Laboratory of Physiology, Institute of Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra , Portugal.
Arch Physiol Biochem. 2013 Dec;119(5):209-18. doi: 10.3109/13813455.2013.812121. Epub 2013 Jul 11.
We previously showed that methylglyoxal-induced glycation induces adipose tissue lesions, including decreased irrigation and macrophage recruitment, independently of obesity. Here, we developed a model of partially decreased adipose tissue irrigation, a common condition in obese individuals. We aimed to study the role of methylglyoxal in the metabolic adaptations to such conditions 1 and 48 hours after decreased blood supply, avoiding other confoundable variables. Irrigation decrease during 1 hour leaded to increased activation of ERK1/2 and degradation of Ikappa-Balpha and Perilipin A in methylglyoxal-treated normal Wistar rats. After 48 hours, all rats showed increased fasting glycaemia and insulinemia. However, methylglyoxal-treated rats had higher free fatty acids and triglycerides levels and decreased adiponectinemia, consequent to decreased PPARgamma levels in partially irrigated adipose tissue. Our data show that besides causing vascular dysfunction, glycation further contributes to impaired adipocyte metabolism after a decrease of tissue irrigation, what may hamper metabolic adaptation during tissue expansion.
我们之前的研究表明，甲基乙二醛诱导的糖化作用会导致脂肪组织损伤，包括灌流减少和巨噬细胞募集，而与肥胖无关。在这里，我们建立了一个部分减少脂肪组织灌流的模型，这是肥胖个体的常见情况。我们的目的是研究甲基乙二醛在血液供应减少后 1 小时和 48 小时的代谢适应中的作用，避免其他混杂的变量。1 小时的灌流减少导致正常 Wistar 大鼠中 ERK1/2 的激活增加和 Ikappa-Balpha 和 perilipin A 的降解增加。48 小时后，所有大鼠的空腹血糖和胰岛素水平均升高。然而，甲基乙二醛处理的大鼠的游离脂肪酸和甘油三酯水平升高，脂联素血症降低，这与部分灌流的脂肪组织中 PPARgamma 水平降低有关。我们的数据表明，除了引起血管功能障碍外，糖化作用还会导致组织灌流减少后脂肪细胞代谢受损，这可能会阻碍组织扩张期间的代谢适应。
