Adipose-specific deletion of Src homology phosphatase 2 does not significantly alter systemic glucose homeostasis
Abstract The SH2 domain-containing protein-tyrosine phosphatase Src homology phosphatase 2 (Shp2) has been implicated in a variety of growth factor signaling pathways, but its metabolic role in some peripheral insulin-responsive tissues remains unknown. To address the metabolic function of Shp2 in a...
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| Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2011-08, Vol.60 (8), p.1193-1201 |
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| container_title | Metabolism, clinical and experimental |
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| creator | Bettaieb, Ahmed Matsuo, Kosuke Matsuo, Izumi Nagata, Naoto Chahed, Samah Liu, Siming Haj, Fawaz G |
| description | Abstract The SH2 domain-containing protein-tyrosine phosphatase Src homology phosphatase 2 (Shp2) has been implicated in a variety of growth factor signaling pathways, but its metabolic role in some peripheral insulin-responsive tissues remains unknown. To address the metabolic function of Shp2 in adipose tissue, we generated mice with adipose-specific Shp2 deletion using adiponectin-Cre transgenic mice. We then analyzed insulin sensitivity, glucose tolerance, and body mass in adipose-specific Shp2-deficient and control mice on regular chow and high-fat diet (HFD). Control mice on HFD exhibited increased Shp2 expression in various adipose depots compared with those on regular chow. Adiponectin-Cre mice enabled efficient and specific deletion of Shp2 in adipose tissue. However, adipose Shp2 deletion did not significantly alter body mass in mice on chow or HFD. In addition, mice with adipose Shp2 deletion exhibited comparable insulin sensitivity and glucose tolerance compared with controls. Consistent with this, basal and insulin-stimulated Erk and Akt phosphorylations were comparable in adipose tissue of Shp2-deficient and control mice. Our findings indicate that adipose-specific Shp2 deletion does not significantly alter systemic insulin sensitivity and glucose homeostasis. |
| doi_str_mv | 10.1016/j.metabol.2011.01.004 |
| format | Article |
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To address the metabolic function of Shp2 in adipose tissue, we generated mice with adipose-specific Shp2 deletion using adiponectin-Cre transgenic mice. We then analyzed insulin sensitivity, glucose tolerance, and body mass in adipose-specific Shp2-deficient and control mice on regular chow and high-fat diet (HFD). Control mice on HFD exhibited increased Shp2 expression in various adipose depots compared with those on regular chow. Adiponectin-Cre mice enabled efficient and specific deletion of Shp2 in adipose tissue. However, adipose Shp2 deletion did not significantly alter body mass in mice on chow or HFD. In addition, mice with adipose Shp2 deletion exhibited comparable insulin sensitivity and glucose tolerance compared with controls. Consistent with this, basal and insulin-stimulated Erk and Akt phosphorylations were comparable in adipose tissue of Shp2-deficient and control mice. Our findings indicate that adipose-specific Shp2 deletion does not significantly alter systemic insulin sensitivity and glucose homeostasis.</description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/j.metabol.2011.01.004</identifier><identifier>PMID: 21353259</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adipose Tissue - metabolism ; Animals ; Biological and medical sciences ; Endocrinology & Metabolism ; Feeding. Feeding behavior ; Fundamental and applied biological sciences. Psychology ; Glucose - genetics ; Glucose - metabolism ; Homeostasis - genetics ; Insulin - genetics ; Insulin - metabolism ; Insulin Resistance - genetics ; Mice ; Mice, Transgenic ; Phosphorylation ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - genetics ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Metabolism, clinical and experimental, 2011-08, Vol.60 (8), p.1193-1201</ispartof><rights>2011</rights><rights>2015 INIST-CNRS</rights><rights>Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c551t-a5bf93e75713eebf389ca2976599a295f7a0fb147505c4103db2bb45aa8cbc4a3</citedby><cites>FETCH-LOGICAL-c551t-a5bf93e75713eebf389ca2976599a295f7a0fb147505c4103db2bb45aa8cbc4a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0026049511000060$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24392820$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21353259$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bettaieb, Ahmed</creatorcontrib><creatorcontrib>Matsuo, Kosuke</creatorcontrib><creatorcontrib>Matsuo, Izumi</creatorcontrib><creatorcontrib>Nagata, Naoto</creatorcontrib><creatorcontrib>Chahed, Samah</creatorcontrib><creatorcontrib>Liu, Siming</creatorcontrib><creatorcontrib>Haj, Fawaz G</creatorcontrib><title>Adipose-specific deletion of Src homology phosphatase 2 does not significantly alter systemic glucose homeostasis</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description>Abstract The SH2 domain-containing protein-tyrosine phosphatase Src homology phosphatase 2 (Shp2) has been implicated in a variety of growth factor signaling pathways, but its metabolic role in some peripheral insulin-responsive tissues remains unknown. To address the metabolic function of Shp2 in adipose tissue, we generated mice with adipose-specific Shp2 deletion using adiponectin-Cre transgenic mice. We then analyzed insulin sensitivity, glucose tolerance, and body mass in adipose-specific Shp2-deficient and control mice on regular chow and high-fat diet (HFD). Control mice on HFD exhibited increased Shp2 expression in various adipose depots compared with those on regular chow. Adiponectin-Cre mice enabled efficient and specific deletion of Shp2 in adipose tissue. However, adipose Shp2 deletion did not significantly alter body mass in mice on chow or HFD. In addition, mice with adipose Shp2 deletion exhibited comparable insulin sensitivity and glucose tolerance compared with controls. Consistent with this, basal and insulin-stimulated Erk and Akt phosphorylations were comparable in adipose tissue of Shp2-deficient and control mice. Our findings indicate that adipose-specific Shp2 deletion does not significantly alter systemic insulin sensitivity and glucose homeostasis.</description><subject>Adipose Tissue - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Endocrinology & Metabolism</subject><subject>Feeding. Feeding behavior</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glucose - genetics</subject><subject>Glucose - metabolism</subject><subject>Homeostasis - genetics</subject><subject>Insulin - genetics</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance - genetics</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Phosphorylation</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - genetics</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFksuLFDEQxoMo7jj6Jyh9kT31mEenH5eVZfEFCx5WzyGdrp7JmE56U5mF-e9NM-P6uAgFdcjv-1LUV4S8ZnTDKKvf7TcTJN0Ht-GUsQ3NRasnZMWk4GVbU_qUrCjldUmrTl6QF4h7SmnTtPVzcsGZyJjsVuT-erBzQChxBmNHa4oBHCQbfBHG4i6aYhem4ML2WMy7gPNOJ41Q8GIIgIUPqUC79YtQ--SOhXYJYoFHTDBls607mOy-mEDALLX4kjwbtUN4de5r8v3jh283n8vbr5--3FzflkZKlkot-7ET0MiGCYB-FG1nNO-aWnZd7nJsNB17VjWSSlMxKoae930ltW5Nbyot1uTq5Dsf-gkGAz5F7dQc7aTjUQVt1d8v3u7UNjyoqhJCZMM1uTwbxHB_AExqsmjAOe0hHFC1TdtyXlddJuWJNDEgRhgff2FULWmpvTqnpZa0FM1Fq6x78-eIj6pf8WTg7RnQaLQbo_bG4m-uEh1v-TLq-xMHeaEPFqJCY8EbGGwEk9QQ7H9HufrHwTjrc6ruBxwB9-EQfU5LMYVcUXW3nNZyWYzlq6I1FT8B9_HOKQ</recordid><startdate>20110801</startdate><enddate>20110801</enddate><creator>Bettaieb, Ahmed</creator><creator>Matsuo, Kosuke</creator><creator>Matsuo, Izumi</creator><creator>Nagata, Naoto</creator><creator>Chahed, Samah</creator><creator>Liu, Siming</creator><creator>Haj, Fawaz G</creator><general>Elsevier Inc</general><general>Elsevier</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>5PM</scope></search><sort><creationdate>20110801</creationdate><title>Adipose-specific deletion of Src homology phosphatase 2 does not significantly alter systemic glucose homeostasis</title><author>Bettaieb, Ahmed ; Matsuo, Kosuke ; Matsuo, Izumi ; Nagata, Naoto ; Chahed, Samah ; Liu, Siming ; Haj, Fawaz G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c551t-a5bf93e75713eebf389ca2976599a295f7a0fb147505c4103db2bb45aa8cbc4a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adipose Tissue - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Endocrinology & Metabolism</topic><topic>Feeding. Feeding behavior</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glucose - genetics</topic><topic>Glucose - metabolism</topic><topic>Homeostasis - genetics</topic><topic>Insulin - genetics</topic><topic>Insulin - metabolism</topic><topic>Insulin Resistance - genetics</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Phosphorylation</topic><topic>Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics</topic><topic>Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - genetics</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bettaieb, Ahmed</creatorcontrib><creatorcontrib>Matsuo, Kosuke</creatorcontrib><creatorcontrib>Matsuo, Izumi</creatorcontrib><creatorcontrib>Nagata, Naoto</creatorcontrib><creatorcontrib>Chahed, Samah</creatorcontrib><creatorcontrib>Liu, Siming</creatorcontrib><creatorcontrib>Haj, Fawaz G</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>PubMed Central (Full Participant titles)</collection><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bettaieb, Ahmed</au><au>Matsuo, Kosuke</au><au>Matsuo, Izumi</au><au>Nagata, Naoto</au><au>Chahed, Samah</au><au>Liu, Siming</au><au>Haj, Fawaz G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adipose-specific deletion of Src homology phosphatase 2 does not significantly alter systemic glucose homeostasis</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>2011-08-01</date><risdate>2011</risdate><volume>60</volume><issue>8</issue><spage>1193</spage><epage>1201</epage><pages>1193-1201</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract>Abstract The SH2 domain-containing protein-tyrosine phosphatase Src homology phosphatase 2 (Shp2) has been implicated in a variety of growth factor signaling pathways, but its metabolic role in some peripheral insulin-responsive tissues remains unknown. To address the metabolic function of Shp2 in adipose tissue, we generated mice with adipose-specific Shp2 deletion using adiponectin-Cre transgenic mice. We then analyzed insulin sensitivity, glucose tolerance, and body mass in adipose-specific Shp2-deficient and control mice on regular chow and high-fat diet (HFD). Control mice on HFD exhibited increased Shp2 expression in various adipose depots compared with those on regular chow. Adiponectin-Cre mice enabled efficient and specific deletion of Shp2 in adipose tissue. However, adipose Shp2 deletion did not significantly alter body mass in mice on chow or HFD. In addition, mice with adipose Shp2 deletion exhibited comparable insulin sensitivity and glucose tolerance compared with controls. Consistent with this, basal and insulin-stimulated Erk and Akt phosphorylations were comparable in adipose tissue of Shp2-deficient and control mice. Our findings indicate that adipose-specific Shp2 deletion does not significantly alter systemic insulin sensitivity and glucose homeostasis.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>21353259</pmid><doi>10.1016/j.metabol.2011.01.004</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adipose Tissue - metabolism Animals Biological and medical sciences Endocrinology & Metabolism Feeding. Feeding behavior Fundamental and applied biological sciences. Psychology Glucose - genetics Glucose - metabolism Homeostasis - genetics Insulin - genetics Insulin - metabolism Insulin Resistance - genetics Mice Mice, Transgenic Phosphorylation Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - genetics Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Adipose-specific deletion of Src homology phosphatase 2 does not significantly alter systemic glucose homeostasis |
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