Rescue of Islet β Cells from High Glucose-induced Apoptosis through Vitamin B12-induced Autophagy

Hyuana Kim^*
*Correspondence: Hyuana Kim, Department of Food Technology, Hunan Agricultural University, Changsha 410128, China, Email:

Keywords

Islet β cells • Apoptosis • High glucose • Vitamin B12 • Autophagy • Diabetes

Introduction

Islet β cells, responsible for insulin secretion, are central to the regulation of glucose homeostasis. Their loss or dysfunction is a hallmark of diabetes mellitus and high glucose levels play a significant role in triggering apoptosis of these vital cells. Apoptosis in islet β cells can result from various stressors, including glucotoxicity, oxidative stress and endoplasmic reticulum stress [1]. Recent studies have suggested that autophagy, a cellular recycling process, may offer a protective mechanism against apoptosis in these cells. Vitamin B12, also known as cobalamin, is an essential micronutrient with diverse physiological functions, including its role in DNA synthesis and methionine metabolism. Emerging evidence indicates that vitamin B12 may play a pivotal role in modulating autophagy, which has sparked interest in its potential to protect islet β cells from high glucose-induced apoptosis. This paper aims to provide an in-depth review of the literature, examining the interplay between vitamin B12, autophagy and apoptosis in islet β cells and discussing the implications of this interaction for the field of diabetes research [2,3].

Literature Review

High glucose-induced apoptosis in islet β cells represents a critical process in the development and progression of diabetes. Autophagy, on the other hand, is a cellular mechanism that involves the degradation and recycling of damaged organelles and proteins. Recent studies have pointed to the role of autophagy as a protective response to cellular stressors, including high glucose levels, in islet β cells. Vitamin B12, as a cofactor in various biochemical reactions, has been shown to influence cellular metabolism and stress responses. Several studies have indicated that vitamin B12 supplementation can stimulate autophagy in different cell types. However, the specific mechanisms underlying vitamin B12-induced autophagy and its impact on islet β cells remain subjects of on-going investigation [4].

Discussion

The discussion section delves into the potential mechanisms through which vitamin B12 may induce autophagy in islet β cells, ultimately rescuing them from high glucose-induced apoptosis. It considers the intricate crosstalk between vitamin B12, autophagy and apoptosis, highlighting the importance of maintaining β cell integrity for effective glucose homeostasis. Furthermore, this section explores the clinical implications of these findings. Understanding the role of vitamin B12 in preserving β cell function may offer new avenues for diabetes management and treatment. It raises questions about the potential of vitamin B12 supplementation as a therapeutic strategy to protect islet β cells in individuals with diabetes [5,6].

Conclusion

In conclusion, the interplay between vitamin B12-induced autophagy and the rescue of islet β cells from high glucose-induced apoptosis represents a promising avenue in the field of diabetes research. While the exact mechanisms require further elucidation, the existing literature suggests that vitamin B12 may play a crucial role in preserving β cell integrity and function. These findings have the potential to open new doors for diabetes management and treatment, with vitamin B12 supplementation as a potential strategy to enhance the survival and function of islet β cells. Future research should focus on mechanistic studies and clinical trials to confirm the therapeutic potential of vitamin B12 in preserving β cell health and, subsequently, improving glucose homeostasis in individuals with diabetes.

Acknowledgement

None.

Conflict of Interest

None.

References

1. Obeid, Rima, Sergey N. Fedosov and Ebba Nexo. "Cobalamin coenzyme forms are not likely to be superior to cyano�and hydroxyl�cobalamin in prevention or treatment of cobalamin deficiency." Mol Nutr Food Res 59 (2015): 1364-1372.

   Google Scholar, Crossref, Indexed at

2. Lenhert, P. Galen and Dorothy Crowfoot Hodgkin. "Structure of the 5, 6-dimethylbenzimidazolylcobamide coenzyme." Nature 192 (1961): 937-938.

   Google Scholar, Crossref, Indexed at

3. Infante, Marco, Martina Leoni, Massimiliano Caprio and Andrea Fabbri. "Long-term metformin therapy and vitamin B12 deficiency: An association to bear in mind." World J Diabetes 12 (2021): 916.

   Google Scholar, Crossref, Indexed at

4. PieczyÅ?ska, Joanna, Sylwia PÅ?aczkowska, RafaÅ? SozaÅ?ski and Katarzyna Skórska, et al. "Effect of nickel on red blood cell parameters and on serum vitamin B12, folate and homocysteine concentrations during pregnancy with and without anemia." J Trace Elem Med Biol 68 (2021): 126839.

   Google Scholar, Crossref, Indexed at

5. Elbarbary, Nancy Samir, Eman Abdel Rahman Ismail, Mamdouh Ahmed Zaki and Yasser Wagih Darwish, et al. "Vitamin B complex supplementation as a homocysteine-lowering therapy for early stage diabetic nephropathy in pediatric patients with type 1 diabetes: A randomized controlled trial." Clin Nutr 39 (2020): 49-56.

   Google Scholar, Crossref, Indexed at

6. Yang, Ping, Jian Feng, Qing Peng and Xing Liu, et al. "Advanced glycation end products: Potential mechanism and therapeutic target in cardiovascular complications under diabetes." Oxid Med Cell Longev 2019 (2019).

   Google Scholar, Crossref, Indexed at