Cellular Stress in the Brain May Contribute to Non-Alcoholic Fatty Liver Disease
George Washington University researchers find a connection between cellular stress in the brain and non-alcoholic fatty liver disease
Disruptions in a protein folding process occurring in the brain, known as endoplasmic reticulum (ER) stress, may cause non-alcoholic fatty liver disease, independent of other factors. A research team at the George Washington University (GW) published their results in the Journal of Clinical Investigation Insight. “Nearly 75 percent of obese adults experience non-alcoholic fatty liver disease. However, its underlying causes are unclear,” said Colin Young, PhD, senior author and assistant professor of pharmacology and physiology at the GW School of Medicine and Health Sciences. “Recent findings have pointed to ER stress as central to its development. What our research shows is that ER stress in the brain is a key contributor.” As the primary site of cellular protein folding, the ER plays a critical role in maintaining cellular function. When there is nutritional excess, the protein load exceeds the ER folding capacity and a collection of conserved signaling pathways, termed the unfolded protein response (UPR), are activated to preserve ER function. While beneficial in the short-term, chronic UPR activation, known as ER stress, is a major pathological mechanism in metabolic disease, such as obesity.
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