The study was authored by Dr Yin Paradies, an epidemiologist from Darwin's Menzies School of Health Research along with two researchers from the United States. It shows that the high rates of diabetes among indigenous people across the globe are rooted in social disadvantage rather than a genetic pre-disposition specific to indigenous populations.

"Around the world, indigenous people suffer from diabetes at 2-5 times the rate of non-indigenous people", says Dr Paradies.

"There is a common misconception that diabetes is 'in the genes' for Indigenous people. This idea stems from the 'thrifty gene hypothesis' which proposes that cycles of feast and famine in indigenous societies created a gene that was very efficient at using nutrients. According to this hypothesis, such efficiency combined with a modern affluent and sedentary lifestyle leads to obesity and diabetes among indigenous people."

"Although there is certainly a genetic component to diabetes that affects people throughout society, the idea that indigenous people have a 'thrifty gene' is dispelled by our research which shows that when it comes to diabetes, genes are no more important for indigenous people than for anyone else."

"Instead, it is aspects of the social environment that are responsible for the high rates of diabetes among indigenous people. Poor diet, reduced physical activity, stress, low birth weight and other factors associated with poverty all contribute to the high rate of diabetes among indigenous people", Dr Paradies said.

"For indigenous people, diabetes will only be tackled by addressing poverty and social disadvantage".

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AVN944 is an oral small molecule drug candidate that inhibits inosine monosphospate dehydrogenase (IMPDH), an enzyme that is critical for cells to be able to synthesize guanosine triphosphate (GTP), a molecule required for DNA synthesis and cellular signaling. IMPDH is over expressed in some cancer cells, especially in the case of hematological malignancies. In laboratory experiments, AVN944 has been shown to inhibit IMPDH activity in cells, and suppress pools of GTP. Anticancer activities of IMPDH inhibitors correlate with sustained depletion of GTP pools both in cellular models and in human subjects. AVN944 appears to have a selective effect on cancer cells in that deprivation of GTP in normal cells results in a temporary slowing of cell growth, while GTP deprivation in cancer cells induces cell death, or apoptosis.

Results from preclinical studies of AVN944 indicate that AVN944 inhibited the proliferation of lymphoid and myeloid cells, the principal cells involved in the most common types of human leukemias. In a single-dose, dose- escalation Phase I clinical trial of AVN944 conducted in the United Kingdom in healthy volunteers, AVN944: (1) was well tolerated at all tested doses with no notable side effects; (2) demonstrated good pharmacokinetic properties; and (3) had a significant inhibitory effect on IMPDH enzyme activity. Avalon filed an IND with the FDA in August 2005 and initiated U.S. Phase I clinical trials in January 2006 for the treatment of hematological cancers.

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