Insulin resistance in an animal model of polycystic ovary disease is aggravated by vitamin D deficiency: Vascular consequences
Insulin resistance in an animal model of polycystic ovary disease is aggravated by vitamin D deficiency: Vascular consequences
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DOI：
10.1177/1479164118758580
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发表时间：
2018-07-01
影响因子：
2.4
通讯作者：
Nadasy, Gyorgy Laszlo
中科院分区：
文献类型：
--
作者：
Hadjadj, Leila;Varbiro, Szabolcs;Nadasy, Gyorgy Laszlo
女性的高雄激素状态伴随着代谢综合征、胰岛素抵抗和血管病变。共有 67%-85% 的高雄激素女性还患有维生素 D 缺乏症。我们的目的是检查高雄激素血症和维生素 D 缺乏之间潜在的相互作用，从而产生胰岛素抵抗以及对冠状动脉抵抗的影响。将青春期雌性大鼠分为四组，每组11-12只。经皮睾酮治疗和媒介物治疗的动物要么缺乏维生素D，要么补充维生素D饮食8周。测定血浆性类固醇、胰岛素、瘦素和维生素D血浆水平，并进行口服葡萄糖耐量试验。在冠状动脉中，通过免疫组织化学检测胰岛素受体和维生素 D 受体的表达，并在离体冠状动脉阻力动脉段上体外测量胰岛素诱导的舒张。睾酮会损害葡萄糖耐量，并减少胰岛素松弛，但不影响血管组织中胰岛素和维生素 D 受体的表达。维生素 D 缺乏会升高餐后胰岛素水平，稳态模型评估胰岛素抵抗。它还可以减少胰岛素引起的冠状动脉松弛，同时提高内皮层和中层中维生素 D 和胰岛素受体的表达。我们的结论是，雄激素过多症和维生素 D 缺乏都会降低冠状血管组织对胰岛素的敏感性，但它们的机制不同。
Hyperandrogenic state in females is accompanied with metabolic syndrome, insulin resistance and vascular pathologies. A total of 67%-85% of hyperandrogenic women suffer also from vitamin D deficiency. We aimed to check a potential interplay between hyperandrogenism and vitamin D deficiency in producing insulin resistance and effects on coronary resistance arteries. Adolescent female rats were divided into four groups, 11-12 animals in each. Transdermal testosterone-treated and vehicle-treated animals were kept either on vitamin D-deficient or on vitamin D-supplemented diet for 8 weeks. Plasma sexual steroid, insulin, leptin and vitamin D plasma levels were measured, and oral glucose tolerance test was performed. In coronary arterioles, insulin receptor and vitamin D receptor expressions were tested by immunohistochemistry, and insulin-induced relaxation was measured in vitro on isolated coronary resistance artery segments. Testosterone impaired glucose tolerance, and it diminished insulin relaxation but did not affect the expression of insulin and vitamin D receptors in vascular tissue. Vitamin D deficiency elevated postprandial insulin levels and homeostatic model assessment insulin resistance. It also diminished insulin-induced coronary arteriole relaxation, while it raised the expression of vitamin D and insulin receptors in the endothelial and medial layers. Our conclusion is that both hyperandrogenism and vitamin D deficiency reduce sensitivity of coronary vascular tissue to insulin, but they do it with different mechanisms.