Peredo H A, Andrade V, Donoso A S, Lee H J, Puyó A M
Cátedra de Anatomía Humana (macro y microscópica) and INFIBIOC, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires; CONICET, Junín 956, 1113, Buenos Aires, Argentina.
Auton Autacoid Pharmacol. 2013 Oct;33(3-4):43-8. doi: 10.1111/aap.12010. Epub 2013 Aug 2.
(1) Fructose (F) overload produces elevated blood pressure (BP), hyperglycaemia, hypertriglyceridemia and insulin resistance, resembling human metabolic syndrome. Previously, we found altered vascular prostanoid (PR) production in this model. (2) Sodium molybdate (Mo), as well as sodium tungstate, causes insulin-like effects and normalizes plasma glucose levels in streptozotocin-treated diabetic rats. We studied the effects of Mo on BP, metabolic parameters and release of PR from the mesenteric vascular bed (MVB) in F-overloaded rats. (3) Four groups of male Sprague-Dawley rats were analysed: Control, tap water to drink; F, F solution 10% W/V to drink; CMo, Mo 100 mg kg day(-1) and FMo, both treatments. After 9 weeks, the animals were killed and MVBs removed and the released PRs measured. (4) F increased BP, glycemia, triglyceridemia and insulinemia. Mo treatment prevented the increases in BP and glycemia, but did not modify triglyceridemia or insulinemia. In addition, Mo decreased BP in controls. (5) Prostaglandins (PG) F2 alpha and E2, PG 6-ketoF1 alpha and thromboxane (TX) B2 , as well as inactive metabolites of prostacyclin (PGI2 ) and TXA2 were detected. F decreased the production of vasodilator PRs PGI2 and PGE2 in MVB. Mo prevented these alterations and increased PGE2 in controls. Vasoconstrict or PRs PGF2 alpha and TXA2 release was not modified. (6) Mo treatment, beyond its known lowering effect on glycemia, prevents the reduction in the vascular release of vasodilator PR observed in this model. This could be one of the mechanisms by which Mo avoids the increase in BP caused by F overload in the rat.
(1) 果糖（F）过载会导致血压（BP）升高、高血糖、高甘油三酯血症和胰岛素抵抗，类似于人类代谢综合征。此前，我们在该模型中发现血管类前列腺素（PR）生成发生改变。(2) 钼酸钠（Mo）以及钨酸钠会产生胰岛素样作用，并使链脲佐菌素处理的糖尿病大鼠的血糖水平恢复正常。我们研究了Mo对F过载大鼠的血压、代谢参数以及肠系膜血管床（MVB）中PR释放的影响。(3) 分析了四组雄性Sprague-Dawley大鼠：对照组，饮用自来水；F组，饮用10%（W/V）的F溶液；CMo组，Mo剂量为100 mg·kg⁻¹·天⁻¹；FMo组，同时进行上述两种处理。9周后，处死动物并取出MVB，测量释放的PR。(4) F会使血压、血糖、甘油三酯水平和胰岛素水平升高。Mo处理可预防血压和血糖升高，但未改变甘油三酯水平或胰岛素水平。此外，Mo可降低对照组的血压。(5) 检测到前列腺素（PG）F2α和E2、PG 6-酮F1α以及血栓素（TX）B2，以及前列环素（PGI2）和血栓素A2（TXA2）的无活性代谢产物。F会降低MVB中血管舒张性PRs PGI2和PGE2的生成。Mo可预防这些改变，并增加对照组中的PGE2。血管收缩性PRs PGF2α和TXA2的释放未发生改变。(6) Mo处理除了对血糖具有已知的降低作用外，还可预防该模型中观察到的血管舒张性PR释放减少。这可能是Mo避免大鼠因F过载导致血压升高的机制之一。
