**1.2 Diabetes- an understanding at the molecular level**

Diabetes is a serious public health challenge, and its types, especially type 1 & 2 are caused by a combination of genetic and environmental risk factors. For instance, an increase in human islet BCL11A expression decreases islet insulin secretion. Thus *BCL11A* expression is elevated during T2D and chronic hyperglycemia [2]. Being **polygenic**, they are related to a change, or defect, in multiple genes. This includes variations in important genes which are vital for glucose metabolism (regulation of fasting & postprandial blood glucose levels), insulin function (mainly insulin resistance) & triglyceride metabolism. The following figure, **Figure 1** illustrates the pathogenesis of diabetes at a molecular level.

Diseases like diabetes are now being diagnosed, monitored and treated through an effective, individualized model of care rather than the 'one size fits all' approach. Owing to its efficiency in personalized care, precision medicine has gained focus worldwide, and its emerging application has diabetes in the forefront [3, 4]. For instance, the gastrointestinal side effects of the hypoglycaemic drug metformin has been linked to the interaction between the genes encoding the organic cation transporter 1 (OCT1) and the serotonin reuptake transporter (SERT). The number of lowexpressing SERT S\* alleles increased the odds of metformin intolerance. Likewise, the presence of two deficient OCT1 alleles was associated with over a nine-fold higher odds of metformin intolerance in patients carrying L\*L\* genotype [5].

Understanding relevant genes may not only help determine who is at high risk for developing the disease, but may also be useful in guiding treatment regimens. Beyond treating diabetes, we have set foot in a new era of curing the disease with pancreatic
