Genes play a deciding factor in the way an organism’s body functions. Several genome studies have indicated that mutation of the genes controlling the production of Human leukocyte antigen (HLA protein) results in Type1 diabetes, while variations in the gene TCF7L2 results in Type2 diabetes. Apart from the gene play, certain congenital autoimmune disorders result in the destruction of Beta cells of the pancreas resulting in late onset Type1 diabetes.
Diabetes was once known as the disease of the affluent, which suggested a connection between the disease and rich diet combined with physical inactivity. Modern science has confirmed this old adage. Obesity reduces insulin sensitivity of the cells resulting in Type2 diabetes. Moreover, high body fat percentage can adversely affect the pancreas, leading to reduced insulin secretion.
Further complicating the etiology is the discovery of the Ob gene. This is a mutant gene found in obese individuals, which plays a role in passing Type2 diabetes to the next generation. Ob gene, purportedly leads to insulin toxicity resulting in age onset diabetes. At the same time, the presence of the gene in healthy and physically active individuals has shown to have no effect on insulin sensitivity, suggesting interplay of nature and nurture.
Thus, according to the present understanding, diabetes mellitus is a result of a combination of genetic predisposition and faulty lifestyle (including both under nutrition and over nutrition).