Increased hepatic PDGF-AA signaling mediates liver insulin resistance in obesity associated type 2 diabetes
Type 2 diabetes (T2D) is closely linked with non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance, but the involved mechanisms are still elusive. Using DNA methylome and transcriptome analyses of livers from obese individuals, we found that both hypomethylation at a CpG site in P...
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| creator | Abderrahmani, Amar Yengo, Loic Caiazzo, Robert Canouil, Mickael Cauchi, Stephane Raverdy, Violeta Plaisance, Valerie Pawlowski, Valerie Lobbens, Stephane Maillet, Julie Rolland, Laure Boutry, Raphael Queniat, Gurvan Kwapich, Maxime Tenenbaum, Mathie Bricambert, Julien Saussenthaler, Sophie Anthony, Elodie Jha, Pooja Derop, Julien Sand, Olivier Rabearivelo, Iandry Leloire, Audrey Pigeyre, Marie Daujat-Chavanieu, Martine Gerbal-Chaloin, Sabine Dayeh, Tasnim Lassailly, Guillaume Mathurin, Philippe Staels, Bart Auwerx, Johan Schurmann, Annette Postic, Catherine Schafmayer, Clemens Hampe, Jochen Bonnefond, Amelie Pattou, Francois Froguel, Philippe |
| description | Type 2 diabetes (T2D) is closely linked with non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance, but the involved mechanisms are still elusive. Using DNA methylome and transcriptome analyses of livers from obese individuals, we found that both hypomethylation at a CpG site in PDGFA (encoding platelet derived growth factor alpha) and PDGFA overexpression are associated with increased T2D risk, hyperinsulinemia, increased insulin resistance and increased steatohepatitis risk. Both genetic risk score studies and human cell modeling pointed to a causative impact of high insulin levels on PDGFA CpG site hypomethylation, PDGFA overexpression, and increased PDGF-AA secretion from liver. We found that PDGF-AA secretion further stimulates its own expression through protein kinase C activity and contributes to insulin resistance through decreased expression of both insulin receptor substrate 1 and of insulin receptor. Importantly, hepatocyte insulin sensitivity can be restored by PDGF-AA blocking antibodies, PDGF receptor inhibitors and by metformin opening therapeutic avenues. Conclusion: Therefore, in the liver of obese patients with T2D, the increased PDGF-AA signaling contributes to insulin resistance, opening new therapeutic avenues against T2D and NAFLD. |
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Using DNA methylome and transcriptome analyses of livers from obese individuals, we found that both hypomethylation at a CpG site in PDGFA (encoding platelet derived growth factor alpha) and PDGFA overexpression are associated with increased T2D risk, hyperinsulinemia, increased insulin resistance and increased steatohepatitis risk. Both genetic risk score studies and human cell modeling pointed to a causative impact of high insulin levels on PDGFA CpG site hypomethylation, PDGFA overexpression, and increased PDGF-AA secretion from liver. We found that PDGF-AA secretion further stimulates its own expression through protein kinase C activity and contributes to insulin resistance through decreased expression of both insulin receptor substrate 1 and of insulin receptor. Importantly, hepatocyte insulin sensitivity can be restored by PDGF-AA blocking antibodies, PDGF receptor inhibitors and by metformin opening therapeutic avenues. Conclusion: Therefore, in the liver of obese patients with T2D, the increased PDGF-AA signaling contributes to insulin resistance, opening new therapeutic avenues against T2D and NAFLD.</description><identifier>EISSN: 2331-8422</identifier><language>eng</language><publisher>Ithaca: Cornell University Library, arXiv.org</publisher><subject>Antibodies ; Deoxyribonucleic acid ; Diabetes ; Diabetes mellitus ; DNA ; Growth factors ; Insulin ; Insulin resistance ; Kinases ; Liver ; Metformin ; Proteins ; Risk ; Signaling ; Substrates</subject><ispartof>arXiv.org, 2017-12</ispartof><rights>2017. This work is published under http://arxiv.org/licenses/nonexclusive-distrib/1.0/ (the “License”). 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Using DNA methylome and transcriptome analyses of livers from obese individuals, we found that both hypomethylation at a CpG site in PDGFA (encoding platelet derived growth factor alpha) and PDGFA overexpression are associated with increased T2D risk, hyperinsulinemia, increased insulin resistance and increased steatohepatitis risk. Both genetic risk score studies and human cell modeling pointed to a causative impact of high insulin levels on PDGFA CpG site hypomethylation, PDGFA overexpression, and increased PDGF-AA secretion from liver. We found that PDGF-AA secretion further stimulates its own expression through protein kinase C activity and contributes to insulin resistance through decreased expression of both insulin receptor substrate 1 and of insulin receptor. Importantly, hepatocyte insulin sensitivity can be restored by PDGF-AA blocking antibodies, PDGF receptor inhibitors and by metformin opening therapeutic avenues. 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Bart</au><au>Auwerx, Johan</au><au>Schurmann, Annette</au><au>Postic, Catherine</au><au>Schafmayer, Clemens</au><au>Hampe, Jochen</au><au>Bonnefond, Amelie</au><au>Pattou, Francois</au><au>Froguel, Philippe</au><format>book</format><genre>document</genre><ristype>GEN</ristype><atitle>Increased hepatic PDGF-AA signaling mediates liver insulin resistance in obesity associated type 2 diabetes</atitle><jtitle>arXiv.org</jtitle><date>2017-12-13</date><risdate>2017</risdate><eissn>2331-8422</eissn><abstract>Type 2 diabetes (T2D) is closely linked with non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance, but the involved mechanisms are still elusive. Using DNA methylome and transcriptome analyses of livers from obese individuals, we found that both hypomethylation at a CpG site in PDGFA (encoding platelet derived growth factor alpha) and PDGFA overexpression are associated with increased T2D risk, hyperinsulinemia, increased insulin resistance and increased steatohepatitis risk. Both genetic risk score studies and human cell modeling pointed to a causative impact of high insulin levels on PDGFA CpG site hypomethylation, PDGFA overexpression, and increased PDGF-AA secretion from liver. We found that PDGF-AA secretion further stimulates its own expression through protein kinase C activity and contributes to insulin resistance through decreased expression of both insulin receptor substrate 1 and of insulin receptor. Importantly, hepatocyte insulin sensitivity can be restored by PDGF-AA blocking antibodies, PDGF receptor inhibitors and by metformin opening therapeutic avenues. Conclusion: Therefore, in the liver of obese patients with T2D, the increased PDGF-AA signaling contributes to insulin resistance, opening new therapeutic avenues against T2D and NAFLD.</abstract><cop>Ithaca</cop><pub>Cornell University Library, arXiv.org</pub><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies Deoxyribonucleic acid Diabetes Diabetes mellitus DNA Growth factors Insulin Insulin resistance Kinases Liver Metformin Proteins Risk Signaling Substrates |
| title | Increased hepatic PDGF-AA signaling mediates liver insulin resistance in obesity associated type 2 diabetes |
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