Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats
Gøtzsche LB-H, Rosenqvist N. Grønbœk H, Flyvbjerg A, Gøtzsche O. Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats. Eur J Endocrinol 1996;134:107–13. ISSN 0804–4643. In order to elucidate further the abnormal my...
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| Veröffentlicht in: | European journal of endocrinology 1996-01, Vol.134 (1), p.107-113 |
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| creator | GOTZSCHE, L. B.-H ROSENQVIST, N GRONBAEK, H FLYVBJERG, A GOTZSCHE, O |
| description | Gøtzsche LB-H, Rosenqvist N. Grønbœk H, Flyvbjerg A, Gøtzsche O. Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats. Eur J Endocrinol 1996;134:107–13. ISSN 0804–4643. In order to elucidate further the abnormal myocardial Ca+ metabolism in diabetes mellitus, voltage-gated Ca2+ channels and β-receptors were quantified in myocardial membranes of short- and long-term diabetic rats. Diabetes was induced by an injection of streptozotocin (STZ). Animals were killed 2, 4, 7, 90 and 200 days after STZ. A group of diabetic animals were treated with insulin for 20 days following 180 days of untreated diabetes. Diabetic animals developed low triiodothyronine syndrome. During short-term diabetes, the maximum binding capacity (MBC) for Ca+ channels was reduced by 25% at day 4 p |
| doi_str_mv | 10.1530/eje.0.1340107 |
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B.-H ; ROSENQVIST, N ; GRONBAEK, H ; FLYVBJERG, A ; GOTZSCHE, O</creator><creatorcontrib>GOTZSCHE, L. B.-H ; ROSENQVIST, N ; GRONBAEK, H ; FLYVBJERG, A ; GOTZSCHE, O</creatorcontrib><description>Gøtzsche LB-H, Rosenqvist N. Grønbœk H, Flyvbjerg A, Gøtzsche O. Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats. Eur J Endocrinol 1996;134:107–13. ISSN 0804–4643. In order to elucidate further the abnormal myocardial Ca+ metabolism in diabetes mellitus, voltage-gated Ca2+ channels and β-receptors were quantified in myocardial membranes of short- and long-term diabetic rats. Diabetes was induced by an injection of streptozotocin (STZ). Animals were killed 2, 4, 7, 90 and 200 days after STZ. A group of diabetic animals were treated with insulin for 20 days following 180 days of untreated diabetes. Diabetic animals developed low triiodothyronine syndrome. During short-term diabetes, the maximum binding capacity (MBC) for Ca+ channels was reduced by 25% at day 4 p<0.05) and the β-receptor MBC was reduced by 48% p<0.05). A normalizing tendency was observed at day 7 for both receptor types; insulin-treated rats did not differ from controls at that time. After 90 and 200 days of untreated diabetes the Ca+ channel MBC had increased by 36% and 27%, respectively (p < 0.05). Twenty days of strictly regulated blood glucose following 180 days of untreated diabetes totally normalized the Ca+ channel MBC. This is in contrast to a previous report where insulin treatment did not normalize the Ca+ channel MBC. Total β-receptor MBCs did not differ from control values 90 and 200 days after STZ. In conclusion, an increase in rat myocardial Ca2+ channel MBC during long-term diabetes was fully normalized by short-term insulin treatment. The increase in sarcolemmal Ca2+ channels could serve to compensate for a defect coupling of the β-receptor to adenylate cyclase. An elevated Ca+ channel number may, at least theoretically, lead to increased Ca2+ flow across the cardiac sarcolemma and in this way contribute to the diabetic cardiomyopathy by increasing the intracellular Ca2+ concentration. Liv Bjørn-Hansen Gøtzsche, Dept. of Internal Medicine M, (Diabetes and Endocrinology), Aarhus Kommunehospital, University Hospital of Aarhus, DK-8000 Aarhus C, Denmark.</description><identifier>ISSN: 0804-4643</identifier><identifier>EISSN: 1479-683X</identifier><identifier>DOI: 10.1530/eje.0.1340107</identifier><identifier>PMID: 8590944</identifier><language>eng</language><publisher>Colchester: Portland Press</publisher><subject>Animals ; Associated diseases and complications ; Biological and medical sciences ; Calcium Channels - metabolism ; Chronic Disease ; Diabetes Mellitus, Experimental - metabolism ; Diabetes. Impaired glucose tolerance ; Electrophysiology ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; EXPERIMENTAL STUDIES ; Female ; Ion Channel Gating ; Medical sciences ; Myocardium - metabolism ; Rats ; Rats, Wistar ; Receptors, Adrenergic, beta - metabolism ; Thyroxine - blood ; Triiodothyronine - blood</subject><ispartof>European journal of endocrinology, 1996-01, Vol.134 (1), p.107-113</ispartof><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b293t-b72c3d56919f0188a847aa5243ad61f7e2656b5ac980626cb952256b55dc1c7e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2955015$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8590944$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GOTZSCHE, L. B.-H</creatorcontrib><creatorcontrib>ROSENQVIST, N</creatorcontrib><creatorcontrib>GRONBAEK, H</creatorcontrib><creatorcontrib>FLYVBJERG, A</creatorcontrib><creatorcontrib>GOTZSCHE, O</creatorcontrib><title>Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats</title><title>European journal of endocrinology</title><addtitle>Eur J Endocrinol</addtitle><description>Gøtzsche LB-H, Rosenqvist N. Grønbœk H, Flyvbjerg A, Gøtzsche O. Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats. Eur J Endocrinol 1996;134:107–13. ISSN 0804–4643. In order to elucidate further the abnormal myocardial Ca+ metabolism in diabetes mellitus, voltage-gated Ca2+ channels and β-receptors were quantified in myocardial membranes of short- and long-term diabetic rats. Diabetes was induced by an injection of streptozotocin (STZ). Animals were killed 2, 4, 7, 90 and 200 days after STZ. A group of diabetic animals were treated with insulin for 20 days following 180 days of untreated diabetes. Diabetic animals developed low triiodothyronine syndrome. During short-term diabetes, the maximum binding capacity (MBC) for Ca+ channels was reduced by 25% at day 4 p<0.05) and the β-receptor MBC was reduced by 48% p<0.05). A normalizing tendency was observed at day 7 for both receptor types; insulin-treated rats did not differ from controls at that time. After 90 and 200 days of untreated diabetes the Ca+ channel MBC had increased by 36% and 27%, respectively (p < 0.05). Twenty days of strictly regulated blood glucose following 180 days of untreated diabetes totally normalized the Ca+ channel MBC. This is in contrast to a previous report where insulin treatment did not normalize the Ca+ channel MBC. Total β-receptor MBCs did not differ from control values 90 and 200 days after STZ. In conclusion, an increase in rat myocardial Ca2+ channel MBC during long-term diabetes was fully normalized by short-term insulin treatment. The increase in sarcolemmal Ca2+ channels could serve to compensate for a defect coupling of the β-receptor to adenylate cyclase. An elevated Ca+ channel number may, at least theoretically, lead to increased Ca2+ flow across the cardiac sarcolemma and in this way contribute to the diabetic cardiomyopathy by increasing the intracellular Ca2+ concentration. Liv Bjørn-Hansen Gøtzsche, Dept. of Internal Medicine M, (Diabetes and Endocrinology), Aarhus Kommunehospital, University Hospital of Aarhus, DK-8000 Aarhus C, Denmark.</description><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Calcium Channels - metabolism</subject><subject>Chronic Disease</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Electrophysiology</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>EXPERIMENTAL STUDIES</subject><subject>Female</subject><subject>Ion Channel Gating</subject><subject>Medical sciences</subject><subject>Myocardium - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Adrenergic, beta - metabolism</subject><subject>Thyroxine - blood</subject><subject>Triiodothyronine - blood</subject><issn>0804-4643</issn><issn>1479-683X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM2KFDEUhYMoY0_r0qWQhbiRjPmtqiylUWdgwI2Cu-JW6laboSppk5QwvoJv44P4TKbpdrau7rn3fJwLh5AXgl8Jo_hbvMOrKpXmgrePyEbo1rKmU18fkw3vuGa60eopucz5jnNRNb8gF52x3Gq9Ib9ugksIGUca1mXARONEl_voII0eZvojzgX2yPZQKrID-Ya6bxACzplCGOkajuu-eiWWyv_5zRI6PJSY_gX6QOcY9qxgWmgu6Wj-jCU6H1j9MWDxjiYo-Rl5MsGc8fl5bsmXD-8_767Z7aePN7t3t2yQVhU2tNKp0TRW2ImLroNOtwBGagVjI6YWZWOawYCzHW9k4wZrpDxezOiEa1FtyetT7iHF7yvm0i8-O5xnCBjX3LettcIIUUF2Al2KOSec-kPyC6T7XvD-WH5fy--rPJVf-Zfn4HVYcHygz21X_9XZh-xgnhIE5_MDJq0xvMZuiTphg4_ZeQzFT97Bf57_BftkoEE</recordid><startdate>199601</startdate><enddate>199601</enddate><creator>GOTZSCHE, L. B.-H</creator><creator>ROSENQVIST, N</creator><creator>GRONBAEK, H</creator><creator>FLYVBJERG, A</creator><creator>GOTZSCHE, O</creator><general>Portland Press</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>199601</creationdate><title>Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats</title><author>GOTZSCHE, L. B.-H ; ROSENQVIST, N ; GRONBAEK, H ; FLYVBJERG, A ; GOTZSCHE, O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b293t-b72c3d56919f0188a847aa5243ad61f7e2656b5ac980626cb952256b55dc1c7e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Calcium Channels - metabolism</topic><topic>Chronic Disease</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Electrophysiology</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>EXPERIMENTAL STUDIES</topic><topic>Female</topic><topic>Ion Channel Gating</topic><topic>Medical sciences</topic><topic>Myocardium - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Adrenergic, beta - metabolism</topic><topic>Thyroxine - blood</topic><topic>Triiodothyronine - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GOTZSCHE, L. B.-H</creatorcontrib><creatorcontrib>ROSENQVIST, N</creatorcontrib><creatorcontrib>GRONBAEK, H</creatorcontrib><creatorcontrib>FLYVBJERG, A</creatorcontrib><creatorcontrib>GOTZSCHE, O</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>European journal of endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GOTZSCHE, L. B.-H</au><au>ROSENQVIST, N</au><au>GRONBAEK, H</au><au>FLYVBJERG, A</au><au>GOTZSCHE, O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats</atitle><jtitle>European journal of endocrinology</jtitle><addtitle>Eur J Endocrinol</addtitle><date>1996-01</date><risdate>1996</risdate><volume>134</volume><issue>1</issue><spage>107</spage><epage>113</epage><pages>107-113</pages><issn>0804-4643</issn><eissn>1479-683X</eissn><abstract>Gøtzsche LB-H, Rosenqvist N. Grønbœk H, Flyvbjerg A, Gøtzsche O. Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats. Eur J Endocrinol 1996;134:107–13. ISSN 0804–4643. In order to elucidate further the abnormal myocardial Ca+ metabolism in diabetes mellitus, voltage-gated Ca2+ channels and β-receptors were quantified in myocardial membranes of short- and long-term diabetic rats. Diabetes was induced by an injection of streptozotocin (STZ). Animals were killed 2, 4, 7, 90 and 200 days after STZ. A group of diabetic animals were treated with insulin for 20 days following 180 days of untreated diabetes. Diabetic animals developed low triiodothyronine syndrome. During short-term diabetes, the maximum binding capacity (MBC) for Ca+ channels was reduced by 25% at day 4 p<0.05) and the β-receptor MBC was reduced by 48% p<0.05). A normalizing tendency was observed at day 7 for both receptor types; insulin-treated rats did not differ from controls at that time. After 90 and 200 days of untreated diabetes the Ca+ channel MBC had increased by 36% and 27%, respectively (p < 0.05). Twenty days of strictly regulated blood glucose following 180 days of untreated diabetes totally normalized the Ca+ channel MBC. This is in contrast to a previous report where insulin treatment did not normalize the Ca+ channel MBC. Total β-receptor MBCs did not differ from control values 90 and 200 days after STZ. In conclusion, an increase in rat myocardial Ca2+ channel MBC during long-term diabetes was fully normalized by short-term insulin treatment. The increase in sarcolemmal Ca2+ channels could serve to compensate for a defect coupling of the β-receptor to adenylate cyclase. An elevated Ca+ channel number may, at least theoretically, lead to increased Ca2+ flow across the cardiac sarcolemma and in this way contribute to the diabetic cardiomyopathy by increasing the intracellular Ca2+ concentration. Liv Bjørn-Hansen Gøtzsche, Dept. of Internal Medicine M, (Diabetes and Endocrinology), Aarhus Kommunehospital, University Hospital of Aarhus, DK-8000 Aarhus C, Denmark.</abstract><cop>Colchester</cop><pub>Portland Press</pub><pmid>8590944</pmid><doi>10.1530/eje.0.1340107</doi><tpages>7</tpages></addata></record> |
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| identifier | ISSN: 0804-4643 |
| ispartof | European journal of endocrinology, 1996-01, Vol.134 (1), p.107-113 |
| issn | 0804-4643 1479-683X |
| language | eng |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Animals Associated diseases and complications Biological and medical sciences Calcium Channels - metabolism Chronic Disease Diabetes Mellitus, Experimental - metabolism Diabetes. Impaired glucose tolerance Electrophysiology Endocrine pancreas. Apud cells (diseases) Endocrinopathies EXPERIMENTAL STUDIES Female Ion Channel Gating Medical sciences Myocardium - metabolism Rats Rats, Wistar Receptors, Adrenergic, beta - metabolism Thyroxine - blood Triiodothyronine - blood |
| title | Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats |
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