循环microrna作为妊娠期和跨代代谢风险的可修改诊断生物标志物:运动能起作用吗?

P. Pinto-Hernández, C. Tomás-Zapico, E. Iglesias-Gutiérrez
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引用次数: 1

摘要

妊娠期糖尿病(GDM)被定义为妊娠期间首次发现的任何程度的葡萄糖耐受不良(1)。根据国际协会和委员会的建议,通常在妊娠24-28周诊断(2)。诊断采用50克1小时葡萄糖激发试验(GCT)的序列模型进行普遍筛查。然后对筛查结果阳性的女性进行100克三小时口服葡萄糖耐量试验(OGTT)诊断(3)。GDM的总体发病率在全球范围内呈上升趋势,约占所有妊娠的7-15%(4)。它被认为是妊娠期间最常见的代谢问题,约占危险妊娠的90%(5)。尽管妊娠合并糖尿病(妊娠期或妊娠前)的患病率在地理位置和不同种族之间存在差异(6)。在健康妊娠期间,由于胎盘分泌一系列胰岛素拮抗剂(皮质醇、催乳素、孕酮和乳原),胰岛素抵抗会增加,最终导致血糖升高(6)。此外,在GDM妇女中,胰岛素分泌不足以抵消这种增加的胰岛素抵抗。由于β-胰腺细胞凋亡率增加,导致胰岛素的产生和分泌异常(7)。由于血糖容易通过胎盘扩散,到达胎儿,产生胎儿高血糖(8)。
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Circulating microRNAs as modifiable diagnostic biomarkers of gestational and transgenerational metabolic risk: can exercise play a role?
Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance at first recognition during pregnancy (1). It is usually diagnosed at 24–28 gestational weeks, according to the recommendations of international associations and committees (2). Diagnosis is made using a sequential model of universal screening with a 50-g one-hour glucose challenge test (GCT), followed by a diagnostic 100-g three-hour oral glucose tolerance test (OGTT) for women with a positive screening test (3). The overall incidence of GDM is increasing worldwide, affecting approximately 7–15% of all pregnancies (4). It is considered the most frequent metabolic problem during pregnancy, representing about 90% of risky pregnancies (5), although the prevalence of pregnancies complicated by diabetes (gestational or pre-gestational) varies geographically and among different ethnic groups (6). During healthy pregnancy insulin resistance increases due to the secretion of a series of placental hormones antagonists to insulin (cortisol, prolactin, progesterone and lactogen), ultimately causing blood glucose to rise (6). Furthermore, in GDM women insulin production is insufficient to counteract this increasing insulin resistance, due to an increase in β-pancreatic cells apoptotic rate which leads to an abnormal production and secretion of insulin (7). Given that blood glucose easily goes through placenta by facilitated diffusion, it reaches the fetus producing fetal hyperglycemia (8).
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