Summary Evidence for a genetic basis for type 2 diabetes and the metabolic syndrome has been derived from studies of families, twins and populations with genetic admixture. Identification of genes associated with disease pathogenesis is now underway using techniques such as genome scanning by positional cloning and the candidate gene approach. Genome scanning in several different ethnic groups has identified chromosome regions harbouring type 2 diabetes susceptibility genes such as the novel gene, calpain 10 (CAPN10). The hepatic nuclear factor 4α (HNF4α) gene partly explains the linkage peak on chromosome 20, while the upstream transcription factor (USF1) is associated with familial combined hyperlipidaemia (FCHL) and maps close to the type 2 diabetes associated 1q peak. Peroxisome proliferator‐activated receptor gamma (PPARγ) was identified as a candidate gene based on its biology. A Pro12Ala variant of this gene has been associated with an increased risk of type 2 diabetes. Many genes accounting for monogenic forms of diabetes have been identified – such as maturity onset diabetes of the young (MODY); glucokinase (GCK) and HNF1α mutations being the most common causes of MODY. GCK variants result in ‘mild’ diabetes or impaired glucose tolerance (IGT) and relatively few cardiovascular complications, while HNF1α‐associated MODY is more typical of type 2 diabetes, frequently being treated with sulphonylureas or insulin and resulting in microvascular complications. Testing for single gene disorders associated with type 2 diabetes and obesity may determine cause, prognosis and appropriate treatment; however, for the more common polygenic diseases this is not the case. In type 2 diabetes, molecular genetics has the potential to enhance understanding of disease pathogenesis, and help formulate preventative and treatment strategies.

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Diabetic retinopathy (DR) is a leading cause of visual impairment and blindness in the working-age population across the globe. The objective of the present study was to assess the drug utilization pattern, risk factors and prevalence of diabetic retinopathy in patients with type 2 diabetes mellitus in a south Indian tertiary care hospital. A cross-sectional observational study was conducted on 745 subjects (386 with diabetic retinopathy and 359 without diabetic retinopathy). Prevalence of diabetic retinopathy was measured and risk factors for the development of diabetic retinopathy were determined by calculating odds ratios using graph-pad prism statistical software and drug utilization pattern was assessed. Retinopathy was significantly higher in the subjects who are married, uneducated, housewives, urban residents, no income group and risk factors were comorbidities (other diseases, hypertension, endocrine diseases, history of cardiovascular diseases, HbA1c, high serum creatinine, duration of diabetes (5-10 years and >10 years, physical inactivity, junk foods (weekly once and weekly twice), soft drinks occasionally and tea/ coffee (daily twice). Metformin (38.21%), combination of Insulin Isophane and Insulin Regular (16.75%), Insulin Regular (15.18%), combination of Glimepiride and Metformin (11.51%), Glimepiride (7.85%), combination of Metformin and Vildagliptin (7.85%) were most commonly prescribed anti-diabetic drugs to the T2DM patients with retinopathy. The present study revealed that risk factors for the development of diabetic retinopathy were multiple