Food, Fitness & Pharma > Research > Genetics/Epid

Genetics /Epidemiology

Main hypothesis:

The development of obesity, type 2 diabetes and associated cardiovascular morbidity and premature mortality is determined by both genetic and environmental risk factors.  Genetics / epidemiology constitute a central, intersecting “bar” in the inter-disciplinary research matrix, addressing environmental, genetic and epigenetic interplays in the pathogenesis of these lifestyle diseases.

State of the art:

Although fifty percent of the between-subject variation in body weight and fasting- and postprandial glucose and insulin levels are determined by genetics changes in the environment must be responsible for the rapid increasing prevalence of obesity and type 2 diabetes.,. A number of common single nucleotide polymorphisms each with modest effect size (relative disease risk of 8-35%) have recently been shown to associate with obesity and type 2 diabetes. Nonetheless, the common variation in these genes can only account for less than 5% of the heritability of these metabolic disorders.. Moreover, our knowledge of the intricate interplay between the multiple genetic and environmental factors in the pathogenesis of lifestyle diseases is its infancy.   

This part of the UNIK is about:

• A DNA biobank will be established based on the large “Diet, Cancer & Health cohort”. This biobank and associated serum samples and phenotypic database with 12 year follow-up will form a national resource for studies of the interactions between genomics and health behavior associated with lifestyle related disorders.

• In addition candidate genes will be identified in pig and dog models of obesity and diabetes, as well as for muscular constitution, fitness and physical activity.

• The genomic basis for the role of GI tract and physical activity effects on body weight regulation and glucose homeostasis will further be investigated in the human and animal studies assessing levels of gene activity in the hormone producing cells of the small intestine and skeletal muscles.
  

This part of the UNIK is expected to lead to:

• Assessment of how the genetic contribution has contributed, alongside with the environmental changes, to the evolvement of the epidemic growth of obesity, type 2 diabetes and vascular co-morbidities.

• Identification of rare and common gene variants by whole genome exome sequencing in 2.000
  individuals, and large scale genome association studies by high-resolution SNP arrays tested
  in the DCH cohort for their roles and interactions in pathogenesis of lifestyle diseases.

• Identification of genomic components involved in gene regulation of the GI-tract (induced by gastric bypass) and muscle (induced by exercise) - including non-coding RNAs.

• Elucidation of the impact of epigenetic effects on phenotypic characteristics.
  

Impact/Implementation:

New knowledge about how to prevent obesity, type 2 diabetes and vascular co-morbidities. Novel drug leads derived from genomics discoveries and the potentials for individualized treatment modalities offering higher efficacy and less side effects.