PTEN Mutations as a Cause of Constitutive Insulin Sensitivity and Obesity
Evidence suggests that protection against cancer confers a risk of type 2 diabetes and vice versa. This study shows that persons susceptible to cancer owing to a constitutive mutation in the tumor-suppressor gene PTEN also have heightened sensitivity to insulin and are obese. Epidemiologic evidence...
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| Veröffentlicht in: | The New England journal of medicine 2012-09, Vol.367 (11), p.1002-1011 |
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| container_title | The New England journal of medicine |
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| creator | Pal, Aparna Barber, Thomas M Van de Bunt, Martijn Rudge, Simon A Zhang, Qifeng Lachlan, Katherine L Cooper, Nicola S Linden, Helen Levy, Jonathan C Wakelam, Michael J.O Walker, Lisa Karpe, Fredrik Gloyn, Anna L |
| description | Evidence suggests that protection against cancer confers a risk of type 2 diabetes and vice versa. This study shows that persons susceptible to cancer owing to a constitutive mutation in the tumor-suppressor gene PTEN also have heightened sensitivity to insulin and are obese.
Epidemiologic evidence for a link among type 2 diabetes, obesity, and cancer has increased interest in the idea that some antidiabetes therapies may increase the risk of susceptibility to cancer, whereas others appear to offer protection.
1
Such a link is also supported by the discovery of several susceptibility loci for type 2 diabetes and their unexpected proximity to genes implicated in cell-cycle regulation.
2
The discovery of common genetic variants that influence both the risk of cancer and the risk of type 2 diabetes, in opposite directions, suggests that the two conditions may result from defects in the same pathway.
3
– . . . |
| doi_str_mv | 10.1056/NEJMoa1113966 |
| format | Article |
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Epidemiologic evidence for a link among type 2 diabetes, obesity, and cancer has increased interest in the idea that some antidiabetes therapies may increase the risk of susceptibility to cancer, whereas others appear to offer protection.
1
Such a link is also supported by the discovery of several susceptibility loci for type 2 diabetes and their unexpected proximity to genes implicated in cell-cycle regulation.
2
The discovery of common genetic variants that influence both the risk of cancer and the risk of type 2 diabetes, in opposite directions, suggests that the two conditions may result from defects in the same pathway.
3
– . . .</description><identifier>ISSN: 0028-4793</identifier><identifier>EISSN: 1533-4406</identifier><identifier>DOI: 10.1056/NEJMoa1113966</identifier><identifier>PMID: 22970944</identifier><identifier>CODEN: NEJMAG</identifier><language>eng</language><publisher>Waltham, MA: Massachusetts Medical Society</publisher><subject>1-Phosphatidylinositol 3-kinase ; Absorptiometry ; Adiponectin - blood ; Adipose Tissue ; Adult ; Aged ; AKT protein ; Anthropomorphism ; Beta cells ; Biological and medical sciences ; Biomedical research ; Biopsy ; Body composition ; Body mass ; Body Mass Index ; Cancer ; Cell growth ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - genetics ; Epidemiology ; Female ; General aspects ; Glucose ; Glucose Tolerance Test ; Haploinsufficiency ; Humans ; Insulin ; Insulin resistance ; Insulin Resistance - genetics ; Laboratories ; Leptin - blood ; Male ; Medical sciences ; Metabolic diseases ; Metabolism ; Middle Aged ; Mutation ; Neoplasms - complications ; Neoplasms - genetics ; Obesity ; Obesity - complications ; Obesity - genetics ; Phosphatase ; Phosphorylation ; Population studies ; PTEN Phosphohydrolase - genetics ; PTEN protein ; Skinfold thickness ; Tensin ; Thyroid gland</subject><ispartof>The New England journal of medicine, 2012-09, Vol.367 (11), p.1002-1011</ispartof><rights>Copyright © 2012 Massachusetts Medical Society. All rights reserved.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Massachusetts Medical Society. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-c2d119228a19b6bf2ea9d8f5bd6f9a05c36073e03dbd8f0b917b961842af34d93</citedby><cites>FETCH-LOGICAL-c541t-c2d119228a19b6bf2ea9d8f5bd6f9a05c36073e03dbd8f0b917b961842af34d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.nejm.org/doi/pdf/10.1056/NEJMoa1113966$$EPDF$$P50$$Gmms$$H</linktopdf><linktohtml>$$Uhttps://www.nejm.org/doi/full/10.1056/NEJMoa1113966$$EHTML$$P50$$Gmms$$H</linktohtml><link.rule.ids>230,314,776,780,881,2746,2747,26080,27901,27902,52357,54039</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26324996$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22970944$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pal, Aparna</creatorcontrib><creatorcontrib>Barber, Thomas M</creatorcontrib><creatorcontrib>Van de Bunt, Martijn</creatorcontrib><creatorcontrib>Rudge, Simon A</creatorcontrib><creatorcontrib>Zhang, Qifeng</creatorcontrib><creatorcontrib>Lachlan, Katherine L</creatorcontrib><creatorcontrib>Cooper, Nicola S</creatorcontrib><creatorcontrib>Linden, Helen</creatorcontrib><creatorcontrib>Levy, Jonathan C</creatorcontrib><creatorcontrib>Wakelam, Michael J.O</creatorcontrib><creatorcontrib>Walker, Lisa</creatorcontrib><creatorcontrib>Karpe, Fredrik</creatorcontrib><creatorcontrib>Gloyn, Anna L</creatorcontrib><title>PTEN Mutations as a Cause of Constitutive Insulin Sensitivity and Obesity</title><title>The New England journal of medicine</title><addtitle>N Engl J Med</addtitle><description>Evidence suggests that protection against cancer confers a risk of type 2 diabetes and vice versa. This study shows that persons susceptible to cancer owing to a constitutive mutation in the tumor-suppressor gene PTEN also have heightened sensitivity to insulin and are obese.
Epidemiologic evidence for a link among type 2 diabetes, obesity, and cancer has increased interest in the idea that some antidiabetes therapies may increase the risk of susceptibility to cancer, whereas others appear to offer protection.
1
Such a link is also supported by the discovery of several susceptibility loci for type 2 diabetes and their unexpected proximity to genes implicated in cell-cycle regulation.
2
The discovery of common genetic variants that influence both the risk of cancer and the risk of type 2 diabetes, in opposite directions, suggests that the two conditions may result from defects in the same pathway.
3
– . . .</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Absorptiometry</subject><subject>Adiponectin - blood</subject><subject>Adipose Tissue</subject><subject>Adult</subject><subject>Aged</subject><subject>AKT protein</subject><subject>Anthropomorphism</subject><subject>Beta cells</subject><subject>Biological and medical sciences</subject><subject>Biomedical research</subject><subject>Biopsy</subject><subject>Body composition</subject><subject>Body mass</subject><subject>Body Mass Index</subject><subject>Cancer</subject><subject>Cell growth</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Epidemiology</subject><subject>Female</subject><subject>General aspects</subject><subject>Glucose</subject><subject>Glucose Tolerance Test</subject><subject>Haploinsufficiency</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Laboratories</subject><subject>Leptin - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neoplasms - complications</subject><subject>Neoplasms - genetics</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - genetics</subject><subject>Phosphatase</subject><subject>Phosphorylation</subject><subject>Population studies</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN protein</subject><subject>Skinfold thickness</subject><subject>Tensin</subject><subject>Thyroid gland</subject><issn>0028-4793</issn><issn>1533-4406</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp10d1r2zAQAHAxVpas3WNfh2AU9uJWX5atl0IJ6ZrSj8GyZ3G25U7BllpLLuS_r9am6VKYEAidftzpOIQOKTmmJJcnN_PLaw-UUq6k_ICmNOc8E4LIj2hKCCszUSg-QZ9DWJG0qFCf0IQxVRAlxBQtfi7nN_h6jBCtdwFD2ngGYzDYt3iWQtHGMdpHgxcujJ11-JdxwaaIjWsMrsG3lUn39QHaa6EL5svm3Ee_z-fL2UV2dftjMTu7yupc0JjVrKFUMVYCVZWsWmZANWWbV41sFZC85pIU3BDeVClMKkWLSklaCgYtF43i--j0Je_9WPWmqY2LA3T6frA9DGvtwerdF2f_6Dv_qAUpWE5ESvB9k2DwD6MJUfc21KbrwBk_Bk0JV2XJCyYT_faOrvw4uNTesxKsSDSp7EXVgw9hMO32M5Tov0PSO0NK_uu_HWz161QSONoACDV07QCutuHNSc6EUvLN9X3Qzqz6_xR8AhscpQw</recordid><startdate>20120913</startdate><enddate>20120913</enddate><creator>Pal, Aparna</creator><creator>Barber, Thomas M</creator><creator>Van de Bunt, Martijn</creator><creator>Rudge, Simon A</creator><creator>Zhang, Qifeng</creator><creator>Lachlan, Katherine L</creator><creator>Cooper, Nicola S</creator><creator>Linden, Helen</creator><creator>Levy, Jonathan C</creator><creator>Wakelam, Michael J.O</creator><creator>Walker, Lisa</creator><creator>Karpe, Fredrik</creator><creator>Gloyn, Anna L</creator><general>Massachusetts Medical Society</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>0TZ</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K0Y</scope><scope>LK8</scope><scope>M0R</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120913</creationdate><title>PTEN Mutations as a Cause of Constitutive Insulin Sensitivity and Obesity</title><author>Pal, Aparna ; Barber, Thomas M ; Van de Bunt, Martijn ; Rudge, Simon A ; Zhang, Qifeng ; Lachlan, Katherine L ; Cooper, Nicola S ; Linden, Helen ; Levy, Jonathan C ; Wakelam, Michael J.O ; Walker, Lisa ; Karpe, Fredrik ; Gloyn, Anna L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-c2d119228a19b6bf2ea9d8f5bd6f9a05c36073e03dbd8f0b917b961842af34d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Absorptiometry</topic><topic>Adiponectin - blood</topic><topic>Adipose Tissue</topic><topic>Adult</topic><topic>Aged</topic><topic>AKT protein</topic><topic>Anthropomorphism</topic><topic>Beta cells</topic><topic>Biological and medical sciences</topic><topic>Biomedical research</topic><topic>Biopsy</topic><topic>Body composition</topic><topic>Body mass</topic><topic>Body Mass Index</topic><topic>Cancer</topic><topic>Cell growth</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Epidemiology</topic><topic>Female</topic><topic>General aspects</topic><topic>Glucose</topic><topic>Glucose Tolerance Test</topic><topic>Haploinsufficiency</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - genetics</topic><topic>Laboratories</topic><topic>Leptin - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Neoplasms - complications</topic><topic>Neoplasms - genetics</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - genetics</topic><topic>Phosphatase</topic><topic>Phosphorylation</topic><topic>Population studies</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN protein</topic><topic>Skinfold thickness</topic><topic>Tensin</topic><topic>Thyroid gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pal, Aparna</creatorcontrib><creatorcontrib>Barber, Thomas M</creatorcontrib><creatorcontrib>Van de Bunt, Martijn</creatorcontrib><creatorcontrib>Rudge, Simon A</creatorcontrib><creatorcontrib>Zhang, Qifeng</creatorcontrib><creatorcontrib>Lachlan, Katherine L</creatorcontrib><creatorcontrib>Cooper, Nicola S</creatorcontrib><creatorcontrib>Linden, Helen</creatorcontrib><creatorcontrib>Levy, Jonathan C</creatorcontrib><creatorcontrib>Wakelam, Michael J.O</creatorcontrib><creatorcontrib>Walker, Lisa</creatorcontrib><creatorcontrib>Karpe, Fredrik</creatorcontrib><creatorcontrib>Gloyn, Anna L</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>Pharma and Biotech Premium PRO</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>New England Journal of Medicine</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The New England journal of medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pal, Aparna</au><au>Barber, Thomas M</au><au>Van de Bunt, Martijn</au><au>Rudge, Simon A</au><au>Zhang, Qifeng</au><au>Lachlan, Katherine L</au><au>Cooper, Nicola S</au><au>Linden, Helen</au><au>Levy, Jonathan C</au><au>Wakelam, Michael J.O</au><au>Walker, Lisa</au><au>Karpe, Fredrik</au><au>Gloyn, Anna L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PTEN Mutations as a Cause of Constitutive Insulin Sensitivity and Obesity</atitle><jtitle>The New England journal of medicine</jtitle><addtitle>N Engl J Med</addtitle><date>2012-09-13</date><risdate>2012</risdate><volume>367</volume><issue>11</issue><spage>1002</spage><epage>1011</epage><pages>1002-1011</pages><issn>0028-4793</issn><eissn>1533-4406</eissn><coden>NEJMAG</coden><abstract>Evidence suggests that protection against cancer confers a risk of type 2 diabetes and vice versa. This study shows that persons susceptible to cancer owing to a constitutive mutation in the tumor-suppressor gene PTEN also have heightened sensitivity to insulin and are obese.
Epidemiologic evidence for a link among type 2 diabetes, obesity, and cancer has increased interest in the idea that some antidiabetes therapies may increase the risk of susceptibility to cancer, whereas others appear to offer protection.
1
Such a link is also supported by the discovery of several susceptibility loci for type 2 diabetes and their unexpected proximity to genes implicated in cell-cycle regulation.
2
The discovery of common genetic variants that influence both the risk of cancer and the risk of type 2 diabetes, in opposite directions, suggests that the two conditions may result from defects in the same pathway.
3
– . . .</abstract><cop>Waltham, MA</cop><pub>Massachusetts Medical Society</pub><pmid>22970944</pmid><doi>10.1056/NEJMoa1113966</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The New England journal of medicine, 2012-09, Vol.367 (11), p.1002-1011 |
| issn | 0028-4793 1533-4406 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; New England Journal of Medicine |
| subjects | 1-Phosphatidylinositol 3-kinase Absorptiometry Adiponectin - blood Adipose Tissue Adult Aged AKT protein Anthropomorphism Beta cells Biological and medical sciences Biomedical research Biopsy Body composition Body mass Body Mass Index Cancer Cell growth Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - genetics Epidemiology Female General aspects Glucose Glucose Tolerance Test Haploinsufficiency Humans Insulin Insulin resistance Insulin Resistance - genetics Laboratories Leptin - blood Male Medical sciences Metabolic diseases Metabolism Middle Aged Mutation Neoplasms - complications Neoplasms - genetics Obesity Obesity - complications Obesity - genetics Phosphatase Phosphorylation Population studies PTEN Phosphohydrolase - genetics PTEN protein Skinfold thickness Tensin Thyroid gland |
| title | PTEN Mutations as a Cause of Constitutive Insulin Sensitivity and Obesity |
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