Interactions of PPAR α and GLUT4 in DOCA/salt-induced renal injury in mice
Diminished insulin sensitivity is a characteristic feature of various pathological conditions such as hypertension and activation of peroxisome proliferator activated receptor α (PPARα) has been shown to enhance insulin resistance and reduce capacity for glucose uptake in muscles. The present study...
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| Veröffentlicht in: | Nigerian journal of physiological sciences 2013-12, Vol.28 (2), p.127-133 |
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| creator | Ighodaro, Igbe Eric, Omogbai Kelly Adebayo, Oyekan |
| description | Diminished insulin sensitivity is a characteristic feature of various pathological conditions such as hypertension and activation of peroxisome proliferator activated receptor α (PPARα) has been shown to enhance insulin resistance and reduce capacity for glucose uptake in muscles. The present study was designed to evaluate the interactions of PPARα and GLUT4 in a model of hypertensive renal injury by studying deoxycorticosterone acetate (DOCA)-salt induced hypertension in wild-type (WT) and PPARα knockout (KO) mice. PPARα WT and KO mice were uninephrectomized (UNx) and implanted subcutaneously DOCA and drank 1% sodium chloride/1% potassium chloride with or without a GLUT4 antagonist, indinavir (20 mg/kg/day, s.c) or PPARα ligand, fenofibrate (100 mg/kg/day, orally). DOCA/salt treatment increased urinary sodium excretion and urine volume (p |
| format | Article |
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The present study was designed to evaluate the interactions of PPARα and GLUT4 in a model of hypertensive renal injury by studying deoxycorticosterone acetate (DOCA)-salt induced hypertension in wild-type (WT) and PPARα knockout (KO) mice. PPARα WT and KO mice were uninephrectomized (UNx) and implanted subcutaneously DOCA and drank 1% sodium chloride/1% potassium chloride with or without a GLUT4 antagonist, indinavir (20 mg/kg/day, s.c) or PPARα ligand, fenofibrate (100 mg/kg/day, orally). DOCA/salt treatment increased urinary sodium excretion and urine volume (p<0.05) in PPARα KO mice compared to WT littermates. Indinavir increased proteinuria (p<0.01) in DOCA/salt-treated PPARα KO mice compared to WT littermates but did not affect heart and kidney weight index in DOCA/salt KO or WT-treated mice. Urinary sodium excretion (UNaV) and urine volume (UV) were increased by indinavir (p<0.01) and fenofibrate (p<0.05) in DOCA/salt-treated PPARα KO mice compared to WT mice. Urinary nitric oxide was greater in both fenofibrate (p<0.05) and indinavir-treated WT mice (p<0.05) compared to KO mice. These data suggest that in hypertensive nephropathy, GLUT4 probably exerts a renoprotective role that was enhanced with the activation of PPARα receptors by a mechanism that may be related to increased nitric oxide production.]]></description><identifier>ISSN: 0794-859X</identifier><identifier>PMID: 24937386</identifier><language>eng</language><publisher>Nigeria</publisher><subject>Animals ; Desoxycorticosterone Acetate ; Disease Models, Animal ; Fenofibrate - pharmacology ; Glucose Transporter Type 4 - antagonists & inhibitors ; Glucose Transporter Type 4 - metabolism ; Indinavir - pharmacology ; Kidney - drug effects ; Kidney - metabolism ; Kidney - physiopathology ; Kidney Diseases - chemically induced ; Kidney Diseases - metabolism ; Kidney Diseases - physiopathology ; Male ; Mice, Knockout ; Nephrectomy ; Nitric Oxide - urine ; Potassium Chloride ; PPAR alpha - agonists ; PPAR alpha - deficiency ; PPAR alpha - genetics ; PPAR alpha - metabolism ; Sodium - urine ; Sodium Chloride ; Time Factors ; Urination - drug effects</subject><ispartof>Nigerian journal of physiological sciences, 2013-12, Vol.28 (2), p.127-133</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24937386$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ighodaro, Igbe</creatorcontrib><creatorcontrib>Eric, Omogbai Kelly</creatorcontrib><creatorcontrib>Adebayo, Oyekan</creatorcontrib><title>Interactions of PPAR α and GLUT4 in DOCA/salt-induced renal injury in mice</title><title>Nigerian journal of physiological sciences</title><addtitle>Niger J Physiol Sci</addtitle><description><![CDATA[Diminished insulin sensitivity is a characteristic feature of various pathological conditions such as hypertension and activation of peroxisome proliferator activated receptor α (PPARα) has been shown to enhance insulin resistance and reduce capacity for glucose uptake in muscles. The present study was designed to evaluate the interactions of PPARα and GLUT4 in a model of hypertensive renal injury by studying deoxycorticosterone acetate (DOCA)-salt induced hypertension in wild-type (WT) and PPARα knockout (KO) mice. PPARα WT and KO mice were uninephrectomized (UNx) and implanted subcutaneously DOCA and drank 1% sodium chloride/1% potassium chloride with or without a GLUT4 antagonist, indinavir (20 mg/kg/day, s.c) or PPARα ligand, fenofibrate (100 mg/kg/day, orally). DOCA/salt treatment increased urinary sodium excretion and urine volume (p<0.05) in PPARα KO mice compared to WT littermates. Indinavir increased proteinuria (p<0.01) in DOCA/salt-treated PPARα KO mice compared to WT littermates but did not affect heart and kidney weight index in DOCA/salt KO or WT-treated mice. Urinary sodium excretion (UNaV) and urine volume (UV) were increased by indinavir (p<0.01) and fenofibrate (p<0.05) in DOCA/salt-treated PPARα KO mice compared to WT mice. Urinary nitric oxide was greater in both fenofibrate (p<0.05) and indinavir-treated WT mice (p<0.05) compared to KO mice. These data suggest that in hypertensive nephropathy, GLUT4 probably exerts a renoprotective role that was enhanced with the activation of PPARα receptors by a mechanism that may be related to increased nitric oxide production.]]></description><subject>Animals</subject><subject>Desoxycorticosterone Acetate</subject><subject>Disease Models, Animal</subject><subject>Fenofibrate - pharmacology</subject><subject>Glucose Transporter Type 4 - antagonists & inhibitors</subject><subject>Glucose Transporter Type 4 - metabolism</subject><subject>Indinavir - pharmacology</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - physiopathology</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - physiopathology</subject><subject>Male</subject><subject>Mice, Knockout</subject><subject>Nephrectomy</subject><subject>Nitric Oxide - urine</subject><subject>Potassium Chloride</subject><subject>PPAR alpha - agonists</subject><subject>PPAR alpha - deficiency</subject><subject>PPAR alpha - genetics</subject><subject>PPAR alpha - metabolism</subject><subject>Sodium - urine</subject><subject>Sodium Chloride</subject><subject>Time Factors</subject><subject>Urination - drug effects</subject><issn>0794-859X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kD1OwzAAhT2AaClcAXlkibBjx47HKEBbEakVaiW2yL9SqsQJdjL0WFyEMxFEmd7wvvcN7wosERc0yTPxsQC3MZ4QophhdAMWKRWEk5wtwdvWjzZIPTa9j7B3cL8v3uH3F5TewHV1PFDYePi8K4unKNsxabyZtDUwWC_buTpN4fxLdI22d-DayTba-0uuwPH15VBukmq33pZFlQw4ZWNCHM-tIjwzCimTK0oRUVLlDGtHnTKci8xZwYjRhBHihOG5ZkSheYYwMmQFHv-8Q-g_JxvHumuitm0rve2nWONslouUMT6jDxd0Up019RCaToZz_X8A-QGUm1Uh</recordid><startdate>20131220</startdate><enddate>20131220</enddate><creator>Ighodaro, Igbe</creator><creator>Eric, Omogbai Kelly</creator><creator>Adebayo, Oyekan</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20131220</creationdate><title>Interactions of PPAR α and GLUT4 in DOCA/salt-induced renal injury in mice</title><author>Ighodaro, Igbe ; Eric, Omogbai Kelly ; Adebayo, Oyekan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p126t-3f78eb375db0bd8b4403bab861cf4fbd7795fe963dc3633f9d78c63b078e010d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Desoxycorticosterone Acetate</topic><topic>Disease Models, Animal</topic><topic>Fenofibrate - pharmacology</topic><topic>Glucose Transporter Type 4 - antagonists & inhibitors</topic><topic>Glucose Transporter Type 4 - metabolism</topic><topic>Indinavir - pharmacology</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - physiopathology</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - physiopathology</topic><topic>Male</topic><topic>Mice, Knockout</topic><topic>Nephrectomy</topic><topic>Nitric Oxide - urine</topic><topic>Potassium Chloride</topic><topic>PPAR alpha - agonists</topic><topic>PPAR alpha - deficiency</topic><topic>PPAR alpha - genetics</topic><topic>PPAR alpha - metabolism</topic><topic>Sodium - urine</topic><topic>Sodium Chloride</topic><topic>Time Factors</topic><topic>Urination - drug effects</topic><toplevel>online_resources</toplevel><creatorcontrib>Ighodaro, Igbe</creatorcontrib><creatorcontrib>Eric, Omogbai Kelly</creatorcontrib><creatorcontrib>Adebayo, Oyekan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Nigerian journal of physiological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ighodaro, Igbe</au><au>Eric, Omogbai Kelly</au><au>Adebayo, Oyekan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interactions of PPAR α and GLUT4 in DOCA/salt-induced renal injury in mice</atitle><jtitle>Nigerian journal of physiological sciences</jtitle><addtitle>Niger J Physiol Sci</addtitle><date>2013-12-20</date><risdate>2013</risdate><volume>28</volume><issue>2</issue><spage>127</spage><epage>133</epage><pages>127-133</pages><issn>0794-859X</issn><abstract><![CDATA[Diminished insulin sensitivity is a characteristic feature of various pathological conditions such as hypertension and activation of peroxisome proliferator activated receptor α (PPARα) has been shown to enhance insulin resistance and reduce capacity for glucose uptake in muscles. The present study was designed to evaluate the interactions of PPARα and GLUT4 in a model of hypertensive renal injury by studying deoxycorticosterone acetate (DOCA)-salt induced hypertension in wild-type (WT) and PPARα knockout (KO) mice. PPARα WT and KO mice were uninephrectomized (UNx) and implanted subcutaneously DOCA and drank 1% sodium chloride/1% potassium chloride with or without a GLUT4 antagonist, indinavir (20 mg/kg/day, s.c) or PPARα ligand, fenofibrate (100 mg/kg/day, orally). DOCA/salt treatment increased urinary sodium excretion and urine volume (p<0.05) in PPARα KO mice compared to WT littermates. Indinavir increased proteinuria (p<0.01) in DOCA/salt-treated PPARα KO mice compared to WT littermates but did not affect heart and kidney weight index in DOCA/salt KO or WT-treated mice. Urinary sodium excretion (UNaV) and urine volume (UV) were increased by indinavir (p<0.01) and fenofibrate (p<0.05) in DOCA/salt-treated PPARα KO mice compared to WT mice. Urinary nitric oxide was greater in both fenofibrate (p<0.05) and indinavir-treated WT mice (p<0.05) compared to KO mice. These data suggest that in hypertensive nephropathy, GLUT4 probably exerts a renoprotective role that was enhanced with the activation of PPARα receptors by a mechanism that may be related to increased nitric oxide production.]]></abstract><cop>Nigeria</cop><pmid>24937386</pmid><tpages>7</tpages></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; African Journals Online (Open Access); Bioline International; Alma/SFX Local Collection |
| subjects | Animals Desoxycorticosterone Acetate Disease Models, Animal Fenofibrate - pharmacology Glucose Transporter Type 4 - antagonists & inhibitors Glucose Transporter Type 4 - metabolism Indinavir - pharmacology Kidney - drug effects Kidney - metabolism Kidney - physiopathology Kidney Diseases - chemically induced Kidney Diseases - metabolism Kidney Diseases - physiopathology Male Mice, Knockout Nephrectomy Nitric Oxide - urine Potassium Chloride PPAR alpha - agonists PPAR alpha - deficiency PPAR alpha - genetics PPAR alpha - metabolism Sodium - urine Sodium Chloride Time Factors Urination - drug effects |
| title | Interactions of PPAR α and GLUT4 in DOCA/salt-induced renal injury in mice |
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