Increased diacylglycerol acyltransferase activity is associated with triglyceride accumulation in tissues of diet-induced insulin-resistant hyperlipidemic hamsters
Over-accumulation of triglyceride (TG) in insulin-sensitive tissues is associated with the development of insulin resistance. We investigated whether enhanced de novo lipogenesis via diacylglycerol acyltransferase (DGAT) may contribute to the over-accumulation of TG in various tissues (liver, adipos...
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Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2005-03, Vol.54 (3), p.403-409 |
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description | Over-accumulation of triglyceride (TG) in insulin-sensitive tissues is associated with the development of insulin resistance. We investigated whether enhanced de novo lipogenesis via diacylglycerol acyltransferase (DGAT) may contribute to the over-accumulation of TG in various tissues (liver, adipose, muscle, and intestine) using 2 well-characterized hyperlipidemic, insulin-resistant hamster models. In general, a marked increase in TG accumulation was noted in most tissues. Interestingly, the increase in TG accumulation corresponded to an increase in microsomal DGAT activity which ranged from 114% to 575% in all of the examined tissues (n = 7 per group). To delineate the mechanism for the increase in DGAT activity, we measured the expression of DGAT-1 and DGAT-2 messenger RNA by relative reverse transcriptase polymerase chain reaction (RT-PCR). In general, DGAT gene expression changed with DGAT-1 changing the most in the liver and adipose tissue, whereas DGAT-2 showed responses mainly in muscle and intestine. The increases in messenger RNA expression were not remarkable (averaging 35%; n = 4 per group) indicating that posttranscriptional mechanism(s) may play a larger role in regulating DGAT activity. In summary, the data suggest that elevated DGAT activity/expression and the subsequent increase in de novo lipogenesis could in part induce the insulin-resistant state. |
doi_str_mv | 10.1016/j.metabol.2004.09.016 |
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We investigated whether enhanced de novo lipogenesis via diacylglycerol acyltransferase (DGAT) may contribute to the over-accumulation of TG in various tissues (liver, adipose, muscle, and intestine) using 2 well-characterized hyperlipidemic, insulin-resistant hamster models. In general, a marked increase in TG accumulation was noted in most tissues. Interestingly, the increase in TG accumulation corresponded to an increase in microsomal DGAT activity which ranged from 114% to 575% in all of the examined tissues (n = 7 per group). To delineate the mechanism for the increase in DGAT activity, we measured the expression of DGAT-1 and DGAT-2 messenger RNA by relative reverse transcriptase polymerase chain reaction (RT-PCR). In general, DGAT gene expression changed with DGAT-1 changing the most in the liver and adipose tissue, whereas DGAT-2 showed responses mainly in muscle and intestine. The increases in messenger RNA expression were not remarkable (averaging 35%; n = 4 per group) indicating that posttranscriptional mechanism(s) may play a larger role in regulating DGAT activity. In summary, the data suggest that elevated DGAT activity/expression and the subsequent increase in de novo lipogenesis could in part induce the insulin-resistant state.</description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/j.metabol.2004.09.016</identifier><identifier>PMID: 15736121</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Acyltransferases - genetics ; Acyltransferases - metabolism ; Adipose Tissue - enzymology ; Adipose Tissue - metabolism ; Animals ; Biological and medical sciences ; Cholesterol - blood ; Cricetinae ; Diabetes. Impaired glucose tolerance ; Diacylglycerol O-Acyltransferase ; Diet ; Dietary Fats - administration & dosage ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. 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We investigated whether enhanced de novo lipogenesis via diacylglycerol acyltransferase (DGAT) may contribute to the over-accumulation of TG in various tissues (liver, adipose, muscle, and intestine) using 2 well-characterized hyperlipidemic, insulin-resistant hamster models. In general, a marked increase in TG accumulation was noted in most tissues. Interestingly, the increase in TG accumulation corresponded to an increase in microsomal DGAT activity which ranged from 114% to 575% in all of the examined tissues (n = 7 per group). To delineate the mechanism for the increase in DGAT activity, we measured the expression of DGAT-1 and DGAT-2 messenger RNA by relative reverse transcriptase polymerase chain reaction (RT-PCR). In general, DGAT gene expression changed with DGAT-1 changing the most in the liver and adipose tissue, whereas DGAT-2 showed responses mainly in muscle and intestine. The increases in messenger RNA expression were not remarkable (averaging 35%; n = 4 per group) indicating that posttranscriptional mechanism(s) may play a larger role in regulating DGAT activity. In summary, the data suggest that elevated DGAT activity/expression and the subsequent increase in de novo lipogenesis could in part induce the insulin-resistant state.</description><subject>Acyltransferases - genetics</subject><subject>Acyltransferases - metabolism</subject><subject>Adipose Tissue - enzymology</subject><subject>Adipose Tissue - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cholesterol - blood</subject><subject>Cricetinae</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diacylglycerol O-Acyltransferase</subject><subject>Diet</subject><subject>Dietary Fats - administration & dosage</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Fatty Acids, Nonesterified - blood</subject><subject>Fructose - administration & dosage</subject><subject>Gene Expression</subject><subject>Hyperlipidemias - enzymology</subject><subject>Hyperlipidemias - metabolism</subject><subject>Insulin - blood</subject><subject>Insulin Resistance</subject><subject>Intestines - enzymology</subject><subject>Intestines - metabolism</subject><subject>Liver - enzymology</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mesocricetus</subject><subject>Muscles - enzymology</subject><subject>Muscles - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>Triglycerides - blood</subject><subject>Triglycerides - metabolism</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhiMEotvCTwDlAreEcT6c5IRQxUelSlzgbHntMTsrJ1k8Tqv8Hv4oXm2kHnuyZvy8M6P3zbJ3AkoBQn46liNGvZ99WQE0JQxl6r7IdqKtq6KXAC-zHUAlC2iG9iq7Zj4CQNf18nV2JdqulqISu-zf3WQCakabW9Jm9X_8ajDMPj8XMeiJHYb0n-pIDxTXnDjXzLMhHZPqkeIhj4EuOrJn0Czj4nWkecppyiMxL8j57NIKjAVNdjFJSRMvnqYiIBNHPcX8sJ4weDqlKSOZ_KBHjhj4TfbKac_4dntvst_fvv66_VHc__x-d_vlvjD1UMei6prGgHOisrXttRVO4gBmb6FvsbeVtWicFY2VjXTQDS2gENpVNdRdM9i-vsk-Xuaewvw3XRzVSGzQez3hvLCSXSM7UVUJbC-gCTNzQKdOgUYdViVAndNRR7Wlo87pKBhU6ibd-23Bsh_RPqm2OBLwYQM0G-1dst8QP3FSiiblmbjPFw6THQ-EQbEhnJKrFNBEZWd65pT_eqi20g</recordid><startdate>20050301</startdate><enddate>20050301</enddate><creator>Casaschi, Adele</creator><creator>Maiyoh, Geoffrey K.</creator><creator>Adeli, Khosrow</creator><creator>Theriault, Andre G.</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>20050301</creationdate><title>Increased diacylglycerol acyltransferase activity is associated with triglyceride accumulation in tissues of diet-induced insulin-resistant hyperlipidemic hamsters</title><author>Casaschi, Adele ; Maiyoh, Geoffrey K. ; Adeli, Khosrow ; Theriault, Andre G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-2744c0ff12d3d8ad1f6e90cbd085e8d2ddecfd14d646f07950e11af2303749d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acyltransferases - genetics</topic><topic>Acyltransferases - metabolism</topic><topic>Adipose Tissue - enzymology</topic><topic>Adipose Tissue - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cholesterol - blood</topic><topic>Cricetinae</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diacylglycerol O-Acyltransferase</topic><topic>Diet</topic><topic>Dietary Fats - administration & dosage</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Fatty Acids, Nonesterified - blood</topic><topic>Fructose - administration & dosage</topic><topic>Gene Expression</topic><topic>Hyperlipidemias - enzymology</topic><topic>Hyperlipidemias - metabolism</topic><topic>Insulin - blood</topic><topic>Insulin Resistance</topic><topic>Intestines - enzymology</topic><topic>Intestines - metabolism</topic><topic>Liver - enzymology</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mesocricetus</topic><topic>Muscles - enzymology</topic><topic>Muscles - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>Triglycerides - blood</topic><topic>Triglycerides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Casaschi, Adele</creatorcontrib><creatorcontrib>Maiyoh, Geoffrey K.</creatorcontrib><creatorcontrib>Adeli, Khosrow</creatorcontrib><creatorcontrib>Theriault, Andre G.</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><collection>MEDLINE - Academic</collection><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Casaschi, Adele</au><au>Maiyoh, Geoffrey K.</au><au>Adeli, Khosrow</au><au>Theriault, Andre G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased diacylglycerol acyltransferase activity is associated with triglyceride accumulation in tissues of diet-induced insulin-resistant hyperlipidemic hamsters</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>2005-03-01</date><risdate>2005</risdate><volume>54</volume><issue>3</issue><spage>403</spage><epage>409</epage><pages>403-409</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract>Over-accumulation of triglyceride (TG) in insulin-sensitive tissues is associated with the development of insulin resistance. We investigated whether enhanced de novo lipogenesis via diacylglycerol acyltransferase (DGAT) may contribute to the over-accumulation of TG in various tissues (liver, adipose, muscle, and intestine) using 2 well-characterized hyperlipidemic, insulin-resistant hamster models. In general, a marked increase in TG accumulation was noted in most tissues. Interestingly, the increase in TG accumulation corresponded to an increase in microsomal DGAT activity which ranged from 114% to 575% in all of the examined tissues (n = 7 per group). To delineate the mechanism for the increase in DGAT activity, we measured the expression of DGAT-1 and DGAT-2 messenger RNA by relative reverse transcriptase polymerase chain reaction (RT-PCR). In general, DGAT gene expression changed with DGAT-1 changing the most in the liver and adipose tissue, whereas DGAT-2 showed responses mainly in muscle and intestine. The increases in messenger RNA expression were not remarkable (averaging 35%; n = 4 per group) indicating that posttranscriptional mechanism(s) may play a larger role in regulating DGAT activity. In summary, the data suggest that elevated DGAT activity/expression and the subsequent increase in de novo lipogenesis could in part induce the insulin-resistant state.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15736121</pmid><doi>10.1016/j.metabol.2004.09.016</doi><tpages>7</tpages></addata></record> |
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subjects | Acyltransferases - genetics Acyltransferases - metabolism Adipose Tissue - enzymology Adipose Tissue - metabolism Animals Biological and medical sciences Cholesterol - blood Cricetinae Diabetes. Impaired glucose tolerance Diacylglycerol O-Acyltransferase Diet Dietary Fats - administration & dosage Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Fatty Acids, Nonesterified - blood Fructose - administration & dosage Gene Expression Hyperlipidemias - enzymology Hyperlipidemias - metabolism Insulin - blood Insulin Resistance Intestines - enzymology Intestines - metabolism Liver - enzymology Liver - metabolism Male Medical sciences Mesocricetus Muscles - enzymology Muscles - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis Triglycerides - blood Triglycerides - metabolism |
title | Increased diacylglycerol acyltransferase activity is associated with triglyceride accumulation in tissues of diet-induced insulin-resistant hyperlipidemic hamsters |
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