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      <dc:title>In vivo tissue specific modulation of rat insulin receptor gene expression in an experimental model of mineralocorticoid excess</dc:title>
      <dc:creator>Campion, Javier</dc:creator>
      <dc:creator>Lahera, Vicente</dc:creator>
      <dc:creator>Cachofeiro, Victoria</dc:creator>
      <dc:creator>Maestro, Begoña</dc:creator>
      <dc:creator>dávila, norma</dc:creator>
      <dc:creator>Carranza, María del Carmen</dc:creator>
      <dc:creator>calle, consuelo</dc:creator>
      <dc:subject>insulin receptor gene expression</dc:subject>
      <dc:subject>mineralocorticoid-treated rats</dc:subject>
      <dc:description>Insulin receptor (IR) gene expression at the mRNA level was investigated in hindlimb skeletal muscle, epididymal adipose&#xd;
tissue and in the liver of rats exposed to prolonged in vivo administration of deoxycorticosterone acetate (DOCA). Following&#xd;
treatment, plasma insulin levels were reduced while glucose levels increased compared to values in control rats. DOCA-treated&#xd;
animals showed an increase in blood pressure and a reduction in body weight. This treatment also induced hypokalemia and&#xd;
decreased plasma protein levels. Sodium levels were unaffected. Moreover, no differences in DNA and protein content or in&#xd;
the indicator of cell size (protein/DNA) were observed in the skeletal muscle or adipose tissue of animals. In contrast, there&#xd;
was a clear increase in the protein and DNA contents of the liver with no change in the indicator of cell size. Northern blot&#xd;
assays revealed 2 major IR mRNA species of approximately 9.5 and 7.5 Kb in the 3 tissues from control animals. DOCA treatment&#xd;
induced no change in the levels of either RNA species in skeletal muscle. However, a decrease of approximately 22% was&#xd;
detected in the levels of both species in adipose tissue whereas the liver showed an increase of 64%. These results provide the&#xd;
first evidence for an in vivo tissue-specific modulation of IR mRNA levels under experimental conditions of mineralocorticoid&#xd;
excess.</dc:description>
      <dc:date>2026-06-18T11:18:15Z</dc:date>
      <dc:date>2026-06-18T11:18:15Z</dc:date>
      <dc:date>1998</dc:date>
      <dc:identifier>1573-4919</dc:identifier>
      <dc:identifier>0300-8177</dc:identifier>
      <dc:identifier>https://hdl.handle.net/20.500.11984/14595</dc:identifier>
      <dc:language>eng</dc:language>
      <dc:rights>© 1998 Kluwer Academic Publishers.</dc:rights>
      <dc:publisher>Springer Nature Link</dc:publisher>
   </ow:Publication>
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