Literature DB >> 9151802

The midcycle increase in ovarian glucose uptake is associated with enhanced expression of glucose transporter 3. Possible role for interleukin-1, a putative intermediary in the ovulatory process.

S Kol1, I Ben-Shlomo, K Ruutiainen, M Ando, T M Davies-Hill, R M Rohan, I A Simpson, E Y Adashi.   

Abstract

This study characterizes the rat ovary as a site of hormonally dependent glucose transporter (Glut) expression, and explores the potential role of interleukin (IL)-1, a putative intermediary in the ovulatory process, in this regard. Molecular probing throughout a simulated estrous cycle revealed a significant surge in ovarian Glut3 (but not Glut1) expression at the time of ovulation. Treatment of cultured whole ovarian dispersates from immature rats with IL-1beta resulted in upregulation of the relative abundance of the Glut1 (4.5-fold) and Glut3 (3.5-fold) proteins as determined by Western blot analysis. Other members of the Glut family (i.e., Gluts 2, 4, and 5) remained undetectable. The ability of IL-1 to upregulate Glut1 and Glut3 transcripts proved time-, dose-, nitric oxide-, and protein biosynthesis-dependent but glucose independent. Other ovarian agonists (i.e., TNF alpha, IGF-I, interferon-gamma, and insulin) were without effect. Taken together, our findings establish the mammalian ovary as a site of cyclically determined Glut1 and Glut3 expression, and disclose the ability of IL-1 to induce the ovarian expression as well as translation of Glut1 and Glut3 (but not of Gluts 2, 4, or 5). Our observations also establish IL-1 as the first known regulator of Glut3, the most efficient Glut known to date. In so doing, IL-1, a putative component of the ovulatory process, may be acting to meet the increased metabolic demands imposed on the growing follicle and the ovulated cumulus-enclosed oocyte.

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Year:  1997        PMID: 9151802      PMCID: PMC508060          DOI: 10.1172/JCI119403

Source DB:  PubMed          Journal:  J Clin Invest        ISSN: 0021-9738            Impact factor:   14.808


  39 in total

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2.  Receptor-mediated stimulatory effect of IL-1 beta on hyaluronic acid and proteoglycan biosynthesis by cultured rat ovarian cells: role for heterologous cell-cell interactions.

Authors:  E Kokia; A Hurwitz; I Ben-Shlomo; E Y Adashi; M Yanagishita
Journal:  Endocrinology       Date:  1993-11       Impact factor: 4.736

3.  Interleukin-1 in human ovarian cells and in peripheral blood monocytes increases during the luteal phase: evidence for a midcycle surge in the human.

Authors:  M L Polan; J A Loukides; J Honig
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4.  Interleukin-1 beta (IL-1 beta) modulates prostaglandin production and the natural IL-1 receptor antagonist inhibits ovulation in the optimally stimulated rat ovarian perfusion model.

Authors:  C M Peterson; H A Hales; H H Hatasaka; M D Mitchell; L Rittenhouse; K P Jones
Journal:  Endocrinology       Date:  1993-11       Impact factor: 4.736

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Journal:  J Clin Invest       Date:  1993-12       Impact factor: 14.808

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Journal:  Biol Reprod       Date:  1994-01       Impact factor: 4.285

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Authors:  F Maher; S J Vannucci; I A Simpson
Journal:  FASEB J       Date:  1994-10       Impact factor: 5.191

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Authors:  C Simón; A Frances; G Piquette; M L Polan
Journal:  Biol Reprod       Date:  1994-02       Impact factor: 4.285

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Authors:  Y Takehara; A M Dharmarajan; G Kaufman; E E Wallach
Journal:  Endocrinology       Date:  1994-04       Impact factor: 4.736

10.  The morphogenic/cytotoxic and prostaglandin-stimulating activities of interleukin-1 beta in the rat ovary are nitric oxide independent.

Authors:  I Ben-Shlomo; E Y Adashi; D W Payne
Journal:  J Clin Invest       Date:  1994-10       Impact factor: 14.808

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7.  Protective effect of vitamin E on cypermethrin-induced follicular atresia in rat ovary: Evidence for energy dependent mechanism.

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

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9.  Alterations of IL-1 and VEGF After Ischemia-Reperfusion Injured Uterus and Ovary in Rats.

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10.  Microglial signalling pathway deficits associated with the patient derived R47H TREM2 variants linked to AD indicate inability to activate inflammasome.

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