Korolenko Tatiana A, Ovsyukova Marina V, Bgatova Nataliya P, Ivanov Igor D, Makarova Svetlana I, Vavilin Valentin A, Popov Alexey V, Yuzhik Ekaterina I, Koldysheva Elena V, Korolenko Erik C, Zavjalov Evgeny L, Amstislavskaya Tamara G
Scientific-Research Institute of Neurosciences and Medicine, Timakov Street 4, 630117 Novosibirsk, Russia.
Laboratory of Ultrastructural Research, Research Institute of Clinical and Experimental Lymphology-Branch of Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, 630060 Novosibirsk, Russia.
Life (Basel). 2022 Mar 17;12(3):442. doi: 10.3390/life12030442.
mice (carrying a mutation in the gene encoding leptin receptor) show autophagy suppression. Our aim was to evaluate the effect of autophagy inducer trehalose on liver and heart autophagy in mice and to study inflammation dysregulation and the suitability of chitinases' expression levels as diabetes markers. Thirty-eight male mice and C57/BL mice (control) were used. The model manifested inflammation symptoms: overexpression of in the spleen and underexpression of in the liver and spleen (cytokine imbalance). Simultaneously, we revealed decreased expression of chitotriosidase () and acid mammalian chitinase () in the liver of mice. expression in mice is significantly lower only in the spleen. Trehalose treatment significantly reduced blood glucose concentration and glycated hemoglobin. Treatment of mice by trehalose was followed by increased autophagy induction in the heart and liver (increased autolysosomes volume density studied by morphometric electron-microscopic method). Trehalose exerted beneficial cardiac effects possibly via increased lipophagy (uptake of lipid droplets). The autophagy activation by trehalose had several positive effects on the heart and liver of mice; therefore, lipophagy activation seems to be a promising therapy for diabetes.
携带瘦素受体编码基因突变的小鼠表现出自噬抑制。我们的目的是评估自噬诱导剂海藻糖对小鼠肝脏和心脏自噬的影响,并研究炎症失调以及几丁质酶表达水平作为糖尿病标志物的适用性。使用了38只雄性小鼠和C57/BL小鼠(对照)。该模型表现出炎症症状:脾脏中[具体基因]过表达,肝脏和脾脏中[具体基因]表达不足(细胞因子失衡)。同时,我们发现小鼠肝脏中壳三糖苷酶([具体酶名称])和酸性哺乳动物几丁质酶([具体酶名称])的表达降低。[具体基因]在小鼠中的表达仅在脾脏中显著较低。海藻糖治疗显著降低了血糖浓度和糖化血红蛋白。用海藻糖治疗小鼠后,心脏和肝脏中的自噬诱导增加(通过形态计量电子显微镜方法研究自噬溶酶体体积密度增加)。海藻糖可能通过增加脂肪自噬(脂滴摄取)对心脏产生有益作用。海藻糖激活自噬对小鼠的心脏和肝脏有几个积极影响;因此,激活脂肪自噬似乎是一种有前途的糖尿病治疗方法。