Currently, the WHO estimates the number of diabetics worldwide to be more than 180 million. A doubling of this number is expected to occur by 2030. In developing countries, the WHO estimates a doubling of diabetics in the age group 20-44 years until 2030 while in the age groups of 45-64 years and 65+ years, the numbers will increase by a factor of ~2.4 and ~3, respectively. Although a large portion of the worldwide increase of diabetes will occur in developing countries, in Europe the incidence of diabetes will also increase. While for the year 2000, the percentage of diabetics in the EU population ranges from 2.7% (in Ireland) to 5.3% (in Finland) (Health Statistics of the EU, Key Data on Health 2002, for the year 2030 estimations range from 3.2% (in Ireland) to 13.8% (in Malta)(Wild et al, 2004, official study for the WHO). The WHO estimates that in upper- and middle-income countries (including Western Europe), the number of diabetes-related deaths will increase by 80% between 2006 and 2015. It is estimated that up to 20% of the total costs of European national health systems may be dedicated to treatment of diabetes or diabetes-associated complications.
The EU health strategy aims to protect and improve health of EU citizens. Strand 2 of the 3 main strands of the EU "Programme of Community action in the field of health and consumer protection (2007-2013)" is dedicated to objectives and measures that are specific to the health field. One of the main aims in this strand is to reduce the incidence of major diseases, such as diabetes mellitus. The overall EU health strategy aims at tackling health determinants, in particular harmful factors related to life style. Though some of the life style-related risk factors for the development of diabetes mellitus are well-known, such as obesity in the case of T2D, the precise underlying molecular pathophysiological mechanisms leading to the decrease in beta-cell mass responsible for the development of impaired glucose tolerance and diabetes still remain to be elucidated. Similarly, many unknowns still exist with regard to the initiation, development, and time course of the islet alterations in T1D.
Reliable, sensitive, specific, and non-invasive methods for a comprehensive structural and functional characterization of living pancreatic beta-cells in vivo and in vitro would enhance our understanding of the pathophysiology of both type 1 and type 2 diabetes. Furthermore, the ongoing development of novel therapeutic approaches to diabetes, whether based on pharmacology or cell replacement also calls for the rapid development of methods for the longitudinal in vivo assessment of the beta-cell mass and function. Apart from direct determination of beta-cell mass, such imaging techniques could also be used for imaging of the response of beta-cells to processes leading to beta-cell dysfunction and eventually apoptosis.
Therefore, BetaImage will: