Depot-specific adipocyte-extracellular matrix metabolic crosstalk in murine obesity
Depot-specific adipocyte-extracellular matrix metabolic crosstalk in murine obesity
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DOI：
10.1080/21623945.2020.1749500
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发表时间：
2020-01-01
期刊：
影响因子：
3.3
通讯作者：
O'Rourke, Robert W.
中科院分区：
文献类型：
--
作者：
Strieder-Barboza, Clarissa;Baker, Nicki A.;O'Rourke, Robert W.
皮下（SAT）和内脏（VAT）脂肪组织具有不同的代谢表型。我们假设细胞外基质（ECM）调节肥胖小鼠脂肪细胞代谢功能的特定差异。将来自瘦或肥胖小鼠的VAT和SAT前脂肪细胞在塑料组织培养板上的标准2D培养物中或在ECM中的3D培养物中进行成脂分化，然后进行代谢谱分析。从VAT相对于SAT脂肪细胞表现出受损的胰岛素刺激的葡萄糖摄取和脂肪形成能力下降。在3D-ECM-脂肪细胞培养中，ECM以储库特异性方式调节脂肪细胞代谢，SAT ECM挽救VAT脂肪细胞中葡萄糖摄取和成脂基因表达的缺陷，而VAT ECM损害SAT脂肪细胞中的成脂基因表达。这些发现表明ECM-脂肪细胞串扰调节小鼠肥胖症中脂肪细胞代谢功能障碍的贮库特异性差异。
Subcutaneous (SAT) and visceral (VAT) adipose tissues have distinct metabolic phenotypes. We hypothesized that the extracellular matrix (ECM) regulates depot-specific differences in adipocyte metabolic function in murine obesity. VAT and SAT preadipocytes from lean or obese mice were subject to adipogenic differentiation in standard 2D culture on plastic tissue culture plates or in 3D culture in ECM, followed by metabolic profiling. Adipocytes from VAT relative to SAT manifested impaired insulin-stimulated glucose uptake and decreased adipogenic capacity. In 3D-ECM-adipocyte culture, ECM regulated adipocyte metabolism in a depot-specific manner, with SAT ECM rescuing defects in glucose uptake and adipogenic gene expression in VAT adipocytes, while VAT ECM impaired adipogenic gene expression in SAT adipocytes. These findings demonstrate that ECM-adipocyte crosstalk regulates depot-specific differences in adipocyte metabolic dysfunction in murine obesity.