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bjective This systematic literature review aims to compare the efficacy and safety of traditional and stem cell (SC) therapies for type 1 (T1DM) and type 2 (T2DM) diabetes mellitus patients. Methods The PubMed, SciELO, BVS, and Medline databases were searched, and 38 original articles were selected, which included 647 control cases and 654 treatments with three-, six- and twelve-month follow-ups of T1DM and T2DM patients. The efficacy of stem cell therapy was validated by comparing laboratory parameters such as fasting blood glucose and C-peptide levels before and after treatment. The REML model was chosen for random effects, and the inverse of variance was used for fixed effects. The statistical analysis was carried out using Bioestat 5.0 and STATA 16.0 software. Results All SC treatments significantly reduced the need for insulin following six and twelve months of treatment, whereas there was no significant decrease after three months. Fasting blood glucose and glycosylated hemoglobin levels were significantly reduced in all follow-ups with SC. In addition, SC treatment caused a significant increase in C-peptide levels. Bone marrow hematopoietic stem cell therapy produced better results than the conventional drug treatment for diabetes mellitus (semagglutide). Conclusion The results with SC were significantly better, regardless of the follow-up period. Studies have proven cell therapy to be beneficial, safe, and effective. [ABSTRACT FROM AUTHOR]

The prevalence of type 1 diabetes (T1D) is rising steadily. A potential contributor to the rise is vitamin D. In this systematic review, we examined the literature around vitamin D and T1D. We identified 22 papers examining the role of vitamin D in cultured β-cell lines, islets, or perfused pancreas, and 28 papers examining vitamin D in humans or human islets. The literature reports strong associations between T1D and low circulating vitamin D. There is also high-level (systematic reviews, meta-analyses) evidence that adequate vitamin D status in early life reduces T1D risk. Several animal studies, particularly in NOD mice, show harm from D-deficiency and benefit in most studies from vitamin D treatment/supplementation. Short-term streptozotocin studies show a β-cell survival effect with supplementation. Human studies report associations between VDR polymorphisms and T1D risk and β-cell function, as assessed by C-peptide. In view of those outcomes, the variable results in human trials are generally disappointing. Most studies using 1,25D, the active form of vitamin D were ineffective. Similarly, studies using other forms of vitamin D were predominantly ineffective. However, it is interesting to note that all but one of the studies testing 25D reported benefit. Together, this suggests that maintenance of optimal circulating 25D levels may reduce the risk of T1D and that it may have potential for benefits in delaying the development of absolute or near-absolute C-peptide deficiency. Given the near-complete loss of β-cells by the time of clinical diagnosis, vitamin D is much less likely to be useful after disease-onset. However, given the very low toxicity of 25D, and the known benefits of preservation of C-peptide positivity for long-term complications risk, we recommend considering daily cholecalciferol supplementation in people with T1D and people at high risk of T1D, especially if they have vitamin D insufficiency. [ABSTRACT FROM AUTHOR]

A major hallmark of diabetes is a constant high blood glucose level (hyperglycaemia), resulting in endothelial dysfunction. Transient or prolonged hyperglycemia can cause diabetic vasculopathy, a secondary systemic damage. C-Peptide is a product of cleavage of proinsulin by a serine protease that occurs within the pancreatic β-cells, being secreted in similar amounts as insulin. The biological activity of human C-peptide is instrumental in the prevention of diabetic neuropathy, nephropathy and other vascular complications. The main feature of type 1 diabetes mellitus is the lack of insulin and of C-peptide, but the progressive β-cell loss is also observed in later stage of type 2 diabetes mellitus. C-peptide has multifaceted effects in animals and diabetic patients due to the activation of multiple cell signalling pathways, highlighting p38 mitogen-activated protein kinase and extracellular signal–regulated kinase 1/2, Akt, as well as endothelial nitric oxide production. Recent works highlight the role of C-peptide in the prevention and amelioration of diabetes and also in organ-specific complications. Benefits of C-peptide in microangiopathy and vasculopathy have been shown through conservation of vascular function, and also in the prevention of endothelial cell death, microvascular permeability, neointima formation, and in vascular inflammation. Improvement of microvascular blood flow by replacing a physiological amount of C-peptide, in several tissues of diabetic animals and humans, mainly in nerve tissue, myocardium, skeletal muscle, and kidney has been described. A review of the multiple cell signalling pathways of human proinsulin C-peptide in vasculopathy protection is proposed, where the approaches to move beyond the state of the art in the development of innovative and effective therapeutic options of diabetic neuropathy and nephropathy are discussed. [ABSTRACT FROM AUTHOR]