The worldwide increase  of obesity and type 2 diabetes is taking on pandemic proportions. According to  current estimates, more than 366 million people have diabetes, and this is  expected to reach 552 million by 2030. Regarding 2008 WHO global estimates,  around 12% of adults aged 20 years or more are obese.  Even more alarming  is the rate of increase in childhood obesity, which has more than doubled  in children and tripled in adolescents in the past 30 years. 
Importantly, this may  evolve to an excessive burden of morbidity and mortality due to an expected  increase in their long-term complications: cardiovascular disease, retinopathy,  neuropathy, kidney and liver diseases, cancer, depression, impaired quality of  life, etc. Moreover, this picture is further complicated by the fact that  obesity and diabetes are interrelated: obesity is associated with insulin  resistance (a risk factor for type 2 diabetes) and may precede diabetes, and  also obesity is observed in an important number of diabetic patients. The term Diabesity has been coined to describe the concomitant presence of both diseases and their  pathogenic association.
This represents a major  challenge in nephrology since a considerable number of the population with diabesity may develop complications such as albuminuria, overt proteinuria and decreasing  renal function which untreated may lead to end-stage renal disease.  Importantly, the pathogenetic pathways of how obesity causes renal disease are  unknown. Furthermore, patients with diabetic nephropathy are at highly  increased risk of cardiovascular morbidity and mortality.

Detailed Aims:
The following specific themes will  be developed in order to extend scientific knowledge and understanding:

  • common pathways of obesity and diabetes associated renal disease.
  • the non-proteinuric pathways of renal damage in type 2 diabetes mellitus and in insulin resistant obesity.
  • the role of glomerular hyperfiltration in renal function loss in diabetes and obesity.
  • the impact of calorie restriction in obese subject with glomerular hyperfiltration.
  • early stages of kidney damage associated with diabesity in humans and in animal models.
  • the renal histology of obesity (with and without insulin resistance), metabolic syndrome, type 2 diabetes with albuminuria, or with overt proteinuria.
  • to find novel biomarkers for diabesity kidney injury (e.g. microRNA, urinary tubular markers, renal metabolic imaging) by establishing large multi-center cohorts.
    To carry into effect the intent of  the Group, international scientific research, from pre-clinical to  translational, will be stimulated. Importantly, a routine mean of exchanging  and verifying scientific results will be established. The Group will also allow  communication with other European entities to promote collaborations and joint  activities.
  • Finally, regular education and  training activities with the goal of improving understanding of diabesity for both the medical community and patients will be encouraged.