Diabetic Phenotype in the Small Intestine of Zucker Diabetic Fatty Rats
Background/Aims: In contrast to streptozotocin (STZ)-induced rodent models of diabetes, there are no thorough characterizations of the intestinal phenotype and the underlying changes in the global gene-expression of genetic models of diabetes, such as the Zucker diabetic fatty (ZDF) rat. The aim of...
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Veröffentlicht in: | Digestion 2016-01, Vol.94 (4), p.199-214 |
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creator | Hvid, Henning Jensen, Stina Rikke Witgen, Brent M. Fledelius, Christian Damgaard, Jesper Pyke, Charles Rasmussen, Thomas Bovbjerg |
description | Background/Aims: In contrast to streptozotocin (STZ)-induced rodent models of diabetes, there are no thorough characterizations of the intestinal phenotype and the underlying changes in the global gene-expression of genetic models of diabetes, such as the Zucker diabetic fatty (ZDF) rat. The aim of the present study was to characterize the intestine in the ZDF rat. Methods: The intestine of ZDF rats and lean controls was examined macroscopically and histologically, and ribonucleic acid sequencing (RNAseq) was performed in samples of jejunal mucosa. Results: We observed an increased mass and length of the small and large intestines in ZDF rats. RNAseq showed an increased expression of Pdk2 and Pdk4, which are involved in the regulation of glucose and fatty acid metabolism, and increased expression of genes involved in gluconeogenesis and peroxisomal beta-oxidation in jejunal mucosa. Conclusion: Intestinal enlargement in ZDF rats is likely driven by increased food intake, since (i) it also occurs in obese and normoglycemic Zucker fatty rats, and (ii) insulin treatment of STZ-induced diabetic rats reduced the food intake and mass of the small intestine. Results from RNAseq indicate that small intestinal epithelial cells in ZDF rats have developed insulin resistance, and support that a normal physiological effect of insulin in the enterocytes is the regulation of glucose metabolism. |
doi_str_mv | 10.1159/000453107 |
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The aim of the present study was to characterize the intestine in the ZDF rat. Methods: The intestine of ZDF rats and lean controls was examined macroscopically and histologically, and ribonucleic acid sequencing (RNAseq) was performed in samples of jejunal mucosa. Results: We observed an increased mass and length of the small and large intestines in ZDF rats. RNAseq showed an increased expression of Pdk2 and Pdk4, which are involved in the regulation of glucose and fatty acid metabolism, and increased expression of genes involved in gluconeogenesis and peroxisomal beta-oxidation in jejunal mucosa. Conclusion: Intestinal enlargement in ZDF rats is likely driven by increased food intake, since (i) it also occurs in obese and normoglycemic Zucker fatty rats, and (ii) insulin treatment of STZ-induced diabetic rats reduced the food intake and mass of the small intestine. Results from RNAseq indicate that small intestinal epithelial cells in ZDF rats have developed insulin resistance, and support that a normal physiological effect of insulin in the enterocytes is the regulation of glucose metabolism.</description><identifier>ISSN: 0012-2823</identifier><identifier>EISSN: 1421-9867</identifier><identifier>DOI: 10.1159/000453107</identifier><identifier>PMID: 27931035</identifier><language>eng</language><publisher>Basel, Switzerland</publisher><subject>Animals ; Diabetes Mellitus, Experimental - genetics ; Diabetes Mellitus, Experimental - metabolism ; Gluconeogenesis ; Glucose - metabolism ; Insulin Resistance ; Intestinal Mucosa - enzymology ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - pathology ; Intestine, Large - pathology ; Intestine, Small - enzymology ; Intestine, Small - metabolism ; Intestine, Small - pathology ; Male ; Obesity - metabolism ; Original Paper ; Phenotype ; Protein-Serine-Threonine Kinases - metabolism ; Rats ; Rats, Sprague-Dawley ; Rats, Zucker ; Sequence Analysis, RNA ; Sucrase - metabolism ; Transcriptome ; Up-Regulation</subject><ispartof>Digestion, 2016-01, Vol.94 (4), p.199-214</ispartof><rights>2016 S. Karger AG, Basel</rights><rights>2016 S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-6fa681d99a6092dd9e5d1960544e17e59c44d0cd1bbe55bb7e39265a9a290f373</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27931035$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hvid, Henning</creatorcontrib><creatorcontrib>Jensen, Stina Rikke</creatorcontrib><creatorcontrib>Witgen, Brent M.</creatorcontrib><creatorcontrib>Fledelius, Christian</creatorcontrib><creatorcontrib>Damgaard, Jesper</creatorcontrib><creatorcontrib>Pyke, Charles</creatorcontrib><creatorcontrib>Rasmussen, Thomas Bovbjerg</creatorcontrib><title>Diabetic Phenotype in the Small Intestine of Zucker Diabetic Fatty Rats</title><title>Digestion</title><addtitle>Digestion</addtitle><description>Background/Aims: In contrast to streptozotocin (STZ)-induced rodent models of diabetes, there are no thorough characterizations of the intestinal phenotype and the underlying changes in the global gene-expression of genetic models of diabetes, such as the Zucker diabetic fatty (ZDF) rat. The aim of the present study was to characterize the intestine in the ZDF rat. Methods: The intestine of ZDF rats and lean controls was examined macroscopically and histologically, and ribonucleic acid sequencing (RNAseq) was performed in samples of jejunal mucosa. Results: We observed an increased mass and length of the small and large intestines in ZDF rats. RNAseq showed an increased expression of Pdk2 and Pdk4, which are involved in the regulation of glucose and fatty acid metabolism, and increased expression of genes involved in gluconeogenesis and peroxisomal beta-oxidation in jejunal mucosa. Conclusion: Intestinal enlargement in ZDF rats is likely driven by increased food intake, since (i) it also occurs in obese and normoglycemic Zucker fatty rats, and (ii) insulin treatment of STZ-induced diabetic rats reduced the food intake and mass of the small intestine. Results from RNAseq indicate that small intestinal epithelial cells in ZDF rats have developed insulin resistance, and support that a normal physiological effect of insulin in the enterocytes is the regulation of glucose metabolism.</description><subject>Animals</subject><subject>Diabetes Mellitus, Experimental - genetics</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Gluconeogenesis</subject><subject>Glucose - metabolism</subject><subject>Insulin Resistance</subject><subject>Intestinal Mucosa - enzymology</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - pathology</subject><subject>Intestine, Large - pathology</subject><subject>Intestine, Small - enzymology</subject><subject>Intestine, Small - metabolism</subject><subject>Intestine, Small - pathology</subject><subject>Male</subject><subject>Obesity - metabolism</subject><subject>Original Paper</subject><subject>Phenotype</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rats, Zucker</subject><subject>Sequence Analysis, RNA</subject><subject>Sucrase - metabolism</subject><subject>Transcriptome</subject><subject>Up-Regulation</subject><issn>0012-2823</issn><issn>1421-9867</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo90DtPwzAQB3ALgWgpDOwIeYQh4Gccj6jQUqkSiMfCEjnOhYbmUWxn6LcnVUuWO530u9Ppj9AlJXeUSn1PCBGSU6KO0JgKRiOdxOoYjQmhLGIJ4yN05v3PbtSCn6IRU7rnXI7R_LE0GYTS4tcVNG3YbgCXDQ4rwO-1qSq8aAL4UDaA2wJ_dXYNDg87MxPCFr-Z4M_RSWEqDxeHPkGfs6eP6XO0fJkvpg_LyHLFQhQXJk5orrWJiWZ5rkHmVMdECgFUgdRWiJzYnGYZSJllCrhmsTTaME0KrvgE3ezvblz72_WfpXXpLVSVaaDtfEoToRJN-trT2z21rvXeQZFuXFkbt00pSXe5pUNuvb0-nO2yGvJB_gfVg6s9WBv3DW4Ah_0_rfxvEA</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Hvid, Henning</creator><creator>Jensen, Stina Rikke</creator><creator>Witgen, Brent M.</creator><creator>Fledelius, Christian</creator><creator>Damgaard, Jesper</creator><creator>Pyke, Charles</creator><creator>Rasmussen, Thomas Bovbjerg</creator><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>20160101</creationdate><title>Diabetic Phenotype in the Small Intestine of Zucker Diabetic Fatty Rats</title><author>Hvid, Henning ; Jensen, Stina Rikke ; Witgen, Brent M. ; Fledelius, Christian ; Damgaard, Jesper ; Pyke, Charles ; Rasmussen, Thomas Bovbjerg</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-6fa681d99a6092dd9e5d1960544e17e59c44d0cd1bbe55bb7e39265a9a290f373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Diabetes Mellitus, Experimental - genetics</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Gluconeogenesis</topic><topic>Glucose - metabolism</topic><topic>Insulin Resistance</topic><topic>Intestinal Mucosa - enzymology</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestinal Mucosa - pathology</topic><topic>Intestine, Large - pathology</topic><topic>Intestine, Small - enzymology</topic><topic>Intestine, Small - metabolism</topic><topic>Intestine, Small - pathology</topic><topic>Male</topic><topic>Obesity - metabolism</topic><topic>Original Paper</topic><topic>Phenotype</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rats, Zucker</topic><topic>Sequence Analysis, RNA</topic><topic>Sucrase - metabolism</topic><topic>Transcriptome</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hvid, Henning</creatorcontrib><creatorcontrib>Jensen, Stina Rikke</creatorcontrib><creatorcontrib>Witgen, Brent M.</creatorcontrib><creatorcontrib>Fledelius, Christian</creatorcontrib><creatorcontrib>Damgaard, Jesper</creatorcontrib><creatorcontrib>Pyke, Charles</creatorcontrib><creatorcontrib>Rasmussen, Thomas Bovbjerg</creatorcontrib><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>Digestion</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hvid, Henning</au><au>Jensen, Stina Rikke</au><au>Witgen, Brent M.</au><au>Fledelius, Christian</au><au>Damgaard, Jesper</au><au>Pyke, Charles</au><au>Rasmussen, Thomas Bovbjerg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diabetic Phenotype in the Small Intestine of Zucker Diabetic Fatty Rats</atitle><jtitle>Digestion</jtitle><addtitle>Digestion</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>94</volume><issue>4</issue><spage>199</spage><epage>214</epage><pages>199-214</pages><issn>0012-2823</issn><eissn>1421-9867</eissn><abstract>Background/Aims: In contrast to streptozotocin (STZ)-induced rodent models of diabetes, there are no thorough characterizations of the intestinal phenotype and the underlying changes in the global gene-expression of genetic models of diabetes, such as the Zucker diabetic fatty (ZDF) rat. The aim of the present study was to characterize the intestine in the ZDF rat. Methods: The intestine of ZDF rats and lean controls was examined macroscopically and histologically, and ribonucleic acid sequencing (RNAseq) was performed in samples of jejunal mucosa. Results: We observed an increased mass and length of the small and large intestines in ZDF rats. RNAseq showed an increased expression of Pdk2 and Pdk4, which are involved in the regulation of glucose and fatty acid metabolism, and increased expression of genes involved in gluconeogenesis and peroxisomal beta-oxidation in jejunal mucosa. Conclusion: Intestinal enlargement in ZDF rats is likely driven by increased food intake, since (i) it also occurs in obese and normoglycemic Zucker fatty rats, and (ii) insulin treatment of STZ-induced diabetic rats reduced the food intake and mass of the small intestine. Results from RNAseq indicate that small intestinal epithelial cells in ZDF rats have developed insulin resistance, and support that a normal physiological effect of insulin in the enterocytes is the regulation of glucose metabolism.</abstract><cop>Basel, Switzerland</cop><pmid>27931035</pmid><doi>10.1159/000453107</doi><tpages>16</tpages></addata></record> |
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subjects | Animals Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - metabolism Gluconeogenesis Glucose - metabolism Insulin Resistance Intestinal Mucosa - enzymology Intestinal Mucosa - metabolism Intestinal Mucosa - pathology Intestine, Large - pathology Intestine, Small - enzymology Intestine, Small - metabolism Intestine, Small - pathology Male Obesity - metabolism Original Paper Phenotype Protein-Serine-Threonine Kinases - metabolism Rats Rats, Sprague-Dawley Rats, Zucker Sequence Analysis, RNA Sucrase - metabolism Transcriptome Up-Regulation |
title | Diabetic Phenotype in the Small Intestine of Zucker Diabetic Fatty Rats |
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