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December 4, 2019 | 4:00 p.m. - 5:00 p.m.
Category: Seminar
Location: Biological Sciences #1167
Cost: free
Audience: Academic Staff, Alumni, Community, Current Graduate Students, Current Undergraduate Students, Faculty, Staff

Please attend our upcoming Lipids@Wayne seminar featuring J. Mark Brown. All are welcome. Pizza will be served.

Speaker: J. Mark Brown, Ph.D., Associate Staff, Director of Research – Center for Microbiome & Human Health, Cleveland Clinic Lerner Research Institute

Title: Obesity-Linked Suppression of Membrane-Bound O-Acyltransferase 7 (MBOAT7) Drives Non-Alcoholic Fatty Liver Disease Progression

Location: 1167 Biological Sciences

Date and Time: 4 pm on Wednesday, December 4, 2019


Recent studies have identified a common genetic variant rs641738 near two genes encoding membrane bound O-acyltransferase domain-containing 7 (MBOAT7) and transmembrane channel-like 4 (TMC4) that associates with increased risk of non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), alcohol-related cirrhosis, and liver fibrosis in those infected with viral hepatitis. Based on hepatic expression quantitative trait loci (eQTL) analysis it has been suggested that MBOAT7 loss of function promotes liver disease progression, but this has never been formally tested. Here we show that Mboat7 loss of function in mice is sufficient to promote the progression of NAFLD in the setting of high fat diet. Mboat7 loss of function is associated with accumulation of its substrate lysophosphatidylinositol (LPI) lipids, and direct administration of LPI promotes hepatic inflammatory and fibrotic programs in an Mboat7-dependent manner. Interestingly, MBOAT7 expression is dramatically reduced in obese humans and rodents, independent of rs641738 status. These studies reveal a novel role for MBOAT7-driven acylation of LPI lipids in suppressing the progression of NAFLD.

For more information about this event, please contact Emilio Mottillo at 313-574-4688 or