Multihormonal regulation of hepatic sinusoidal Ntcp gene expression
Bile acids are efficiently removed from sinusoidal blood by a number of transporters including the Na+-taurocholate-cotransporting polypeptide (Ntcp). Na+-dependent bile salt uptake, as well as Ntcp, are expressed twofold higher in male compared with female rat livers. Also, estrogen administration...
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Veröffentlicht in: | American journal of physiology: Gastrointestinal and liver physiology 2004-10, Vol.287 (4), p.G782-G794 |
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creator | Simon, Francis R Fortune, John Iwahashi, Mieko Qadri, Ishtiaq Sutherland, Eileen |
description | Bile acids are efficiently removed from sinusoidal blood by a number of transporters including the Na+-taurocholate-cotransporting polypeptide (Ntcp). Na+-dependent bile salt uptake, as well as Ntcp, are expressed twofold higher in male compared with female rat livers. Also, estrogen administration to male rats decreases Ntcp expression. The aims of this study were to determine the hormonal mechanism(s) responsible for this sexually dimorphic expression of Ntcp. We examined castrated and hypophysectomized rats of both sexes. Sex steroid hormones, growth hormone, thyroid, and glucocorticoids were administered, and livers were examined for changes in Ntcp messenger RNA (mRNA). Ntcp mRNA and protein content were selectively increased in males. Estradiol selectively decreased Ntcp expression in males, whereas ovariectomy increased Ntcp in females, confirming the importance of estrogens in regulating Ntcp. Hypophysectomy decreased Ntcp mRNA levels in males and prevented estrogen administration from decreasing Ntcp, indicating the importance of pituitary hormones. Although constant infusion of growth hormone to intact males reduced Ntcp, its replacement alone after hypophysectomy did not restore the sex differences. In contrast, thyroid hormone and corticosterone increased Ntcp mRNA in hypophysectomized rats. Sex differences in Ntcp mRNA levels were produced only when the female pattern of growth hormone was administered to animals also receiving thyroid and corticosterone. Thyroid and dexamethasone also increased Ntcp mRNA in isolated rat hepatocytes, whereas growth hormone decreased Ntcp. These findings demonstrate the essential role that pituitary hormones play in the sexually dimorphic control of Ntcp expression in adult rat liver and in the mediation of estrogen effects. |
doi_str_mv | 10.1152/ajpgi.00379.2003 |
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Na+-dependent bile salt uptake, as well as Ntcp, are expressed twofold higher in male compared with female rat livers. Also, estrogen administration to male rats decreases Ntcp expression. The aims of this study were to determine the hormonal mechanism(s) responsible for this sexually dimorphic expression of Ntcp. We examined castrated and hypophysectomized rats of both sexes. Sex steroid hormones, growth hormone, thyroid, and glucocorticoids were administered, and livers were examined for changes in Ntcp messenger RNA (mRNA). Ntcp mRNA and protein content were selectively increased in males. Estradiol selectively decreased Ntcp expression in males, whereas ovariectomy increased Ntcp in females, confirming the importance of estrogens in regulating Ntcp. Hypophysectomy decreased Ntcp mRNA levels in males and prevented estrogen administration from decreasing Ntcp, indicating the importance of pituitary hormones. Although constant infusion of growth hormone to intact males reduced Ntcp, its replacement alone after hypophysectomy did not restore the sex differences. In contrast, thyroid hormone and corticosterone increased Ntcp mRNA in hypophysectomized rats. Sex differences in Ntcp mRNA levels were produced only when the female pattern of growth hormone was administered to animals also receiving thyroid and corticosterone. Thyroid and dexamethasone also increased Ntcp mRNA in isolated rat hepatocytes, whereas growth hormone decreased Ntcp. 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Na+-dependent bile salt uptake, as well as Ntcp, are expressed twofold higher in male compared with female rat livers. Also, estrogen administration to male rats decreases Ntcp expression. The aims of this study were to determine the hormonal mechanism(s) responsible for this sexually dimorphic expression of Ntcp. We examined castrated and hypophysectomized rats of both sexes. Sex steroid hormones, growth hormone, thyroid, and glucocorticoids were administered, and livers were examined for changes in Ntcp messenger RNA (mRNA). Ntcp mRNA and protein content were selectively increased in males. Estradiol selectively decreased Ntcp expression in males, whereas ovariectomy increased Ntcp in females, confirming the importance of estrogens in regulating Ntcp. Hypophysectomy decreased Ntcp mRNA levels in males and prevented estrogen administration from decreasing Ntcp, indicating the importance of pituitary hormones. Although constant infusion of growth hormone to intact males reduced Ntcp, its replacement alone after hypophysectomy did not restore the sex differences. In contrast, thyroid hormone and corticosterone increased Ntcp mRNA in hypophysectomized rats. Sex differences in Ntcp mRNA levels were produced only when the female pattern of growth hormone was administered to animals also receiving thyroid and corticosterone. Thyroid and dexamethasone also increased Ntcp mRNA in isolated rat hepatocytes, whereas growth hormone decreased Ntcp. These findings demonstrate the essential role that pituitary hormones play in the sexually dimorphic control of Ntcp expression in adult rat liver and in the mediation of estrogen effects.</description><subject>Androgens - pharmacology</subject><subject>Animals</subject><subject>ATP Binding Cassette Subfamily B Member 11</subject><subject>ATP-Binding Cassette Transporters - genetics</subject><subject>Carrier Proteins - genetics</subject><subject>Corticosterone - pharmacology</subject><subject>Estradiol - pharmacology</subject><subject>Female</subject><subject>Gene Expression - drug effects</subject><subject>Gene Expression - physiology</subject><subject>Growth Hormone - pharmacology</subject><subject>Hormones - pharmacology</subject><subject>Liver - physiology</subject><subject>Male</subject><subject>Membrane Transport Proteins</subject><subject>Multidrug Resistance-Associated Proteins - genetics</subject><subject>Organic Anion Transporters, Sodium-Dependent</subject><subject>Pituitary Gland - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - analysis</subject><subject>Sex Characteristics</subject><subject>Symporters</subject><subject>Testosterone - pharmacology</subject><subject>Thyroxine - pharmacology</subject><issn>0193-1857</issn><issn>1522-1547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtLAzEQxoMotlbvnmRP3rbm0Tz2KMUXVL3oOaTZSZuyu1mTXdD_3tQWhIFvmPnmG_ghdE3wnBBO78yu3_g5xkxWc5rlBE3zmJaEL-QpmmJSsZIoLifoIqUdxphTQs7RhHAmSK4pWr6OzeC3IbahM00RYTM2ZvChK4IrttDn3hbJd2MKvs6Gt8H2xQY6KOC7j5BStl6iM2eaBFdHnaHPx4eP5XO5en96Wd6vSksrPpRcsIWhrOZKYgyMKCrpmslaOcDCEVcJW-V1xa1TjFK7AOekBMOkxBILxWbo9pDbx_A1Qhp065OFpjEdhDFpIZTIT2Q24oPRxpBSBKf76FsTfzTBeg9O_4HTf-D0Hlw-uTlmj-sW6v-DIyn2C7BbadQ</recordid><startdate>200410</startdate><enddate>200410</enddate><creator>Simon, Francis R</creator><creator>Fortune, John</creator><creator>Iwahashi, Mieko</creator><creator>Qadri, Ishtiaq</creator><creator>Sutherland, Eileen</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>200410</creationdate><title>Multihormonal regulation of hepatic sinusoidal Ntcp gene expression</title><author>Simon, Francis R ; Fortune, John ; Iwahashi, Mieko ; Qadri, Ishtiaq ; Sutherland, Eileen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c295t-5634a23d58700e318272b37d8fe06f1f96c923d95cf8322c4eff77ea377070683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Androgens - pharmacology</topic><topic>Animals</topic><topic>ATP Binding Cassette Subfamily B Member 11</topic><topic>ATP-Binding Cassette Transporters - genetics</topic><topic>Carrier Proteins - genetics</topic><topic>Corticosterone - pharmacology</topic><topic>Estradiol - pharmacology</topic><topic>Female</topic><topic>Gene Expression - drug effects</topic><topic>Gene Expression - physiology</topic><topic>Growth Hormone - pharmacology</topic><topic>Hormones - pharmacology</topic><topic>Liver - physiology</topic><topic>Male</topic><topic>Membrane Transport Proteins</topic><topic>Multidrug Resistance-Associated Proteins - genetics</topic><topic>Organic Anion Transporters, Sodium-Dependent</topic><topic>Pituitary Gland - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - analysis</topic><topic>Sex Characteristics</topic><topic>Symporters</topic><topic>Testosterone - pharmacology</topic><topic>Thyroxine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Simon, Francis R</creatorcontrib><creatorcontrib>Fortune, John</creatorcontrib><creatorcontrib>Iwahashi, Mieko</creatorcontrib><creatorcontrib>Qadri, Ishtiaq</creatorcontrib><creatorcontrib>Sutherland, Eileen</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>American journal of physiology: Gastrointestinal and liver physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Simon, Francis R</au><au>Fortune, John</au><au>Iwahashi, Mieko</au><au>Qadri, Ishtiaq</au><au>Sutherland, Eileen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Multihormonal regulation of hepatic sinusoidal Ntcp gene expression</atitle><jtitle>American journal of physiology: Gastrointestinal and liver physiology</jtitle><addtitle>Am J Physiol Gastrointest Liver Physiol</addtitle><date>2004-10</date><risdate>2004</risdate><volume>287</volume><issue>4</issue><spage>G782</spage><epage>G794</epage><pages>G782-G794</pages><issn>0193-1857</issn><eissn>1522-1547</eissn><abstract>Bile acids are efficiently removed from sinusoidal blood by a number of transporters including the Na+-taurocholate-cotransporting polypeptide (Ntcp). Na+-dependent bile salt uptake, as well as Ntcp, are expressed twofold higher in male compared with female rat livers. Also, estrogen administration to male rats decreases Ntcp expression. The aims of this study were to determine the hormonal mechanism(s) responsible for this sexually dimorphic expression of Ntcp. We examined castrated and hypophysectomized rats of both sexes. Sex steroid hormones, growth hormone, thyroid, and glucocorticoids were administered, and livers were examined for changes in Ntcp messenger RNA (mRNA). Ntcp mRNA and protein content were selectively increased in males. Estradiol selectively decreased Ntcp expression in males, whereas ovariectomy increased Ntcp in females, confirming the importance of estrogens in regulating Ntcp. Hypophysectomy decreased Ntcp mRNA levels in males and prevented estrogen administration from decreasing Ntcp, indicating the importance of pituitary hormones. Although constant infusion of growth hormone to intact males reduced Ntcp, its replacement alone after hypophysectomy did not restore the sex differences. In contrast, thyroid hormone and corticosterone increased Ntcp mRNA in hypophysectomized rats. Sex differences in Ntcp mRNA levels were produced only when the female pattern of growth hormone was administered to animals also receiving thyroid and corticosterone. Thyroid and dexamethasone also increased Ntcp mRNA in isolated rat hepatocytes, whereas growth hormone decreased Ntcp. These findings demonstrate the essential role that pituitary hormones play in the sexually dimorphic control of Ntcp expression in adult rat liver and in the mediation of estrogen effects.</abstract><cop>United States</cop><pmid>15361361</pmid><doi>10.1152/ajpgi.00379.2003</doi></addata></record> |
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subjects | Androgens - pharmacology Animals ATP Binding Cassette Subfamily B Member 11 ATP-Binding Cassette Transporters - genetics Carrier Proteins - genetics Corticosterone - pharmacology Estradiol - pharmacology Female Gene Expression - drug effects Gene Expression - physiology Growth Hormone - pharmacology Hormones - pharmacology Liver - physiology Male Membrane Transport Proteins Multidrug Resistance-Associated Proteins - genetics Organic Anion Transporters, Sodium-Dependent Pituitary Gland - physiology Rats Rats, Sprague-Dawley RNA, Messenger - analysis Sex Characteristics Symporters Testosterone - pharmacology Thyroxine - pharmacology |
title | Multihormonal regulation of hepatic sinusoidal Ntcp gene expression |
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