Serum leptin levels, hepatic leptin receptor transcription, and clinical predictors of non-alcoholic steatohepatitis in obese bariatric surgery patients
Non-alcoholic steatohepatitis (NASH) is a major cause of liver disease in morbidly obese patients. Clinical predictors of NASH remain elusive, as do molecular mechanisms of pathogenesis. A series of 35 morbidly obese patients undergoing bariatric surgery had a liver biopsy performed for standard his...
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| Veröffentlicht in: | Surgical endoscopy 2007-09, Vol.21 (9), p.1593-1599 |
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| creator | LE, D MARKS, D O'ROURKE, R. W LYLE, E CORLESS, C. L DIGGS, B. S JOBE, B. A KAY, T DEVENEY, C. W WOLFE, B. M ROBERTS, C. T |
| description | Non-alcoholic steatohepatitis (NASH) is a major cause of liver disease in morbidly obese patients. Clinical predictors of NASH remain elusive, as do molecular mechanisms of pathogenesis.
A series of 35 morbidly obese patients undergoing bariatric surgery had a liver biopsy performed for standard histologic analysis. In addition, RNA was obtained from liver tissue and analyzed for leptin receptor gene expression. Regression analysis was used to correlate clinical variables, including serum leptin levels and hepatic leptin receptor gene expression, with the presence of histologically confirmed NASH.
Of the 35 subjects enrolled, 29% had steatosis only, 60% had NASH, and 11% had normal liver histology. Among the clinical variables studied, only diabetes mellitus was an independent predictor of NASH. There was a trend toward lower levels of mRNA encoding the long form of the leptin receptor in hepatic tissue from patients with NASH compared to those with steatosis only.
Diabetes mellitus is associated with an increased risk of NASH in obese patients. Downregulation of hepatic leptin receptor may play a role in the pathogenesis of NASH. |
| doi_str_mv | 10.1007/s00464-006-9185-5 |
| format | Article |
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A series of 35 morbidly obese patients undergoing bariatric surgery had a liver biopsy performed for standard histologic analysis. In addition, RNA was obtained from liver tissue and analyzed for leptin receptor gene expression. Regression analysis was used to correlate clinical variables, including serum leptin levels and hepatic leptin receptor gene expression, with the presence of histologically confirmed NASH.
Of the 35 subjects enrolled, 29% had steatosis only, 60% had NASH, and 11% had normal liver histology. Among the clinical variables studied, only diabetes mellitus was an independent predictor of NASH. There was a trend toward lower levels of mRNA encoding the long form of the leptin receptor in hepatic tissue from patients with NASH compared to those with steatosis only.
Diabetes mellitus is associated with an increased risk of NASH in obese patients. Downregulation of hepatic leptin receptor may play a role in the pathogenesis of NASH.</description><identifier>ISSN: 0930-2794</identifier><identifier>EISSN: 1432-2218</identifier><identifier>DOI: 10.1007/s00464-006-9185-5</identifier><identifier>PMID: 17294310</identifier><identifier>CODEN: SUREEX</identifier><language>eng</language><publisher>New York, NY: Springer</publisher><subject>Adult ; Alcohol use ; Bariatric Surgery ; Biological and medical sciences ; Biomarkers - blood ; Biopsy ; Diabetes ; Fatty Liver - diagnosis ; Fatty Liver - etiology ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gastrointestinal surgery ; Gene expression ; Histology ; Humans ; Laparoscopy ; Leptin - blood ; Liver - metabolism ; Liver cirrhosis ; Liver diseases ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Metabolic diseases ; Middle Aged ; Obesity ; Obesity, Morbid - complications ; Obesity, Morbid - metabolism ; Obesity, Morbid - surgery ; Other diseases. Semiology ; Pathogenesis ; Patients ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - metabolism ; Receptors, Leptin ; Risk Factors ; Stomach, duodenum, intestine, rectum, anus ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the digestive system ; Transcription, Genetic ; Variables</subject><ispartof>Surgical endoscopy, 2007-09, Vol.21 (9), p.1593-1599</ispartof><rights>2007 INIST-CNRS</rights><rights>Springer Science+Business Media, LLC 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-f6a30c9302275aa784bb2fee10f54de07e27a5dd53a1366d3513dfda4b416ade3</citedby><cites>FETCH-LOGICAL-c356t-f6a30c9302275aa784bb2fee10f54de07e27a5dd53a1366d3513dfda4b416ade3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19110351$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17294310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LE, D</creatorcontrib><creatorcontrib>MARKS, D</creatorcontrib><creatorcontrib>O'ROURKE, R. W</creatorcontrib><creatorcontrib>LYLE, E</creatorcontrib><creatorcontrib>CORLESS, C. L</creatorcontrib><creatorcontrib>DIGGS, B. S</creatorcontrib><creatorcontrib>JOBE, B. A</creatorcontrib><creatorcontrib>KAY, T</creatorcontrib><creatorcontrib>DEVENEY, C. W</creatorcontrib><creatorcontrib>WOLFE, B. M</creatorcontrib><creatorcontrib>ROBERTS, C. T</creatorcontrib><title>Serum leptin levels, hepatic leptin receptor transcription, and clinical predictors of non-alcoholic steatohepatitis in obese bariatric surgery patients</title><title>Surgical endoscopy</title><addtitle>Surg Endosc</addtitle><description>Non-alcoholic steatohepatitis (NASH) is a major cause of liver disease in morbidly obese patients. Clinical predictors of NASH remain elusive, as do molecular mechanisms of pathogenesis.
A series of 35 morbidly obese patients undergoing bariatric surgery had a liver biopsy performed for standard histologic analysis. In addition, RNA was obtained from liver tissue and analyzed for leptin receptor gene expression. Regression analysis was used to correlate clinical variables, including serum leptin levels and hepatic leptin receptor gene expression, with the presence of histologically confirmed NASH.
Of the 35 subjects enrolled, 29% had steatosis only, 60% had NASH, and 11% had normal liver histology. Among the clinical variables studied, only diabetes mellitus was an independent predictor of NASH. There was a trend toward lower levels of mRNA encoding the long form of the leptin receptor in hepatic tissue from patients with NASH compared to those with steatosis only.
Diabetes mellitus is associated with an increased risk of NASH in obese patients. Downregulation of hepatic leptin receptor may play a role in the pathogenesis of NASH.</description><subject>Adult</subject><subject>Alcohol use</subject><subject>Bariatric Surgery</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Biopsy</subject><subject>Diabetes</subject><subject>Fatty Liver - diagnosis</subject><subject>Fatty Liver - etiology</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gastrointestinal surgery</subject><subject>Gene expression</subject><subject>Histology</subject><subject>Humans</subject><subject>Laparoscopy</subject><subject>Leptin - blood</subject><subject>Liver - metabolism</subject><subject>Liver cirrhosis</subject><subject>Liver diseases</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Middle Aged</subject><subject>Obesity</subject><subject>Obesity, Morbid - complications</subject><subject>Obesity, Morbid - metabolism</subject><subject>Obesity, Morbid - surgery</subject><subject>Other diseases. Semiology</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Receptors, Leptin</subject><subject>Risk Factors</subject><subject>Stomach, duodenum, intestine, rectum, anus</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. 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W ; LYLE, E ; CORLESS, C. L ; DIGGS, B. S ; JOBE, B. A ; KAY, T ; DEVENEY, C. W ; WOLFE, B. M ; ROBERTS, C. T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-f6a30c9302275aa784bb2fee10f54de07e27a5dd53a1366d3513dfda4b416ade3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Alcohol use</topic><topic>Bariatric Surgery</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Biopsy</topic><topic>Diabetes</topic><topic>Fatty Liver - diagnosis</topic><topic>Fatty Liver - etiology</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gastrointestinal surgery</topic><topic>Gene expression</topic><topic>Histology</topic><topic>Humans</topic><topic>Laparoscopy</topic><topic>Leptin - blood</topic><topic>Liver - metabolism</topic><topic>Liver cirrhosis</topic><topic>Liver diseases</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Middle Aged</topic><topic>Obesity</topic><topic>Obesity, Morbid - complications</topic><topic>Obesity, Morbid - metabolism</topic><topic>Obesity, Morbid - surgery</topic><topic>Other diseases. Semiology</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Receptors, Leptin</topic><topic>Risk Factors</topic><topic>Stomach, duodenum, intestine, rectum, anus</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. 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W</au><au>LYLE, E</au><au>CORLESS, C. L</au><au>DIGGS, B. S</au><au>JOBE, B. A</au><au>KAY, T</au><au>DEVENEY, C. W</au><au>WOLFE, B. M</au><au>ROBERTS, C. T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serum leptin levels, hepatic leptin receptor transcription, and clinical predictors of non-alcoholic steatohepatitis in obese bariatric surgery patients</atitle><jtitle>Surgical endoscopy</jtitle><addtitle>Surg Endosc</addtitle><date>2007-09-01</date><risdate>2007</risdate><volume>21</volume><issue>9</issue><spage>1593</spage><epage>1599</epage><pages>1593-1599</pages><issn>0930-2794</issn><eissn>1432-2218</eissn><coden>SUREEX</coden><abstract>Non-alcoholic steatohepatitis (NASH) is a major cause of liver disease in morbidly obese patients. Clinical predictors of NASH remain elusive, as do molecular mechanisms of pathogenesis.
A series of 35 morbidly obese patients undergoing bariatric surgery had a liver biopsy performed for standard histologic analysis. In addition, RNA was obtained from liver tissue and analyzed for leptin receptor gene expression. Regression analysis was used to correlate clinical variables, including serum leptin levels and hepatic leptin receptor gene expression, with the presence of histologically confirmed NASH.
Of the 35 subjects enrolled, 29% had steatosis only, 60% had NASH, and 11% had normal liver histology. Among the clinical variables studied, only diabetes mellitus was an independent predictor of NASH. There was a trend toward lower levels of mRNA encoding the long form of the leptin receptor in hepatic tissue from patients with NASH compared to those with steatosis only.
Diabetes mellitus is associated with an increased risk of NASH in obese patients. Downregulation of hepatic leptin receptor may play a role in the pathogenesis of NASH.</abstract><cop>New York, NY</cop><pub>Springer</pub><pmid>17294310</pmid><doi>10.1007/s00464-006-9185-5</doi><tpages>7</tpages></addata></record> |
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| subjects | Adult Alcohol use Bariatric Surgery Biological and medical sciences Biomarkers - blood Biopsy Diabetes Fatty Liver - diagnosis Fatty Liver - etiology Female Gastroenterology. Liver. Pancreas. Abdomen Gastrointestinal surgery Gene expression Histology Humans Laparoscopy Leptin - blood Liver - metabolism Liver cirrhosis Liver diseases Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Metabolic diseases Middle Aged Obesity Obesity, Morbid - complications Obesity, Morbid - metabolism Obesity, Morbid - surgery Other diseases. Semiology Pathogenesis Patients Receptors, Cell Surface - genetics Receptors, Cell Surface - metabolism Receptors, Leptin Risk Factors Stomach, duodenum, intestine, rectum, anus Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the digestive system Transcription, Genetic Variables |
| title | Serum leptin levels, hepatic leptin receptor transcription, and clinical predictors of non-alcoholic steatohepatitis in obese bariatric surgery patients |
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