Abstract
Introduction: Scientists are considering the possibility of treating diabetes mellitus (DM) using a personalized approach in which various forms of the diseases will be treated based on the causal gene and its pathogenesis. To this end, scientists have identified mutations in certain genes as probable causes of Type 2 diabetes mellitus (T2DM) with diverse mechanisms.
Aim: This review was aimed at articulating already identified T2DM genes with their mechanisms of action and phenotypic presentations for the awareness of all stakeholders.
Method: The Google search engine was used to retrieve relevant information on the subject from reliable academic databases such as PubMed, Medline, and Google Scholar, among others.
Results: At least seventy (70) genes are currently being suspected in the biogenesis of T2DM. However, mutations in, or variants of KCNJ11, PPARG, HNF1B and WFS1 genes, are the most suspected and reported in the pathogenesis of the disease. Mutations in these genes can cause disruption of insulin biosynthesis through the destruction of pancreatic beta cells, change of beta cell morphology, destruction of insulin receptors, among others. These cellular events may lead to insulin resistance and hyperglycemia and, along with environmental triggers such as obesity and overweight, culminate in T2DM. It was observed that each identified gene has its distinct mechanism by which it interacts with other genes and environmental factors to cause T2DM.
Conclusion: Healthcare providers are advised to formulate T2DM drugs or treatment by targeting the causal genes along with their mechanisms.
Keywords: Beta cells, hyperglycemia, insulin resistance, mutation, obesity, type 2 diabetes.
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