Mechanisms of Alcoholic and Nonalcoholic Fatty Liver (Steatosis) (R01)

The summary for the Mechanisms of Alcoholic and Nonalcoholic Fatty Liver (Steatosis) (R01) grant is detailed below. This summary states who is eligible for the grant, how much grant money will be awarded, current and past deadlines, Catalog of Federal Domestic Assistance (CFDA) numbers, and a sampling of similar government grants. Verify the accuracy of the data FederalGrants.com provides by visiting the webpage noted in the Link to Full Announcement section or by contacting the appropriate person listed as the Grant Announcement Contact. If any section is incomplete, please visit the website for the National Institutes of Health, which is the U.S. government agency offering this grant.

Mechanisms of Alcoholic and Nonalcoholic Fatty Liver (Steatosis) (R01): Purpose. This Funding Opportunity Announcement (FOA) issued by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and the Office of Dietary Supplements (ODS), National Institutes of Health (NIH), solicits grant applications from institutions/organizations that propose to employ an integrative approach using state-of-the-art technologies to gain insight into the molecular and biochemical mechanisms of alcoholic and nonalcoholic fatty liver. This FOA addresses several areas considered to be high priority for liver disease research as delineated in the recently published Trans-NIH Action Plan for Liver Disease Research (http://liverplan.niddk.nih.gov), specifically in the area of fatty liver disease. The areas of focus include investigations of mechanisms by which alcohol and nonalcoholic physiologic processes: a) accelerate import of free fatty acids into hepatocytes; b) impair mitochondrial oxidation of fatty acids; c) impede the entry of free fatty acids into mitochondria; d) promote de novo fatty acid synthesis; e) promote esterification of free fatty acids into triglycerides; and f) disrupt export of triglycerides from hepatocytes. Research to develop non-invasive biomarkers for fatty liver using genomics, proteomics, and metabolomics, is also encouraged. Applications investigating the modulating effects of dietary fatty acids, obesity, diabetes, insulin resistance, and components of the metabolic syndrome on alcoholic and nonalcoholic fatty liver are also encouraged. Understanding these mechanisms may help develop strategies for the prevention of accumulation of fat within the liver which may block or delay the progression of fatty liver to active hepatitis, fibrosis, and cirrhosis.