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Hypoxia increases glucose transporter 1 expression in bovine corpus luteum at the early luteal stage

A major role of the corpus luteum (CL) is to produce progesterone (P4). The CL has immature vasculature shortly after ovulation, suggesting it exists under hypoxic conditions. Hypoxia-inducible factor-1 (HIF1) induces the expression of glucose transporter 1 (GLUT1). To clarify the physiological role...

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Detalles Bibliográficos
Autores principales: NISHIMURA, Ryo, HASEGAWA, Hiroki, YAMASHITA, Masamichi, ITO, Norihiko, OKAMOTO, Yoshiharu, TAKEUCHI, Takashi, KUBO, Tomoaki, IGA, Kosuke, KIMURA, Koji, HISHINUMA, Mitsugu, OKUDA, Kiyoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Japanese Society of Veterinary Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5709568/
https://www.ncbi.nlm.nih.gov/pubmed/29046497
http://dx.doi.org/10.1292/jvms.17-0284
Descripción
Sumario:A major role of the corpus luteum (CL) is to produce progesterone (P4). The CL has immature vasculature shortly after ovulation, suggesting it exists under hypoxic conditions. Hypoxia-inducible factor-1 (HIF1) induces the expression of glucose transporter 1 (GLUT1). To clarify the physiological roles of GLUT1 in bovine CL, we examined GLUT1 mRNA expression in the CL under hypoxic conditions by quantitative RT-PCR. We also measured the effects of glucose (0–25 mM) and GLUT1 inhibitors (cytochalasin B, STF-31) on P4 production in bovine luteal cells. GLUT1 mRNA expression in bovine CL was higher at the early luteal stage compared to the other later stages. Hypoxia (3% O(2)) increased GLUT1 mRNA expression in early luteal cells, but not in mid luteal cells. Glucose (0–25 mM) increased P4 production in early luteal cells, but not in mid luteal cells. Both GLUT1 inhibitors decreased P4 production in early and mid luteal cells. Overall, the results suggest that GLUT1 (possibly induced by hypoxic conditions in the early CL) plays a role in the establishment and development of bovine CL, especially in supporting luteal P4 synthesis at the early luteal stage.