Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, 60 Murray Street, Suite-L5-039, Mailbox-21, Toronto, ON, Canada.
Diabetologia. 2010 Feb;53(2):268-76. doi: 10.1007/s00125-009-1600-8. Epub 2009 Nov 24.
AIMS/HYPOTHESIS: The postpartum phase following gestational diabetes (GDM) is characterised by subtle metabolic defects, including the beta cell dysfunction that is believed to mediate the increased future risk of type 2 diabetes in this patient population. Low circulating levels of adiponectin and increased leptin and C-reactive protein (CRP) have recently emerged as novel diabetic risk factors, although their relevance to GDM and subsequent diabetes has not been characterised. Thus, we sought to determine whether adiponectin, leptin and CRP levels during pregnancy relate to the postpartum metabolic defects linking GDM with type 2 diabetes.
Metabolic characterisation, including oral glucose tolerance testing, was undertaken in 487 women during pregnancy and at 3 months postpartum. Based on the antepartum OGTT, there were 137 women with GDM, 91 with gestational impaired glucose tolerance and 259 with normal glucose tolerance.
Adiponectin levels were lowest (p < 0.0001) and CRP levels highest (p = 0.0008) in women with GDM. Leptin did not differ between the glucose tolerance groups (p = 0.4483). Adiponectin (r = 0.41, p < 0.0001), leptin (r = -0.36, p < 0.0001) and CRP (r = -0.30, p < 0.0001) during pregnancy were all associated with postpartum insulin sensitivity (determined using the insulin sensitivity index of Matsuda and DeFronzo [IS(OGTT)]). Intriguingly, adiponectin levels were also related to postpartum beta cell function (insulinogenic index/HOMA of insulin resistance; r = 0.16, p = 0.0009). Indeed, on multiple linear regression analyses, adiponectin levels during pregnancy independently predicted both postpartum insulin sensitivity (t = 3.97, p < 0.0001) and beta cell function (t = 2.37, p = 0.0181), even after adjustment for GDM. Furthermore, adiponectin emerged as a significant negative independent determinant of postpartum fasting glucose (t = -3.01, p = 0.0027).
CONCLUSIONS/INTERPRETATION: Hypoadiponectinaemia during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia, and hence may be relevant to the pathophysiology relating GDM with type 2 diabetes.
目的/假设：妊娠糖尿病（GDM）后的产后阶段表现出微妙的代谢缺陷，包括β细胞功能障碍，据信这会增加该患者群体未来患 2 型糖尿病的风险。最近，循环中脂联素水平降低、瘦素和 C 反应蛋白（CRP）增加已成为新的糖尿病危险因素，但它们与 GDM 及随后的糖尿病的关系尚未确定。因此，我们试图确定妊娠期间脂联素、瘦素和 CRP 水平是否与将 GDM 与 2 型糖尿病联系起来的产后代谢缺陷有关。
在妊娠期间和产后 3 个月对 487 名女性进行代谢特征分析，包括口服葡萄糖耐量试验。根据产前 OGTT，137 名女性患有 GDM，91 名患有妊娠期糖耐量受损，259 名女性糖耐量正常。
GDM 女性的脂联素水平最低（p < 0.0001），CRP 水平最高（p = 0.0008）。瘦素在葡萄糖耐量组之间没有差异（p = 0.4483）。妊娠期间的脂联素（r = 0.41，p < 0.0001）、瘦素（r = -0.36，p < 0.0001）和 CRP（r = -0.30，p < 0.0001）均与产后胰岛素敏感性相关（使用 Matsuda 和 DeFronzo 的胰岛素敏感性指数[IS（OGTT）]来确定）。有趣的是，脂联素水平也与产后β细胞功能有关（胰岛素原指数/HOMA 胰岛素抵抗；r = 0.16，p = 0.0009）。事实上，在多元线性回归分析中，妊娠期间的脂联素水平独立预测了产后胰岛素敏感性（t = 3.97，p < 0.0001）和β细胞功能（t = 2.37，p = 0.0181），即使在调整了 GDM 后也是如此。此外，脂联素是产后空腹血糖的显著负独立决定因素（t = -3.01，p = 0.0027）。
结论/解释：妊娠期间的低脂联素血症预测产后胰岛素抵抗、β细胞功能障碍和空腹血糖，因此可能与 GDM 与 2 型糖尿病相关的病理生理学有关。
