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  <controlfield tag="005">20240125162930.0</controlfield>
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    <subfield code="2">doi</subfield>
    <subfield code="a">10.1055/s-0028-1128146</subfield>
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    <subfield code="2">sideral</subfield>
    <subfield code="a">116143</subfield>
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    <subfield code="a">ART-2009-116143</subfield>
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    <subfield code="a">eng</subfield>
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  <datafield tag="100" ind1=" " ind2=" ">
    <subfield code="a">Gómez, O.</subfield>
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  <datafield tag="245" ind1=" " ind2=" ">
    <subfield code="a">Expression and Regulation of Insulin and the Glucose Transporter GLUT8 in the Testes of Diabetic Rats</subfield>
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  <datafield tag="260" ind1=" " ind2=" ">
    <subfield code="c">2009</subfield>
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  <datafield tag="520" ind1="3" ind2=" ">
    <subfield code="a">Diabetes induces several malfunctions in male germ cells. The aim of this study was to analyze the levels and localization of the glucose transporter GLUT8 and insulin in the testes of rats induced to a diabetic status by a single dose of streptozotocin. One month after inducing diabetes, the GLUT8 immunoreactivity in diabetic rats was mainly located associated to the acrosomic system of spermatids, and at low levels in Leydig cells. Neither the immunohistochemical localization of this transporter nor its levels showed any difference when compared to control rats. Furthermore, it was observed that control rat testes expressed insulin, which was diffusely located in the cytoplasm of both Leydig cells and early elongated spermatids and concentrated in a cytoplasmic compartment in the more mature spermatids. Testicular insulin levels measured by western blot were reduced by more than half in diabetic rats, although the distribution of the hormone was unchanged. These results indicate that i) insulin is produced by testicular cells, ii) insulin is depleted by streptozotocin-induced diabetes, and iii) that insulin depletion and hyperglycemia do not regulate the expression of GLUT8 in testes. These results also suggest that testicular production of insulin could play a role in regulating spermatogenesis and/or glucose metabolism in these organs.</subfield>
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    <subfield code="a">All rights reserved</subfield>
    <subfield code="u">http://www.europeana.eu/rights/rr-f/</subfield>
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    <subfield code="a">2.686</subfield>
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    <subfield code="a">ENDOCRINOLOGY &amp; METABOLISM</subfield>
    <subfield code="b">51 / 104 = 0.49</subfield>
    <subfield code="c">2009</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Ballester, B.</subfield>
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    <subfield code="a">Romero, A.</subfield>
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    <subfield code="a">Arnal, E.</subfield>
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    <subfield code="a">Almansa, I.</subfield>
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    <subfield code="a">Miranda, M.</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Mesonero, J.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0003-4758-3998</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Terrado, J.</subfield>
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  <datafield tag="710" ind1="2" ind2=" ">
    <subfield code="1">1005</subfield>
    <subfield code="2">410</subfield>
    <subfield code="a">Universidad de Zaragoza</subfield>
    <subfield code="b">Dpto. Farmacología y Fisiolog.</subfield>
    <subfield code="c">Área Fisiología</subfield>
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  <datafield tag="773" ind1=" " ind2=" ">
    <subfield code="g">41, 5 (2009), 343-349</subfield>
    <subfield code="p">Horm. Metab. Res.</subfield>
    <subfield code="t">HORMONE AND METABOLIC RESEARCH</subfield>
    <subfield code="x">0018-5043</subfield>
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    <subfield code="a">2024-01-25-15:11:19</subfield>
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