Importance of changes in adipose tissue insulin resistance to histological response during thiazolidinedione treatment of patients with nonalcoholic steatohepatitis
Pioglitazone treatment improves insulin resistance (IR), glucose metabolism, hepatic steatosis, and necroinflammation in patients with nonalcoholic steatohepatitis (NASH). Because abnormal lipid metabolism/elevated plasma free fatty acids (FFAs) are important to the pathophysiology of NASH, we exami...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 2009-10, Vol.50 (4), p.1087-1093 |
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| creator | Gastaldelli, Amalia Harrison, Stephen A. Belfort‐Aguilar, Renata Hardies, Lou Jean Balas, Bogdan Schenker, Steven Cusi, Kenneth |
| description | Pioglitazone treatment improves insulin resistance (IR), glucose metabolism, hepatic steatosis, and necroinflammation in patients with nonalcoholic steatohepatitis (NASH). Because abnormal lipid metabolism/elevated plasma free fatty acids (FFAs) are important to the pathophysiology of NASH, we examined the impact of pioglitazone therapy on adipose tissue insulin resistance (Adipo‐IR) during the treatment of patients with NASH. To this end, we assessed glucose/lipid metabolism in 47 patients with impaired glucose tolerance/type 2 diabetes mellitus and NASH and 20 nondiabetic controls. All individuals underwent a 75‐g oral glucose tolerance test (OGTT) in which we measured glucose tolerance, IR, and suppression of plasma FFAs. We also measured Adipo‐IR index (fasting, FFAs × insulin), hepatic fat by magnetic resonance spectroscopy, and liver histology (liver biopsy). Patients were randomized (double‐blind) to diet plus pioglitazone (45 mg/day) or placebo for 6 months, and all measurements were repeated. We found that patients with NASH had severe Adipo‐IR and low adiponectin levels. Fasting FFAs were increased and their suppression during the OGTT was impaired. Adipo‐IR was strongly associated with hepatic fat (r= 0.54) and reduced glucose clearance both fasting (r=0.34) and during the OGTT (r=0.40, all P |
| doi_str_mv | 10.1002/hep.23116 |
| format | Article |
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Because abnormal lipid metabolism/elevated plasma free fatty acids (FFAs) are important to the pathophysiology of NASH, we examined the impact of pioglitazone therapy on adipose tissue insulin resistance (Adipo‐IR) during the treatment of patients with NASH. To this end, we assessed glucose/lipid metabolism in 47 patients with impaired glucose tolerance/type 2 diabetes mellitus and NASH and 20 nondiabetic controls. All individuals underwent a 75‐g oral glucose tolerance test (OGTT) in which we measured glucose tolerance, IR, and suppression of plasma FFAs. We also measured Adipo‐IR index (fasting, FFAs × insulin), hepatic fat by magnetic resonance spectroscopy, and liver histology (liver biopsy). Patients were randomized (double‐blind) to diet plus pioglitazone (45 mg/day) or placebo for 6 months, and all measurements were repeated. We found that patients with NASH had severe Adipo‐IR and low adiponectin levels. Fasting FFAs were increased and their suppression during the OGTT was impaired. Adipo‐IR was strongly associated with hepatic fat (r= 0.54) and reduced glucose clearance both fasting (r=0.34) and during the OGTT (r=0.40, all P <0.002). Pioglitazone significantly improved glucose tolerance and glucose clearance, steatosis and necroinflammation (all P<0.01‐0.001 versus placebo). Fasting/postprandial plasma FFAs decreased to levels of controls with pioglitazone (P<0.02 versus placebo). Adipo‐IR decreased by 47% and correlated with the reduction of hepatic fat (r=0.46, P=0.009) and with the reduction in hepatic necroinflammation (r=0.47, P=0.0007). Conclusion: Patients with NASH have severe Adipo‐IR independent of the degree of obesity. Amelioration of Adipo‐IR by pioglitazone is closely related to histological improvement and plays an important role during treatment of patients with NASH. (HEPATOLOGY 2009)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.23116</identifier><identifier>PMID: 19670459</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adipose Tissue - drug effects ; Adipose Tissue - metabolism ; Adipose Tissue - pathology ; Adult ; Biological and medical sciences ; Blood Glucose ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - metabolism ; Double-Blind Method ; Fatty Acids, Nonesterified - blood ; Fatty Liver - complications ; Fatty Liver - drug therapy ; Fatty Liver - metabolism ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; Insulin - metabolism ; Insulin Resistance - physiology ; Lipid Metabolism - drug effects ; Lipid Metabolism - physiology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Middle Aged ; Obesity - metabolism ; Obesity - pathology ; Thiazolidinediones - pharmacology ; Thiazolidinediones - therapeutic use</subject><ispartof>Hepatology (Baltimore, Md.), 2009-10, Vol.50 (4), p.1087-1093</ispartof><rights>Copyright © 2009 American Association for the Study of Liver Diseases</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3886-6e7677b73256a45d0d8502f6aca49ebc017c3231b922c13bf8f2f4c3d57903383</citedby><cites>FETCH-LOGICAL-c3886-6e7677b73256a45d0d8502f6aca49ebc017c3231b922c13bf8f2f4c3d57903383</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.23116$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.23116$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22013399$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19670459$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gastaldelli, Amalia</creatorcontrib><creatorcontrib>Harrison, Stephen A.</creatorcontrib><creatorcontrib>Belfort‐Aguilar, Renata</creatorcontrib><creatorcontrib>Hardies, Lou Jean</creatorcontrib><creatorcontrib>Balas, Bogdan</creatorcontrib><creatorcontrib>Schenker, Steven</creatorcontrib><creatorcontrib>Cusi, Kenneth</creatorcontrib><title>Importance of changes in adipose tissue insulin resistance to histological response during thiazolidinedione treatment of patients with nonalcoholic steatohepatitis</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>Pioglitazone treatment improves insulin resistance (IR), glucose metabolism, hepatic steatosis, and necroinflammation in patients with nonalcoholic steatohepatitis (NASH). Because abnormal lipid metabolism/elevated plasma free fatty acids (FFAs) are important to the pathophysiology of NASH, we examined the impact of pioglitazone therapy on adipose tissue insulin resistance (Adipo‐IR) during the treatment of patients with NASH. To this end, we assessed glucose/lipid metabolism in 47 patients with impaired glucose tolerance/type 2 diabetes mellitus and NASH and 20 nondiabetic controls. All individuals underwent a 75‐g oral glucose tolerance test (OGTT) in which we measured glucose tolerance, IR, and suppression of plasma FFAs. We also measured Adipo‐IR index (fasting, FFAs × insulin), hepatic fat by magnetic resonance spectroscopy, and liver histology (liver biopsy). Patients were randomized (double‐blind) to diet plus pioglitazone (45 mg/day) or placebo for 6 months, and all measurements were repeated. We found that patients with NASH had severe Adipo‐IR and low adiponectin levels. Fasting FFAs were increased and their suppression during the OGTT was impaired. Adipo‐IR was strongly associated with hepatic fat (r= 0.54) and reduced glucose clearance both fasting (r=0.34) and during the OGTT (r=0.40, all P <0.002). Pioglitazone significantly improved glucose tolerance and glucose clearance, steatosis and necroinflammation (all P<0.01‐0.001 versus placebo). Fasting/postprandial plasma FFAs decreased to levels of controls with pioglitazone (P<0.02 versus placebo). Adipo‐IR decreased by 47% and correlated with the reduction of hepatic fat (r=0.46, P=0.009) and with the reduction in hepatic necroinflammation (r=0.47, P=0.0007). Conclusion: Patients with NASH have severe Adipo‐IR independent of the degree of obesity. Amelioration of Adipo‐IR by pioglitazone is closely related to histological improvement and plays an important role during treatment of patients with NASH. (HEPATOLOGY 2009)</description><subject>Adipose Tissue - drug effects</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - pathology</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Double-Blind Method</subject><subject>Fatty Acids, Nonesterified - blood</subject><subject>Fatty Liver - complications</subject><subject>Fatty Liver - drug therapy</subject><subject>Fatty Liver - metabolism</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance - physiology</subject><subject>Lipid Metabolism - drug effects</subject><subject>Lipid Metabolism - physiology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Obesity - metabolism</subject><subject>Obesity - pathology</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Thiazolidinediones - therapeutic use</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kLtOwzAUhi0EglIYeAHkhYEh1JckjkeEykVCggHmyHGcxii1I9sVgufhQTklFUxMPjr-jv_jD6EzSq4oIWzRm_GKcUrLPTSjBRMZ5wXZRzPCBMkk5fIIHcf4RgiROasO0RGVpSB5IWfo62E9-pCU0wb7DuteuZWJ2DqsWjv6aHCyMW4MdOJmgHYw0caJTx73UPvBr6xWw_Zq9A5G2k2wboVTb9WnH2xrnWmtdzARjEpr49I2a1TJQhnxu009dt6pQfseeI1jAs7DtwCB_BN00KkhmtPdOUevt8uXm_vs8enu4eb6MdO8qsqsNKIUohGcFaXKi5a0VUFYVyqtcmkaTajQHDw1kjFNedNVHetyzdtCSMJ5xefocnpXBx9jMF09BrtW4aOmpN6armGl-sc0sOcTO26atWn_yJ1aAC52gIpgpwvgzMZfjjFCOZdbbjFx73YwH_8n1vfL5yn6Gwijmio</recordid><startdate>200910</startdate><enddate>200910</enddate><creator>Gastaldelli, Amalia</creator><creator>Harrison, Stephen A.</creator><creator>Belfort‐Aguilar, Renata</creator><creator>Hardies, Lou Jean</creator><creator>Balas, Bogdan</creator><creator>Schenker, Steven</creator><creator>Cusi, Kenneth</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</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></search><sort><creationdate>200910</creationdate><title>Importance of changes in adipose tissue insulin resistance to histological response during thiazolidinedione treatment of patients with nonalcoholic steatohepatitis</title><author>Gastaldelli, Amalia ; Harrison, Stephen A. ; Belfort‐Aguilar, Renata ; Hardies, Lou Jean ; Balas, Bogdan ; Schenker, Steven ; Cusi, Kenneth</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3886-6e7677b73256a45d0d8502f6aca49ebc017c3231b922c13bf8f2f4c3d57903383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adipose Tissue - drug effects</topic><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - pathology</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Double-Blind Method</topic><topic>Fatty Acids, Nonesterified - blood</topic><topic>Fatty Liver - complications</topic><topic>Fatty Liver - drug therapy</topic><topic>Fatty Liver - metabolism</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Insulin - metabolism</topic><topic>Insulin Resistance - physiology</topic><topic>Lipid Metabolism - drug effects</topic><topic>Lipid Metabolism - physiology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Obesity - metabolism</topic><topic>Obesity - pathology</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Thiazolidinediones - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gastaldelli, Amalia</creatorcontrib><creatorcontrib>Harrison, Stephen A.</creatorcontrib><creatorcontrib>Belfort‐Aguilar, Renata</creatorcontrib><creatorcontrib>Hardies, Lou Jean</creatorcontrib><creatorcontrib>Balas, Bogdan</creatorcontrib><creatorcontrib>Schenker, Steven</creatorcontrib><creatorcontrib>Cusi, Kenneth</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><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gastaldelli, Amalia</au><au>Harrison, Stephen A.</au><au>Belfort‐Aguilar, Renata</au><au>Hardies, Lou Jean</au><au>Balas, Bogdan</au><au>Schenker, Steven</au><au>Cusi, Kenneth</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Importance of changes in adipose tissue insulin resistance to histological response during thiazolidinedione treatment of patients with nonalcoholic steatohepatitis</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>2009-10</date><risdate>2009</risdate><volume>50</volume><issue>4</issue><spage>1087</spage><epage>1093</epage><pages>1087-1093</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>Pioglitazone treatment improves insulin resistance (IR), glucose metabolism, hepatic steatosis, and necroinflammation in patients with nonalcoholic steatohepatitis (NASH). Because abnormal lipid metabolism/elevated plasma free fatty acids (FFAs) are important to the pathophysiology of NASH, we examined the impact of pioglitazone therapy on adipose tissue insulin resistance (Adipo‐IR) during the treatment of patients with NASH. To this end, we assessed glucose/lipid metabolism in 47 patients with impaired glucose tolerance/type 2 diabetes mellitus and NASH and 20 nondiabetic controls. All individuals underwent a 75‐g oral glucose tolerance test (OGTT) in which we measured glucose tolerance, IR, and suppression of plasma FFAs. We also measured Adipo‐IR index (fasting, FFAs × insulin), hepatic fat by magnetic resonance spectroscopy, and liver histology (liver biopsy). Patients were randomized (double‐blind) to diet plus pioglitazone (45 mg/day) or placebo for 6 months, and all measurements were repeated. We found that patients with NASH had severe Adipo‐IR and low adiponectin levels. Fasting FFAs were increased and their suppression during the OGTT was impaired. Adipo‐IR was strongly associated with hepatic fat (r= 0.54) and reduced glucose clearance both fasting (r=0.34) and during the OGTT (r=0.40, all P <0.002). Pioglitazone significantly improved glucose tolerance and glucose clearance, steatosis and necroinflammation (all P<0.01‐0.001 versus placebo). Fasting/postprandial plasma FFAs decreased to levels of controls with pioglitazone (P<0.02 versus placebo). Adipo‐IR decreased by 47% and correlated with the reduction of hepatic fat (r=0.46, P=0.009) and with the reduction in hepatic necroinflammation (r=0.47, P=0.0007). Conclusion: Patients with NASH have severe Adipo‐IR independent of the degree of obesity. Amelioration of Adipo‐IR by pioglitazone is closely related to histological improvement and plays an important role during treatment of patients with NASH. (HEPATOLOGY 2009)</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>19670459</pmid><doi>10.1002/hep.23116</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adipose Tissue - drug effects Adipose Tissue - metabolism Adipose Tissue - pathology Adult Biological and medical sciences Blood Glucose Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Double-Blind Method Fatty Acids, Nonesterified - blood Fatty Liver - complications Fatty Liver - drug therapy Fatty Liver - metabolism Female Gastroenterology. Liver. Pancreas. Abdomen Humans Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Insulin - metabolism Insulin Resistance - physiology Lipid Metabolism - drug effects Lipid Metabolism - physiology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Middle Aged Obesity - metabolism Obesity - pathology Thiazolidinediones - pharmacology Thiazolidinediones - therapeutic use |
| title | Importance of changes in adipose tissue insulin resistance to histological response during thiazolidinedione treatment of patients with nonalcoholic steatohepatitis |
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