Nikola Lukic, Iva Lukic
Laboratory for Molecular Biology and Endocrinology, Institute of Nuclear Sciences "Vinca", National Institute of the Republic of Serbia, University of Belgrade, Serbia.
Laboratory for Molecular Biology and Endocrinology, Institute of Nuclear Sciences "Vinca", National Institute of the Republic of Serbia, University of Belgrade, Serbia.
Life Sci. 2024 Dec 15;359:123187. doi: 10.1016/j.lfs.2024.123187. Epub 2024 Oct 31.
Type 1 diabetes (T1D) is defined as an autoimmune metabolic disorder, characterized by destruction of pancreatic β-cells and high blood sugar levels. If left untreated, T1D results in severe health complications, including cardiovascular and kidney disease, as well as nerve damage, with ultimately grave consequences. Besides the role of genetic and certain environmental factors in T1D development, in the last decade, one new player emerged to affect T1D pathology as well, and that is a gut microbiota. Dysbiosis of gut bacteria can contribute to T1D by gut barrier disruption and the activation of autoimmune response, leading to the destruction of insulin producing cells, causing the development and aggravation of T1D symptoms. The relationship between gut microbiota and diabetes is complex and varies between individuals and additional research is needed to fully understand the effects of gut microbiome alternations in T1D pathogenesis. Therefore, the goal of this review is to understand the current knowledge in underlying molecular mechanism of gut microbiota effects, which leads to the new approaches for further studies in the prevention and treatment of T1D.
1型糖尿病（T1D）被定义为一种自身免疫性代谢紊乱疾病，其特征是胰腺β细胞被破坏以及血糖水平升高。如果不进行治疗，T1D会导致严重的健康并发症，包括心血管疾病和肾脏疾病，以及神经损伤，最终会产生严重后果。除了遗传因素和某些环境因素在T1D发病过程中的作用外，在过去十年中，一个新的因素也出现并影响了T1D的病理过程，即肠道微生物群。肠道细菌的失调可通过破坏肠道屏障和激活自身免疫反应导致T1D，进而导致产生胰岛素的细胞被破坏，引发T1D症状的出现和加重。肠道微生物群与糖尿病之间的关系很复杂，且因人而异，需要更多的研究来全面了解肠道微生物组变化在T1D发病机制中的作用。因此，本综述的目的是了解目前关于肠道微生物群作用的潜在分子机制的知识，从而为T1D预防和治疗的进一步研究提供新方法。
