size relative to body fat was significantly higher in PWS vs OCs. scAT in PWS patients was characterized by a transcriptomic functional signature with enrichment of themes related to immunoinflammation, the extracellular matrix, and angiogenesis. A RT-PCR targeted study revealed that candidate genes encoding proinflammatory markers and remodeling molecules, CD68, CD3e, IL-1β, chemokine (C-C motif) ligand 5, collagen type 4-α, and lysyl oxidase, were down-regulated.
Conclusion:
Matched for FM, PWS subjects have a better metabolic profile, a phenotype that could be linked to changes in scAT remodeling and promotion of adipocyte growth.</description><subject>Adiposity - genetics</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Body Fat Distribution</subject><subject>Case-Control Studies</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Female</subject><subject>Gene Expression Profiling</subject><subject>Humans</subject><subject>Male</subject><subject>Microarray Analysis</subject><subject>Obesity - complications</subject><subject>Obesity - genetics</subject><subject>Obesity - metabolism</subject><subject>Prader-Willi Syndrome - complications</subject><subject>Prader-Willi Syndrome - genetics</subject><subject>Prader-Willi Syndrome - metabolism</subject><subject>Subcutaneous Fat - metabolism</subject><subject>Transcriptome</subject><subject>Young Adult</subject><issn>0021-972X</issn><issn>1945-7197</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNptkM9rFDEUx4Modq3ePEuOHkzNr5nseFtK_QEtCq3UW8gkb9yMmck2yVD3vzfLrp4MPEJ4n_cl74PQa0YvGGf0_WgvOGWSCMbVE7RinWyIYp16ilaUckY6xX-coRc5j7RishHP0RlvpFp3Qq7QeAPF9DF4i83s8Mb5XcyA73zOC-Bb_3M2ZUmQsZ9rcwkl43tftvhbMg4SufcheHy7n12KE3zAG3wTHQQcB3z1uySY4BTpy_4lejaYkOHV6T5H3z9e3V1-JtdfP3253FwTK9maEWEH1dddhs5Q6XhvjGKycWvu2qHrJdB2YA1lyqqWdg21raybm77nXBirBivO0dtj7i7FhwVy0ZPPFkIwM8Qla9Y2SnDBlarouyNqU8w5waB3yU8m7TWj-mBXj1Yf7OqD3Yq_OSUv_QTuH_xXZwXkEXiMoUDKv8LyCElvwYSy1bQe2ao1qYkNFfVFajFWx8RxDGYXbfIz7KryrMe4pLmq-v9v_gDNLpVO</recordid><startdate>201503</startdate><enddate>201503</enddate><creator>Lacroix, Delphine</creator><creator>Moutel, Sandrine</creator><creator>Coupaye, Muriel</creator><creator>Huvenne, Hélène</creator><creator>Faucher, Pauline</creator><creator>Pelloux, Véronique</creator><creator>Rouault, Christine</creator><creator>Bastard, Jean-Philippe</creator><creator>Cagnard, Nicolas</creator><creator>Dubern, Béatrice</creator><creator>Clément, Karine</creator><creator>Poitou, Christine</creator><general>Endocrine Society</general><general>Copyright by The Endocrine Society</general><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></search><sort><creationdate>201503</creationdate><title>Metabolic and Adipose Tissue Signatures in Adults With Prader-Willi Syndrome: A Model of Extreme Adiposity</title><author>Lacroix, Delphine ; Moutel, Sandrine ; Coupaye, Muriel ; Huvenne, Hélène ; Faucher, Pauline ; Pelloux, Véronique ; Rouault, Christine ; Bastard, Jean-Philippe ; Cagnard, Nicolas ; Dubern, Béatrice ; Clément, Karine ; Poitou, Christine</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4181-3cf7b127f9a04d2baa7145d82d6f9b4e06f15017c760950c64312abb223ac7fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adiposity - genetics</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Body Fat Distribution</topic><topic>Case-Control Studies</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Female</topic><topic>Gene Expression Profiling</topic><topic>Humans</topic><topic>Male</topic><topic>Microarray Analysis</topic><topic>Obesity - complications</topic><topic>Obesity - genetics</topic><topic>Obesity - metabolism</topic><topic>Prader-Willi Syndrome - complications</topic><topic>Prader-Willi Syndrome - genetics</topic><topic>Prader-Willi Syndrome - metabolism</topic><topic>Subcutaneous Fat - metabolism</topic><topic>Transcriptome</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lacroix, Delphine</creatorcontrib><creatorcontrib>Moutel, Sandrine</creatorcontrib><creatorcontrib>Coupaye, Muriel</creatorcontrib><creatorcontrib>Huvenne, Hélène</creatorcontrib><creatorcontrib>Faucher, Pauline</creatorcontrib><creatorcontrib>Pelloux, Véronique</creatorcontrib><creatorcontrib>Rouault, Christine</creatorcontrib><creatorcontrib>Bastard, Jean-Philippe</creatorcontrib><creatorcontrib>Cagnard, Nicolas</creatorcontrib><creatorcontrib>Dubern, Béatrice</creatorcontrib><creatorcontrib>Clément, Karine</creatorcontrib><creatorcontrib>Poitou, Christine</creatorcontrib><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><jtitle>The journal of clinical endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lacroix, Delphine</au><au>Moutel, Sandrine</au><au>Coupaye, Muriel</au><au>Huvenne, Hélène</au><au>Faucher, Pauline</au><au>Pelloux, Véronique</au><au>Rouault, Christine</au><au>Bastard, Jean-Philippe</au><au>Cagnard, Nicolas</au><au>Dubern, Béatrice</au><au>Clément, Karine</au><au>Poitou, Christine</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabolic and Adipose Tissue Signatures in Adults With Prader-Willi Syndrome: A Model of Extreme Adiposity</atitle><jtitle>The journal of clinical endocrinology and metabolism</jtitle><addtitle>J Clin Endocrinol Metab</addtitle><date>2015-03</date><risdate>2015</risdate><volume>100</volume><issue>3</issue><spage>850</spage><epage>859</epage><pages>850-859</pages><issn>0021-972X</issn><eissn>1945-7197</eissn><abstract>Context:
Prader-Willi syndrome (PWS), the most frequent syndrome of obesity, is a model of early fat mass (FM) development, but scarce data exist on adipose tissue characteristics.
Objective:
The objective of the study was to compare metabolic, fat distribution, and transcriptomic signatures of sc adipose tissue (scAT) in PWS adults, with matched obese adults with primary obesities.
Main Outcomes and Measures:
Hormonal and metabolic assessments, systemic inflammation, and gene expression in scAT were compared between PWS patients and obese controls (OCs). Each 42nd PWS patient was matched with one randomly paired control with primary obesity. Matching factors were age, gender, fat mass (percentage), and diabetic status.
Results:
Compared with OCs, the PWS group had a decreased percentage of trunk FM and a better metabolic profile with decreased insulin and homeostasis model assessment, an index of insulin-resistance, and increased concentrations of serum adiponectin and ghrelin. Adipocyte size relative to body fat was significantly higher in PWS vs OCs. scAT in PWS patients was characterized by a transcriptomic functional signature with enrichment of themes related to immunoinflammation, the extracellular matrix, and angiogenesis. A RT-PCR targeted study revealed that candidate genes encoding proinflammatory markers and remodeling molecules, CD68, CD3e, IL-1β, chemokine (C-C motif) ligand 5, collagen type 4-α, and lysyl oxidase, were down-regulated.
Conclusion:
Matched for FM, PWS subjects have a better metabolic profile, a phenotype that could be linked to changes in scAT remodeling and promotion of adipocyte growth.</abstract><cop>United States</cop><pub>Endocrine Society</pub><pmid>25478934</pmid><doi>10.1210/jc.2014-3127</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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source | Oxford Journals Online |
subjects | Adiposity - genetics Adolescent Adult Body Fat Distribution Case-Control Studies Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Female Gene Expression Profiling Humans Male Microarray Analysis Obesity - complications Obesity - genetics Obesity - metabolism Prader-Willi Syndrome - complications Prader-Willi Syndrome - genetics Prader-Willi Syndrome - metabolism Subcutaneous Fat - metabolism Transcriptome Young Adult |
title | Metabolic and Adipose Tissue Signatures in Adults With Prader-Willi Syndrome: A Model of Extreme Adiposity |
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