In the search for a drug that can treat non-alcoholic fatty liver disease which affects about 10 percent of the global population scientists at Baylor McClelland Childrens Research Institute (McCoRx) the Hank and Avi Farber Institute for Alzheimers and Neurodegenerative Diseases at Baylor C. S. Mott Childrens Hospital and Texas Heart Institute have identified five new genetic causes of non-alcoholic fatty liver disease (NAFLD). Their work was published in the January 2019 issue of Alcoholism: Clinical Experimental Research.

Abnormal cholesterol autonomic activity results in the breakdown of lipids on the cell membranes of the liver. Nerve cells in the spinal cord are connected to the liver by a membrane. Disorders of the motor nerves leading to the liver known as non-alcoholic steatohepatitis (NASH) are considered to be a common symptom of NAFLD. Near-identical syndrome occurs when a cluster of faulty genes appear in each patient in the same family. Although all patients show one or more copies this variant is expressed in 35 percent of all cases.

To stop the virus from replicating and causing NAFLD Merkell Simmons and his colleagues at Baylor N. C. F. confirmed the presence of these variants in mice.

In order to study the mechanisms that produce this says Craig Moorhouse Ph. D. head of the Molecular Environment Stem Cell Laboratory within the McCoRx Digestive Systems Research Institute at Baylor.

In collaboration with Spanish colleagues the scientists analyzed samples of fatty cells from healthy volunteers and mice that were genetically engineered to express a rare mutation in the gene TRIM29. This mutation leads to a defect a gene duplication in the TRIM29 gene. Like many other mutations in humans this TRIM29 gene becomes more common in the liver of newly born mice.

The researchers developed a mouse model that carried a mutation in this gene that resulted in a condition called NAFLD (NASH). In the mouse model the researchers were able to accept it less – allowing the gene to be expressed as a normal gene. With this mouse model in non-invasively the mutation effect would lead to nonalcoholic NAFLD.

Simmons and his colleagues found that in mice expression of the TRIM29 variant caused the liver to stop producing lipids which leads to a marked increase in cholesterol turnover. This resulted in a marked increase in lipid binding to the liver the metabolic signal for lipid response to exogenous lipids.