Impact of telomere attrition on diabetes mellitus and its complications

Abstract

Diabetes mellitus is a chronic metabolic condition marked by persistent hyperglycemia. It is a major issue of public health with wide-ranging effects. Telomeres are protective caps at chromosome ends, essential for preserving genomic stability and cellular integrity. Research highlights the complex link between diabetes and telomere biology and the potential interactions between the two. This review aims to present a summary of the relationship between diabetes and telomeres, highlighting significant discoveries and probable underlying mechanisms. Telomere shortening in those with diabetes and those at risk of getting the condition provides evidence that telomere dysfunction is linked to diabetes. It is said that telomere attrition, which is influenced by elements such as oxidative stress, inflammation, insulin resistance, and hyperglycemia, plays a major role in the pathophysiology of diabetes. Diabetes Mellitus's hallmark symptoms are chronic inflammation and oxidative stress, accelerating telomere shortening via pro-inflammatory cytokines production and reactive oxygen species, respectively. Telomere dysfunction is enhanced further by the long-term effects of insulin resistance and hyperglycemia. The onset of diabetic comorbidities such as cardiovascular disease, nephropathy, retinopathy, and neuropathy has also been linked to telomere shortening. Understanding how telomeres contribute to these issues may offer new therapeutic ideas. Diabetes and its consequences may be treated with telomere-targeted medicines, such as telomerase activators, telomerase gene therapy, and treatments that target telomere-associated proteins. However, more investigation is required to assess these strategies' security, effectiveness, and long-term impacts.