Non-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent disorder with no approved drug treatment. It occurs with a spectrum of pathological severity including fatty liver, steatohepatitis, and steatonecrosis, which can lead to cirrhosis and hepatocellular carcinoma. It is currently estimated that over 64 million people in the United States have NAFLD, while in Germany, France, Italy, and the United Kingdom combined there are ~52 million with NAFLD. The associated annual direct medical costs are $103 billion and €35 billion, respectively. NAFLD is also highly associated with obesity, cardiovascular disease, and diabetes mellitus, the latter of which afflicts up to ~10 % of the U.S. and European populations and over 422 million people worldwide. In the United States alone, the directly associated medical cost of diabetes mellitus is $237 billion per year. Barish laboratory has made surprising discoveries regarding the role for BCL6 in metabolic control which have novel implications for NAFLD therapeutics via BCL6 reduction or inhibition. Genetic ablation of Bcl6 confers protection against insulin resistance and steatosis, raising the possibility that small molecules or genetic strategeies to degrade or interfere with BCL6 could be therapeutic for obesity-related metabolic pathologies including type 2 diabetes mellitus and nonalcoholic fatty liver disease. We hypothesize that reducing BCL6 levels will ameliorate obesity-related conditions including nonalcoholic fatty liver disease and type 2 diabetes mellitus.
|Effective start/end date||12/23/20 → 6/22/22|
- Boehringer Ingelheim International GmbH (Agmt 12/23/20)
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