A Systematic Review on Prevention of Beta Cell Apoptosis in Type 2 Diabetes Miletus Using Verapamil: A Calcium Channel Blocker

Type 2 Diabetes Miletus is a growing public health issue characterized by peripheral insulin resistance and decompensation of the pancreatic cells that can no longer keep up with the increased insulin requirements, resulting in hyperglycemia. These elevated glucose levels have detrimental effects on various tissues including the pancreatic cell. Cell glucose toxicity leads to progressive cell dysfunction, impaired insulin gene transcription and irreversible cell loss by apoptosis, resulting in a vicious cycle with worsening hyperglycemia. Novel approaches that could promote pancreatic beta cell reserve, protect against apoptotic beta-cell loss, and help prevent diabetes are therefore urgently needed. The calcium-channel blocker verapamil effectively lowers beta cell TXNIP expression in rodent beta cells and islets as well as in human islets. This effect is based on the established mode of action of verapamil, i. e. , blockade of L-type calcium channels and the resulting decrease in intracellular free calcium leading to inhibition of TXNIP transcription. Tissues with high expression of L-type calcium channels, such as beta cells and the heart, are therefore most likely to benefit from the resulting TXNIP inhibition