Contact

Adress

Lund University, Dept of Clinical Sciences Malmö
CRC, Jan Waldenströms gata 35, SE-205 02 Malmö, Sweden

Phone

+46 40 391214

Fax

+46 40 391222

E-mail

Rashmi.Prasad@remove-this-part.med.lu.se

 

Rashmi Prasad

Associated researcher

Current project

The etiology of type 2 diabetes

Type 2 diabetes is a complex heterogeneous disease whose etiology includes genetic and epigenetic factors interacting with diverse environmental factors. The social determinants of environmental factors tend to vary across populations and have changed rapidly over the last few hundred years. A higher energy consuming lifestyle has now changed to a more sedentary one with little or no exercise and high fat – rich sugar diet. Meanwhile genetic factors tend to evolve at a slower rate across generations, and tend to remain constant within a generation. Consistent with the ‘thrifty genotype’ hypothesis, retention of the ‘thrifty-genotype’ which ‘stores’ rather than ‘spends’ and interaction with the environment has resulted in a dramatic increase in diabetes incidences.

Genome wide association studies have identified about 55 genetic variants associated with diabetes and related traits, including insulin resistance and beta cell dysfunction. However, this explains only about 15% of the underlying genetics of type 2 diabetes. One source of the missing heritability could be the more recent or rare variants with stronger effects segregating in families with a clear transmission of the disease. Another source of missing heritability includes the distinct parent specific transmission where risk is conferred when transmitted by one parent and not the other. My projects are aimed at identifying these common and rare variants associated with type 2 diabetes, and their interactions with non-genetic factors. Additional focus will be on determining parent of origin of the risk alleles and subsequent attempts to understand genetic programming effects during intrauterine period. This will be achieved through a combination of genetic, epigenetic and transcriptomic approaches and will lead to identification of key pathways leading to pathological glucose levels and T2D risk. Identification of genetic and non-genetic factors increasing risk of diabetes could potentially be used to design more effective preventive strategies, in diagnostics, risk classifications and in therapeutics.

Last updated: January 25, 2013
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LUDC, CRC, SUS Malmö, Entrance 72, House 91:12. SE-205 02 Malmö. Telephone: +46 40 39 10 00