Institute of Physiology and Institute of Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra (FMUC), Portugal; Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, Portugal; Clinical Academic Center of Coimbra (CACC), Coimbra, Portugal.
Institute of Physiology and Institute of Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra (FMUC), Portugal.
Pharmacol Res. 2020 Nov;161:105198. doi: 10.1016/j.phrs.2020.105198. Epub 2020 Sep 14.
Methylglyoxal was shown to impair adipose tissue capillarization and insulin sensitivity in obese models. We hypothesized that glyoxalase-1 (GLO-1) activity could be diminished in the adipose tissue of type 2 diabetic obese patients. Moreover, we assessed whether such activity could be increased by GLP-1-based therapies in order to improve adipose tissue capillarization and insulin sensitivity. GLO-1 activity was assessed in visceral adipose tissue of a cohort of obese patients. The role of GLP-1 in modulating GLO-1 was assessed in type 2 diabetic GK rats submitted to sleeve gastrectomy or Liraglutide treatment, in the adipose tissue angiogenesis assay and in the HUVEC cell line. Glyoxalase-1 activity was decreased in visceral adipose tissue of pre-diabetic and diabetic obese patients, together with other markers of adipose tissue dysfunction and correlated with increased HbA1c levels. Decreased adipose tissue GLO-1 levels in GK rats were increased by sleeve gastrectomy and Liraglutide, being associated with overexpression of angiogenic and vasoactive factors, as well as insulin receptor phosphorylation (Tyr1161). Moreover, GLP-1 increased adipose tissue capillarization and HUVEC proliferation in a glyoxalase-dependent manner. Lower adipose tissue GLO-1 activity was observed in dysmetabolic patients, being a target for GLP-1 in improving adipose tissue capillarization and insulin sensitivity.
甲基乙二醛被证明会损害肥胖模型中的脂肪组织毛细血管化和胰岛素敏感性。我们假设 2 型糖尿病肥胖患者的脂肪组织中糖氧还蛋白-1(GLO-1)活性可能会降低。此外,我们评估了基于 GLP-1 的治疗是否可以增加这种活性,以改善脂肪组织的毛细血管化和胰岛素敏感性。评估了肥胖患者内脏脂肪组织中的 GLO-1 活性。在接受袖状胃切除术或利拉鲁肽治疗的 2 型糖尿病 GK 大鼠的脂肪组织血管生成测定和 HUVEC 细胞系中评估了 GLP-1 在调节 GLO-1 中的作用。在糖尿病前期和糖尿病肥胖患者的内脏脂肪组织中,GLO-1 活性降低,同时还存在其他脂肪组织功能障碍的标志物,并且与 HbA1c 水平升高相关。GK 大鼠的脂肪组织 GLO-1 水平降低通过袖状胃切除术和利拉鲁肽增加,与血管生成和血管活性因子的过表达以及胰岛素受体磷酸化(Tyr1161)相关。此外,GLP-1 以依赖糖氧还酶的方式增加脂肪组织的毛细血管化和 HUVEC 增殖。代谢紊乱患者的脂肪组织 GLO-1 活性较低,是 GLP-1 改善脂肪组织毛细血管化和胰岛素敏感性的靶点。