Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asian men
Background and Aim: Although insulin resistance is often considered the link between obesity and non‐alcoholic fatty liver disease (NAFLD), the role of insulin resistance, independent of obesity, as a NAFLD risk factor in non‐obese men has been less well established. Systemic inflammation may be ac...
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Veröffentlicht in: | Journal of gastroenterology and hepatology 2004-06, Vol.19 (6), p.694-698 |
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creator | PARK, SEUNG HA KIM, BYUNG IK YUN, JUNG WON KIM, JEONG WOOK PARK, DONG IL CHO, YONG KYUN SUNG, IN KYUNG PARK, CHANG YOUNG SOHN, CHONG IL JEON, WOO KYU KIM, HYANG RHEE, EUN JUNG LEE, WON YOUNG KIM, SUN WOO |
description | Background and Aim: Although insulin resistance is often considered the link between obesity and non‐alcoholic fatty liver disease (NAFLD), the role of insulin resistance, independent of obesity, as a NAFLD risk factor in non‐obese men has been less well established. Systemic inflammation may be accompanied by insulin resistance in healthy subjects. The goal of the present study was to examine if insulin resistance and systemic inflammatory markers are independent predictors of NAFLD in non‐obese men.
Methods: The authors conducted a cross‐sectional survey of 120 patients with NAFLD and 240 controls matched by age and body mass index. Controls had no evidence of alcohol abuse, hepatitis B or C, obesity, or previous history of diabetes, fasting hyperglycemia or hypertension. Diagnosis of NAFLD was based on an elevated alanine aminotransferase level and sonographic evidence of a fatty liver. Insulin resistance was determined using a homeostasis model assessment (HOMA‐IR).
Results: The age‐adjusted risk of developing NAFLD was strongly associated with the elevated levels in measurements of uric acid, fasting blood sugar, triglycerides, apolipoprotein B, C‐reactive protein (CRP) and HOMA‐IR, and decreased levels of high density lipoprotein cholesterol and apolipoprotein A‐I. Multivariate analysis based on univariate analysis indicated that an increase in CRP (odds ratio [OR] = 1.37; 95% confidence interval [CI]: 1.06–1.77) per 1 SD (1.48 mg/L) and HOMA‐IR (OR = 2.28; 95% CI: 1.67–3.11) per 1 SD (0.63) were independent risk factors for NAFLD.
Conclusion: Insulin resistance and systemic inflammatory response are of key importance for inducing NAFLD, particularly in apparently healthy non‐obese men. |
doi_str_mv | 10.1111/j.1440-1746.2004.03362.x |
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fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71943559</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>71943559</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4992-dc40bf0ff0e4d21d60fba00111815ba035b16baa60162e578d9775c1fd2dc4893</originalsourceid><addsrcrecordid>eNqNkcGO0zAQhi0EYsvCKyBf4JZgJ3GcHDgsFXQXVoAQiKPlOGPhbup0PSm0V56cybZaOGJL9lj-_vHMb8a4FLmk8Wqdy6oSmdRVnRdCVLkoy7rI9w_Y4v7iIVuIRqqsLWV7xp4grgWRQqvH7EwqmnVRL9jvq4i7IUSeAANONjrgNvZ8mSWwbgo_gW_TOAERFnmIPWyBljjxFPCGe2LGhNyPiccxZnZw449xCI5upunAB0qQeB8QLALJ76CxAzpcYLCRbyA-ZY-8HRCenfZz9u3d26_Ly-z60-pqeXGduapti6x3lei88F5A1Reyr4XvrBBkB3VJUak6WXfW1oI6A6WbvtVaOen7gqRNW56zl8e81NDtDnAym4AOhsFGGHdotGyrUqkZbI6gSyNiAm-2KWxsOhgpzOy_WZvZZjPbbGb_zZ3_Zk_S56c3dt0G-r_Ck-EEvDgBFp0dfCLHA_7DUaGynLnXR-5XGODw3wWY96vLOSJ9dtTTp8L-Xm_Tjal1qZX5_nFlis-rD80bXZgv5R-oTrFO</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>71943559</pqid></control><display><type>article</type><title>Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asian men</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>PARK, SEUNG HA ; KIM, BYUNG IK ; YUN, JUNG WON ; KIM, JEONG WOOK ; PARK, DONG IL ; CHO, YONG KYUN ; SUNG, IN KYUNG ; PARK, CHANG YOUNG ; SOHN, CHONG IL ; JEON, WOO KYU ; KIM, HYANG ; RHEE, EUN JUNG ; LEE, WON YOUNG ; KIM, SUN WOO</creator><creatorcontrib>PARK, SEUNG HA ; KIM, BYUNG IK ; YUN, JUNG WON ; KIM, JEONG WOOK ; PARK, DONG IL ; CHO, YONG KYUN ; SUNG, IN KYUNG ; PARK, CHANG YOUNG ; SOHN, CHONG IL ; JEON, WOO KYU ; KIM, HYANG ; RHEE, EUN JUNG ; LEE, WON YOUNG ; KIM, SUN WOO</creatorcontrib><description>Background and Aim: Although insulin resistance is often considered the link between obesity and non‐alcoholic fatty liver disease (NAFLD), the role of insulin resistance, independent of obesity, as a NAFLD risk factor in non‐obese men has been less well established. Systemic inflammation may be accompanied by insulin resistance in healthy subjects. The goal of the present study was to examine if insulin resistance and systemic inflammatory markers are independent predictors of NAFLD in non‐obese men.
Methods: The authors conducted a cross‐sectional survey of 120 patients with NAFLD and 240 controls matched by age and body mass index. Controls had no evidence of alcohol abuse, hepatitis B or C, obesity, or previous history of diabetes, fasting hyperglycemia or hypertension. Diagnosis of NAFLD was based on an elevated alanine aminotransferase level and sonographic evidence of a fatty liver. Insulin resistance was determined using a homeostasis model assessment (HOMA‐IR).
Results: The age‐adjusted risk of developing NAFLD was strongly associated with the elevated levels in measurements of uric acid, fasting blood sugar, triglycerides, apolipoprotein B, C‐reactive protein (CRP) and HOMA‐IR, and decreased levels of high density lipoprotein cholesterol and apolipoprotein A‐I. Multivariate analysis based on univariate analysis indicated that an increase in CRP (odds ratio [OR] = 1.37; 95% confidence interval [CI]: 1.06–1.77) per 1 SD (1.48 mg/L) and HOMA‐IR (OR = 2.28; 95% CI: 1.67–3.11) per 1 SD (0.63) were independent risk factors for NAFLD.
Conclusion: Insulin resistance and systemic inflammatory response are of key importance for inducing NAFLD, particularly in apparently healthy non‐obese men.</description><identifier>ISSN: 0815-9319</identifier><identifier>EISSN: 1440-1746</identifier><identifier>DOI: 10.1111/j.1440-1746.2004.03362.x</identifier><identifier>PMID: 15151626</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Science Pty</publisher><subject>Adult ; Asian Continental Ancestry Group ; Biological and medical sciences ; C-reactive protein ; C-Reactive Protein - analysis ; Case-Control Studies ; Confidence Intervals ; Cross-Sectional Studies ; Fatty Liver - epidemiology ; Gastroenterology. Liver. Pancreas. Abdomen ; Homeostasis ; homeostasis model assessment ; Humans ; inflammation ; Insulin Resistance ; Male ; Medical sciences ; Metabolic diseases ; Models, Biological ; Multivariate Analysis ; non-alcoholic fatty liver disease ; Obesity ; Odds Ratio ; Risk Factors</subject><ispartof>Journal of gastroenterology and hepatology, 2004-06, Vol.19 (6), p.694-698</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4992-dc40bf0ff0e4d21d60fba00111815ba035b16baa60162e578d9775c1fd2dc4893</citedby><cites>FETCH-LOGICAL-c4992-dc40bf0ff0e4d21d60fba00111815ba035b16baa60162e578d9775c1fd2dc4893</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%2Fj.1440-1746.2004.03362.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1440-1746.2004.03362.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,782,786,1419,27931,27932,45581,45582</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15893136$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15151626$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>PARK, SEUNG HA</creatorcontrib><creatorcontrib>KIM, BYUNG IK</creatorcontrib><creatorcontrib>YUN, JUNG WON</creatorcontrib><creatorcontrib>KIM, JEONG WOOK</creatorcontrib><creatorcontrib>PARK, DONG IL</creatorcontrib><creatorcontrib>CHO, YONG KYUN</creatorcontrib><creatorcontrib>SUNG, IN KYUNG</creatorcontrib><creatorcontrib>PARK, CHANG YOUNG</creatorcontrib><creatorcontrib>SOHN, CHONG IL</creatorcontrib><creatorcontrib>JEON, WOO KYU</creatorcontrib><creatorcontrib>KIM, HYANG</creatorcontrib><creatorcontrib>RHEE, EUN JUNG</creatorcontrib><creatorcontrib>LEE, WON YOUNG</creatorcontrib><creatorcontrib>KIM, SUN WOO</creatorcontrib><title>Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asian men</title><title>Journal of gastroenterology and hepatology</title><addtitle>J Gastroenterol Hepatol</addtitle><description>Background and Aim: Although insulin resistance is often considered the link between obesity and non‐alcoholic fatty liver disease (NAFLD), the role of insulin resistance, independent of obesity, as a NAFLD risk factor in non‐obese men has been less well established. Systemic inflammation may be accompanied by insulin resistance in healthy subjects. The goal of the present study was to examine if insulin resistance and systemic inflammatory markers are independent predictors of NAFLD in non‐obese men.
Methods: The authors conducted a cross‐sectional survey of 120 patients with NAFLD and 240 controls matched by age and body mass index. Controls had no evidence of alcohol abuse, hepatitis B or C, obesity, or previous history of diabetes, fasting hyperglycemia or hypertension. Diagnosis of NAFLD was based on an elevated alanine aminotransferase level and sonographic evidence of a fatty liver. Insulin resistance was determined using a homeostasis model assessment (HOMA‐IR).
Results: The age‐adjusted risk of developing NAFLD was strongly associated with the elevated levels in measurements of uric acid, fasting blood sugar, triglycerides, apolipoprotein B, C‐reactive protein (CRP) and HOMA‐IR, and decreased levels of high density lipoprotein cholesterol and apolipoprotein A‐I. Multivariate analysis based on univariate analysis indicated that an increase in CRP (odds ratio [OR] = 1.37; 95% confidence interval [CI]: 1.06–1.77) per 1 SD (1.48 mg/L) and HOMA‐IR (OR = 2.28; 95% CI: 1.67–3.11) per 1 SD (0.63) were independent risk factors for NAFLD.
Conclusion: Insulin resistance and systemic inflammatory response are of key importance for inducing NAFLD, particularly in apparently healthy non‐obese men.</description><subject>Adult</subject><subject>Asian Continental Ancestry Group</subject><subject>Biological and medical sciences</subject><subject>C-reactive protein</subject><subject>C-Reactive Protein - analysis</subject><subject>Case-Control Studies</subject><subject>Confidence Intervals</subject><subject>Cross-Sectional Studies</subject><subject>Fatty Liver - epidemiology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Homeostasis</subject><subject>homeostasis model assessment</subject><subject>Humans</subject><subject>inflammation</subject><subject>Insulin Resistance</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Models, Biological</subject><subject>Multivariate Analysis</subject><subject>non-alcoholic fatty liver disease</subject><subject>Obesity</subject><subject>Odds Ratio</subject><subject>Risk Factors</subject><issn>0815-9319</issn><issn>1440-1746</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcGO0zAQhi0EYsvCKyBf4JZgJ3GcHDgsFXQXVoAQiKPlOGPhbup0PSm0V56cybZaOGJL9lj-_vHMb8a4FLmk8Wqdy6oSmdRVnRdCVLkoy7rI9w_Y4v7iIVuIRqqsLWV7xp4grgWRQqvH7EwqmnVRL9jvq4i7IUSeAANONjrgNvZ8mSWwbgo_gW_TOAERFnmIPWyBljjxFPCGe2LGhNyPiccxZnZw449xCI5upunAB0qQeB8QLALJ76CxAzpcYLCRbyA-ZY-8HRCenfZz9u3d26_Ly-z60-pqeXGduapti6x3lei88F5A1Reyr4XvrBBkB3VJUak6WXfW1oI6A6WbvtVaOen7gqRNW56zl8e81NDtDnAym4AOhsFGGHdotGyrUqkZbI6gSyNiAm-2KWxsOhgpzOy_WZvZZjPbbGb_zZ3_Zk_S56c3dt0G-r_Ck-EEvDgBFp0dfCLHA_7DUaGynLnXR-5XGODw3wWY96vLOSJ9dtTTp8L-Xm_Tjal1qZX5_nFlis-rD80bXZgv5R-oTrFO</recordid><startdate>200406</startdate><enddate>200406</enddate><creator>PARK, SEUNG HA</creator><creator>KIM, BYUNG IK</creator><creator>YUN, JUNG WON</creator><creator>KIM, JEONG WOOK</creator><creator>PARK, DONG IL</creator><creator>CHO, YONG KYUN</creator><creator>SUNG, IN KYUNG</creator><creator>PARK, CHANG YOUNG</creator><creator>SOHN, CHONG IL</creator><creator>JEON, WOO KYU</creator><creator>KIM, HYANG</creator><creator>RHEE, EUN JUNG</creator><creator>LEE, WON YOUNG</creator><creator>KIM, SUN WOO</creator><general>Blackwell Science Pty</general><general>Blackwell Science</general><scope>BSCLL</scope><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>7X8</scope></search><sort><creationdate>200406</creationdate><title>Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asian men</title><author>PARK, SEUNG HA ; KIM, BYUNG IK ; YUN, JUNG WON ; KIM, JEONG WOOK ; PARK, DONG IL ; CHO, YONG KYUN ; SUNG, IN KYUNG ; PARK, CHANG YOUNG ; SOHN, CHONG IL ; JEON, WOO KYU ; KIM, HYANG ; RHEE, EUN JUNG ; LEE, WON YOUNG ; KIM, SUN WOO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4992-dc40bf0ff0e4d21d60fba00111815ba035b16baa60162e578d9775c1fd2dc4893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Asian Continental Ancestry Group</topic><topic>Biological and medical sciences</topic><topic>C-reactive protein</topic><topic>C-Reactive Protein - analysis</topic><topic>Case-Control Studies</topic><topic>Confidence Intervals</topic><topic>Cross-Sectional Studies</topic><topic>Fatty Liver - epidemiology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Homeostasis</topic><topic>homeostasis model assessment</topic><topic>Humans</topic><topic>inflammation</topic><topic>Insulin Resistance</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Models, Biological</topic><topic>Multivariate Analysis</topic><topic>non-alcoholic fatty liver disease</topic><topic>Obesity</topic><topic>Odds Ratio</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>PARK, SEUNG HA</creatorcontrib><creatorcontrib>KIM, BYUNG IK</creatorcontrib><creatorcontrib>YUN, JUNG WON</creatorcontrib><creatorcontrib>KIM, JEONG WOOK</creatorcontrib><creatorcontrib>PARK, DONG IL</creatorcontrib><creatorcontrib>CHO, YONG KYUN</creatorcontrib><creatorcontrib>SUNG, IN KYUNG</creatorcontrib><creatorcontrib>PARK, CHANG YOUNG</creatorcontrib><creatorcontrib>SOHN, CHONG IL</creatorcontrib><creatorcontrib>JEON, WOO KYU</creatorcontrib><creatorcontrib>KIM, HYANG</creatorcontrib><creatorcontrib>RHEE, EUN JUNG</creatorcontrib><creatorcontrib>LEE, WON YOUNG</creatorcontrib><creatorcontrib>KIM, SUN WOO</creatorcontrib><collection>Istex</collection><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>MEDLINE - Academic</collection><jtitle>Journal of gastroenterology and hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>PARK, SEUNG HA</au><au>KIM, BYUNG IK</au><au>YUN, JUNG WON</au><au>KIM, JEONG WOOK</au><au>PARK, DONG IL</au><au>CHO, YONG KYUN</au><au>SUNG, IN KYUNG</au><au>PARK, CHANG YOUNG</au><au>SOHN, CHONG IL</au><au>JEON, WOO KYU</au><au>KIM, HYANG</au><au>RHEE, EUN JUNG</au><au>LEE, WON YOUNG</au><au>KIM, SUN WOO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asian men</atitle><jtitle>Journal of gastroenterology and hepatology</jtitle><addtitle>J Gastroenterol Hepatol</addtitle><date>2004-06</date><risdate>2004</risdate><volume>19</volume><issue>6</issue><spage>694</spage><epage>698</epage><pages>694-698</pages><issn>0815-9319</issn><eissn>1440-1746</eissn><abstract>Background and Aim: Although insulin resistance is often considered the link between obesity and non‐alcoholic fatty liver disease (NAFLD), the role of insulin resistance, independent of obesity, as a NAFLD risk factor in non‐obese men has been less well established. Systemic inflammation may be accompanied by insulin resistance in healthy subjects. The goal of the present study was to examine if insulin resistance and systemic inflammatory markers are independent predictors of NAFLD in non‐obese men.
Methods: The authors conducted a cross‐sectional survey of 120 patients with NAFLD and 240 controls matched by age and body mass index. Controls had no evidence of alcohol abuse, hepatitis B or C, obesity, or previous history of diabetes, fasting hyperglycemia or hypertension. Diagnosis of NAFLD was based on an elevated alanine aminotransferase level and sonographic evidence of a fatty liver. Insulin resistance was determined using a homeostasis model assessment (HOMA‐IR).
Results: The age‐adjusted risk of developing NAFLD was strongly associated with the elevated levels in measurements of uric acid, fasting blood sugar, triglycerides, apolipoprotein B, C‐reactive protein (CRP) and HOMA‐IR, and decreased levels of high density lipoprotein cholesterol and apolipoprotein A‐I. Multivariate analysis based on univariate analysis indicated that an increase in CRP (odds ratio [OR] = 1.37; 95% confidence interval [CI]: 1.06–1.77) per 1 SD (1.48 mg/L) and HOMA‐IR (OR = 2.28; 95% CI: 1.67–3.11) per 1 SD (0.63) were independent risk factors for NAFLD.
Conclusion: Insulin resistance and systemic inflammatory response are of key importance for inducing NAFLD, particularly in apparently healthy non‐obese men.</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Science Pty</pub><pmid>15151626</pmid><doi>10.1111/j.1440-1746.2004.03362.x</doi><tpages>5</tpages></addata></record> |
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subjects | Adult Asian Continental Ancestry Group Biological and medical sciences C-reactive protein C-Reactive Protein - analysis Case-Control Studies Confidence Intervals Cross-Sectional Studies Fatty Liver - epidemiology Gastroenterology. Liver. Pancreas. Abdomen Homeostasis homeostasis model assessment Humans inflammation Insulin Resistance Male Medical sciences Metabolic diseases Models, Biological Multivariate Analysis non-alcoholic fatty liver disease Obesity Odds Ratio Risk Factors |
title | Insulin resistance and C-reactive protein as independent risk factors for non-alcoholic fatty liver disease in non-obese Asian men |
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