Investigation of PNPLA3 and IL28B Genotypes on Diabetes and Obesity After Liver Transplantation: Insight Into Mechanisms of Disease
To identify genetic risks for obesity and diabetes postliver transplantation (LT), LT recipients underwent genotyping for IL28B rs12979860 (n = 295) and PNPLA3 rs738409 (n = 205) polymorphism in both donors and recipients. The development of obesity and diabetes/impaired fasting glucose (IFG) was de...
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container_title | American journal of transplantation |
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creator | Watt, K. D. Dierkhising, R. Fan, C. Heimbach, J. K. Tillman, H. Goldstein, D. Thompson, A. Krishnan, A. Charlton, M. R. |
description | To identify genetic risks for obesity and diabetes postliver transplantation (LT), LT recipients underwent genotyping for IL28B rs12979860 (n = 295) and PNPLA3 rs738409 (n = 205) polymorphism in both donors and recipients. The development of obesity and diabetes/impaired fasting glucose (IFG) was determined 1–5 years post‐LT. Recipient PNPLA‐3 genotype was independently associated with obesity (BMI > 30) at 3 years posttransplant (genotype CC 33.7%, CG 48.3% and GG 82.4%, p = 0.002), with an odds ratio (OR 2.54, CI 1.38–4.66, p = 0.003), associated with the G allele. Diabetes/IFG diagnosed within 5 years posttransplant associated with PNPLA‐3 non‐CC genotype (HR 1.59, 1.12–2.26, p = 0.010), but not IL28B TT genotype (HR 1.46, 0.94–2.27, p = 0.092). No genotype variable was independently predictive of diabetes/IFG. The combination of PNPLA‐3 non‐CC and IL28B TT genotype was associated with increased risk of diabetes/IFG compared to PNPLA‐3 CC, IL28B non‐TT (HR 2.64, CI 1.30–5.39, p = 0.008). Donor genotypes were not associated with any of the outcomes analyzed. In conclusion, PNPLA‐3 non‐CC genotype is associated with posttransplant obesity but not independently with diabetes/IFG. The lack of donor related risk suggests a peripheral rather than central mechanism of insulin resistance in liver transplant recipients.
Analysis of donor and recipient genetic risk factors for obesity and diabetes after transplant finds that recipient, but not donor, PNPLA‐3 G allele is independently associated with obesity after liver transplantation, pointing to a peripheral rather than central mechanism of action and explaining some of the risk for posttransplant obesity. |
doi_str_mv | 10.1111/ajt.12355 |
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Analysis of donor and recipient genetic risk factors for obesity and diabetes after transplant finds that recipient, but not donor, PNPLA‐3 G allele is independently associated with obesity after liver transplantation, pointing to a peripheral rather than central mechanism of action and explaining some of the risk for posttransplant obesity.</description><identifier>ISSN: 1600-6135</identifier><identifier>EISSN: 1600-6143</identifier><identifier>DOI: 10.1111/ajt.12355</identifier><identifier>PMID: 23859071</identifier><language>eng</language><publisher>Hoboken, NJ: Wiley</publisher><subject>Adult ; Biological and medical sciences ; Diabetes ; Diabetes Mellitus - genetics ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; genetic risk ; Health risk assessment ; Humans ; insulin resistance ; Insulin Resistance - genetics ; Interferons ; Interleukins - genetics ; Lipase - genetics ; liver transplant ; Liver Transplantation - adverse effects ; Liver, biliary tract, pancreas, portal circulation, spleen ; Medical sciences ; Membrane Proteins - genetics ; Metabolic diseases ; Middle Aged ; Obesity ; Obesity - genetics ; Polymorphism, Single Nucleotide ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the digestive system ; Tissue Donors ; Transplants & implants</subject><ispartof>American journal of transplantation, 2013-09, Vol.13 (9), p.2450-2457</ispartof><rights>Copyright 2013 The American Society of Transplantation and the American Society of Transplant Surgeons</rights><rights>2014 INIST-CNRS</rights><rights>Copyright 2013 The American Society of Transplantation and the American Society of Transplant Surgeons.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4515-3fe7cd759467587cb432a268501a4996f16c672dd442997d084fe824189e8fca3</citedby><cites>FETCH-LOGICAL-c4515-3fe7cd759467587cb432a268501a4996f16c672dd442997d084fe824189e8fca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fajt.12355$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fajt.12355$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27864161$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23859071$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Watt, K. D.</creatorcontrib><creatorcontrib>Dierkhising, R.</creatorcontrib><creatorcontrib>Fan, C.</creatorcontrib><creatorcontrib>Heimbach, J. K.</creatorcontrib><creatorcontrib>Tillman, H.</creatorcontrib><creatorcontrib>Goldstein, D.</creatorcontrib><creatorcontrib>Thompson, A.</creatorcontrib><creatorcontrib>Krishnan, A.</creatorcontrib><creatorcontrib>Charlton, M. R.</creatorcontrib><title>Investigation of PNPLA3 and IL28B Genotypes on Diabetes and Obesity After Liver Transplantation: Insight Into Mechanisms of Disease</title><title>American journal of transplantation</title><addtitle>Am J Transplant</addtitle><description>To identify genetic risks for obesity and diabetes postliver transplantation (LT), LT recipients underwent genotyping for IL28B rs12979860 (n = 295) and PNPLA3 rs738409 (n = 205) polymorphism in both donors and recipients. The development of obesity and diabetes/impaired fasting glucose (IFG) was determined 1–5 years post‐LT. Recipient PNPLA‐3 genotype was independently associated with obesity (BMI > 30) at 3 years posttransplant (genotype CC 33.7%, CG 48.3% and GG 82.4%, p = 0.002), with an odds ratio (OR 2.54, CI 1.38–4.66, p = 0.003), associated with the G allele. Diabetes/IFG diagnosed within 5 years posttransplant associated with PNPLA‐3 non‐CC genotype (HR 1.59, 1.12–2.26, p = 0.010), but not IL28B TT genotype (HR 1.46, 0.94–2.27, p = 0.092). No genotype variable was independently predictive of diabetes/IFG. The combination of PNPLA‐3 non‐CC and IL28B TT genotype was associated with increased risk of diabetes/IFG compared to PNPLA‐3 CC, IL28B non‐TT (HR 2.64, CI 1.30–5.39, p = 0.008). Donor genotypes were not associated with any of the outcomes analyzed. In conclusion, PNPLA‐3 non‐CC genotype is associated with posttransplant obesity but not independently with diabetes/IFG. The lack of donor related risk suggests a peripheral rather than central mechanism of insulin resistance in liver transplant recipients.
Analysis of donor and recipient genetic risk factors for obesity and diabetes after transplant finds that recipient, but not donor, PNPLA‐3 G allele is independently associated with obesity after liver transplantation, pointing to a peripheral rather than central mechanism of action and explaining some of the risk for posttransplant obesity.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Diabetes</subject><subject>Diabetes Mellitus - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>genetic risk</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Interferons</subject><subject>Interleukins - genetics</subject><subject>Lipase - genetics</subject><subject>liver transplant</subject><subject>Liver Transplantation - adverse effects</subject><subject>Liver, biliary tract, pancreas, portal circulation, spleen</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Metabolic diseases</subject><subject>Middle Aged</subject><subject>Obesity</subject><subject>Obesity - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the digestive system</subject><subject>Tissue Donors</subject><subject>Transplants & implants</subject><issn>1600-6135</issn><issn>1600-6143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtvEzEUhS0Eog9Y8AeQJYQEi7R-29NdaKEEDbSLsB45nuvW0cQTxk6rrPnjeJpQJCSEF75X8qdzfO9B6BUlJ7ScU7vMJ5RxKZ-gQ6oImSgq-NPHnssDdJTSkhCqmWHP0QHjRlZE00P0cxbvIOVwY3PoI-49vv52XU85trHFs5qZD_gSYp-3a0i4ABfBLiCXfny_WkAKeYunPsOA63BX7vlgY1p3NuYHxTM8iync3OZSc4-_gru1MaRVGq0uQgKb4AV65m2X4OW-HqPvnz7Ozz9P6qvL2fm0njghqZxwD9q1WlZCaWm0WwjOLFNGEmpFVSlPlVOata0QrKp0S4zwYJigpgLjneXH6N1Odz30PzZl6mYVkoOufBb6TWqoNpJxJcsq_4sKzpnmlKqCvvkLXfabIZZBCsWMYoLpkXq_o9zQpzSAb9ZDWNlh21DSjCE2JcTmIcTCvt4rbhYraB_J36kV4O0esMnZzpeVu5D-cNooQdXIne64-9DB9t-OzfTLfGf9C4N-sBU</recordid><startdate>201309</startdate><enddate>201309</enddate><creator>Watt, K. D.</creator><creator>Dierkhising, R.</creator><creator>Fan, C.</creator><creator>Heimbach, J. K.</creator><creator>Tillman, H.</creator><creator>Goldstein, D.</creator><creator>Thompson, A.</creator><creator>Krishnan, A.</creator><creator>Charlton, M. R.</creator><general>Wiley</general><general>Elsevier Limited</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>7QP</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201309</creationdate><title>Investigation of PNPLA3 and IL28B Genotypes on Diabetes and Obesity After Liver Transplantation: Insight Into Mechanisms of Disease</title><author>Watt, K. D. ; Dierkhising, R. ; Fan, C. ; Heimbach, J. K. ; Tillman, H. ; Goldstein, D. ; Thompson, A. ; Krishnan, A. ; Charlton, M. 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Target tissue resistance</topic><topic>genetic risk</topic><topic>Health risk assessment</topic><topic>Humans</topic><topic>insulin resistance</topic><topic>Insulin Resistance - genetics</topic><topic>Interferons</topic><topic>Interleukins - genetics</topic><topic>Lipase - genetics</topic><topic>liver transplant</topic><topic>Liver Transplantation - adverse effects</topic><topic>Liver, biliary tract, pancreas, portal circulation, spleen</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Metabolic diseases</topic><topic>Middle Aged</topic><topic>Obesity</topic><topic>Obesity - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the digestive system</topic><topic>Tissue Donors</topic><topic>Transplants & implants</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Watt, K. D.</creatorcontrib><creatorcontrib>Dierkhising, R.</creatorcontrib><creatorcontrib>Fan, C.</creatorcontrib><creatorcontrib>Heimbach, J. K.</creatorcontrib><creatorcontrib>Tillman, H.</creatorcontrib><creatorcontrib>Goldstein, D.</creatorcontrib><creatorcontrib>Thompson, A.</creatorcontrib><creatorcontrib>Krishnan, A.</creatorcontrib><creatorcontrib>Charlton, M. 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R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Investigation of PNPLA3 and IL28B Genotypes on Diabetes and Obesity After Liver Transplantation: Insight Into Mechanisms of Disease</atitle><jtitle>American journal of transplantation</jtitle><addtitle>Am J Transplant</addtitle><date>2013-09</date><risdate>2013</risdate><volume>13</volume><issue>9</issue><spage>2450</spage><epage>2457</epage><pages>2450-2457</pages><issn>1600-6135</issn><eissn>1600-6143</eissn><abstract>To identify genetic risks for obesity and diabetes postliver transplantation (LT), LT recipients underwent genotyping for IL28B rs12979860 (n = 295) and PNPLA3 rs738409 (n = 205) polymorphism in both donors and recipients. The development of obesity and diabetes/impaired fasting glucose (IFG) was determined 1–5 years post‐LT. Recipient PNPLA‐3 genotype was independently associated with obesity (BMI > 30) at 3 years posttransplant (genotype CC 33.7%, CG 48.3% and GG 82.4%, p = 0.002), with an odds ratio (OR 2.54, CI 1.38–4.66, p = 0.003), associated with the G allele. Diabetes/IFG diagnosed within 5 years posttransplant associated with PNPLA‐3 non‐CC genotype (HR 1.59, 1.12–2.26, p = 0.010), but not IL28B TT genotype (HR 1.46, 0.94–2.27, p = 0.092). No genotype variable was independently predictive of diabetes/IFG. The combination of PNPLA‐3 non‐CC and IL28B TT genotype was associated with increased risk of diabetes/IFG compared to PNPLA‐3 CC, IL28B non‐TT (HR 2.64, CI 1.30–5.39, p = 0.008). Donor genotypes were not associated with any of the outcomes analyzed. In conclusion, PNPLA‐3 non‐CC genotype is associated with posttransplant obesity but not independently with diabetes/IFG. The lack of donor related risk suggests a peripheral rather than central mechanism of insulin resistance in liver transplant recipients.
Analysis of donor and recipient genetic risk factors for obesity and diabetes after transplant finds that recipient, but not donor, PNPLA‐3 G allele is independently associated with obesity after liver transplantation, pointing to a peripheral rather than central mechanism of action and explaining some of the risk for posttransplant obesity.</abstract><cop>Hoboken, NJ</cop><pub>Wiley</pub><pmid>23859071</pmid><doi>10.1111/ajt.12355</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Biological and medical sciences Diabetes Diabetes Mellitus - genetics Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance genetic risk Health risk assessment Humans insulin resistance Insulin Resistance - genetics Interferons Interleukins - genetics Lipase - genetics liver transplant Liver Transplantation - adverse effects Liver, biliary tract, pancreas, portal circulation, spleen Medical sciences Membrane Proteins - genetics Metabolic diseases Middle Aged Obesity Obesity - genetics Polymorphism, Single Nucleotide Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the digestive system Tissue Donors Transplants & implants |
title | Investigation of PNPLA3 and IL28B Genotypes on Diabetes and Obesity After Liver Transplantation: Insight Into Mechanisms of Disease |
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