Teams of U.S. medical researchers have described new evidence that it may be possible to slow the progression of heart-disease-linked non-alcoholic fatty liver disease (NOD), a highly debilitating condition that can develop in patients who don’t normally have the condition. In a meta-analysis involving 31 previously published studies, researchers identified new protein markers that could help physicians with better prevention and diagnosis strategies for NOD.
Co-lead author Kathryn Smith, BSc, MSN, RHC, of Weill Cornell Medicine, New York, New York, published the study in Scientific Reports, a journal of Nature. “We’ve known about the potential role of these proteins in NOD for quite some time,” says co-lead author Ted Arison, PhD, of the Department of Medicine at the University of Minnesota, Minneapolis. “The new findings, along with genomic data, suggest that these protein markers may be targets for drug and clinical development.”
Non-alcoholic steatohepatitis is an umbrella term for multiple syndromes linked to fatty liver. One of these, non-alcoholic fatty liver disease, or NAFLD, is a broad condition. Known in the medical literature as non-alcoholic fatty liver disease (NAFLD), it can include both alcoholic and non-alcoholic beverages that are high in fat, even if no alcohol was consumed.
“A somewhat surprising finding from our study was the discovery of two distinct markers of NOD,” says Dr. Arison. “Until now, these two proteins were considered independent of each other; however, they don’t appear to play the same role in NOD. This is important because several approaches to treating NOD may change their functions.”
“We hope that this work will help shape next-generation therapeutic approaches for preventing and treating this potentially lethal disease,” adds Dr. Smith.
The research was funded by the National Institutes of Health and the Medical College of Wisconsin.
Article: ABB VIII phosphorylation is sensitive to NOD in the absence of polyunsaturated fatty acids and expression of the Ganglion 2 FFC1 H2OF7 gene, G. Szymanksy D, et al., Scientific Reports, doi: 10.1038/srep24014, published 11 March 2018.