CONTEXT Gestational diabetes mellitus (GDM) is a complex obstetric condition affecting localised glucose metabolism resulting in systemic metabolic dysfunction. OBJECTIVE This cross-sectional study aimed to explore visceral adipose tissue (VAT) as an integral contributor to GDM, focusing on elucidating the specific contribution of obesity and GDM pathology to maternal outcomes. METHODS Fifty-six nulliparous pregnant women were recruited including normal glucose tolerant (NGT) (n = 30) and GDM (n = 26) participants. Participants were subgrouped as nonobese (BMI <30 kg/m2) or obese (BMI ≥30 kg/m2). Metabolic markers in circulation, VAT and placenta were determined. Morphological analysis of VAT and immunoblotting of the insulin signalling cascade were performed. RESULTS GDM participants demonstrated hyperinsulinaemia and elevated HOMA-IR scores relative to NGT participants. The GDM-obese subgroup had significant VAT adipocyte hypoplasia relative to NGT-nonobese tissue. GDM-obese VAT had significantly lower IRS-2 expression, with elevated ser312 phosphorylation of IRS-1, relative to NGT-nonobese. GDM-obese participants had significantly elevated circulating leptin levels and placental adipsin secretion, while GDM-nonobese participants had elevated circulating adipsin levels with reduced placental adiponectin secretion. CONCLUSIONS These findings suggest that GDM-obese pregnancy is specifically characterised by inadequate VAT remodelling and dysfunctional molecular signalling which contribute to insulin resistance and hinder metabolic health.

中文翻译：

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妊娠糖尿病中内脏脂肪组织适应缺陷。

背景 妊娠糖尿病 (GDM) 是一种复杂的产科疾病，影响局部葡萄糖代谢，导致全身代谢功能障碍。目的 这项横断面研究旨在探讨内脏脂肪组织 (VAT) 作为 GDM 的一个不可分割的贡献者，重点是阐明肥胖和 GDM 病理对孕产妇结局的具体贡献。方法 招募了 56 名未产孕妇，其中包括正常糖耐量 (NGT) (n = 30) 和 GDM (n = 26) 参与者。参与者被分为非肥胖（BMI <30 kg/m2）或肥胖（BMI ≥30 kg/m2）。测定了循环、VAT 和胎盘中的代谢标志物。对 VAT 进行形态学分析并进行胰岛素信号级联的免疫印迹。结果 相对于 NGT 参与者，GDM 参与者表现出高胰岛素血症和 HOMA-IR 评分升高。相对于 NGT 非肥胖组织，GDM 肥胖亚组具有显着的 VAT 脂肪细胞发育不全。相对于 NGT 非肥胖者，GDM 肥胖者 VAT 的 IRS-2 表达显着降低，IRS-1 的 Ser312 磷酸化升高。GDM 肥胖参与者的循环瘦素水平和胎盘脂联素分泌显着升高，而 GDM 非肥胖参与者的循环脂联素水平升高，胎盘脂联素分泌减少。结论 这些研究结果表明，GDM 肥胖妊娠的具体特征是 VAT 重塑不足和分子信号传导功能失调，从而导致胰岛素抵抗并阻碍代谢健康。