Artificial sweeteners and their implications in diabetes: a review

Diabetes is a significant global health concern, highlighting the critical role of dietary strategies in its management and prevention. Artificial sweeteners (ASs), due to their capacity to provide sweetness without contributing to caloric intake, have emerged as a potential tool in diabetes management. This review thoroughly examines the nuanced relationship between artificial sweeteners and diabetes, addressing their benefits and potential risks. ASs have been shown to aid in weight management, a key factor in reducing diabetes risk, and do not impact immediate blood glucose levels, offering improved glucose control for individuals with diabetes. Beyond these benefits, however, artificial sweeteners may interact complexly with gut microbiota, potentially altering its composition and affecting metabolic health. This interaction introduces concerns regarding insulin sensitivity and the risk of insulin resistance, with studies reporting conflicting findings. This comprehensive review highlights the importance of a nuanced approach to understanding the implications of artificial sweeteners in diabetes management. Given the mixed evidence on their health effects, there is a clear need for further research to fully elucidate the role of artificial sweeteners in metabolic health and their suitability as part of dietary interventions for diabetes

Metabolic consequences of alterations in gut microbiota induced by antidiabetic medications

The mutualistic relationship between human health and gut microbiota has gained growing attention as a result of its far-reaching consequences. Diabetes medications, essential for managing type 2 diabetes, which regulate glucose metabolism, have shown effects that go beyond glycemic control by receiving attention for their possible influence on gut microbiota. Notably, metformin, a cornerstone therapy, has received a lot of attention for its ability to influence the gut microbiota. Metformin administration has been linked to changes in the abundance of specific bacterial taxa, including an uprise in beneficial microbes like Akkermansia muciniphila. These modifications have been linked to increased insulin sensitivity and better metabolic outcomes. Other classes of diabetes drugs, in addition to metformin, have shown potential effects on the gut microbiota. SGLT-2 inhibitors, for example, may contribute to changes in gut microbial communities, which could explain their cardiovascular and metabolic benefits. However, the processes underlying these interactions, are complicated and not entirely understood. Direct interactions between the gut microbiota and drug, changes in intestinal permeability, and modulation of bile acid metabolism are all possible mechanisms. Individual differences and genetic factors complicate the relationship even more. Understanding the intricate interplay between diabetes drugs and gut microbiota holds promise for developing personalized diabetes management approaches. Taking advantage of these interactions could lead to novel therapeutic strategies that improve drug efficacy and overall metabolic health. More studies are required to determine the exact mechanisms underlying these effects and to capitalize on their potential for improved patient outcomes. This review provides a concise overview of the effects of diabetes medications on gut microbiota composition and its importance

Impact of telomere attrition on diabetes mellitus and its complications

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