Hyperglycaemia is a life-threatening risk factor that occurs in both chronic and acute phases and has been linked to causing injury to many organs. Protein modification was triggered by hyperglycaemic stress, which resulted in pathogenic alterations such as impaired cellular function and tissue damage. Dysregulation in cellular function increases the condition associated with metabolic disorders, including cardiovascular diseases, nephropathy, retinopathy, and neuropathy. Hyperglycaemic stress also increases the proliferation of cancer cells. The major areas of experimental biomedical research have focused on the underlying mechanisms involved in the cellular signalling systems involved in diabetes-associated chronic hyperglycaemia. Reactive oxygen species and oxidative stress generated by hyperglycaemia modify many intracellular signalling pathways that result in insulin resistance and β-cell function degradation. The dysregulation of post translational modification in β cells is clinically associated with the development of diabetes mellitus and its associated diseases. This review will discuss the effect of hyperglycaemic stress on protein modification and the cellular signalling involved in it. The focus will be on the significant molecular changes associated with severe metabolic disorders.

高血糖是一种危及生命的危险因素，发生在慢性和急性期，并与许多器官损伤有关。高血糖应激引发蛋白质修饰，导致细胞功能受损和组织损伤等致病性改变。细胞功能失调会增加与代谢紊乱相关的疾病，包括心血管疾病、肾病、视网膜病和神经病。高血糖应激还会增加癌细胞的增殖。实验生物医学研究的主要领域集中于与糖尿病相关的慢性高血糖相关的细胞信号系统的潜在机制。高血糖产生的活性氧和氧化应激会改变许多细胞内信号传导途径，导致胰岛素抵抗和 β 细胞功能退化。β细胞翻译后修饰的失调在临床上与糖尿病及其相关疾病的发生有关。这篇综述将讨论高血糖应激对蛋白质修饰及其所涉及的细胞信号传导的影响。重点将放在与严重代谢紊乱相关的显着分子变化上。