Wednesday, January 4, 2012

Does copper deficiency lead to liver disease?

The liver is the second largest organ in the body, located under the right rib. It weights three pounds and is shaped like a football, but flat on one side.

The liver processes what we eat and drink into energy and nutrients the body can use. It also removes harmful substances from the body.

Nonalcoholic fatty liver disease occurs when the liver has trouble breaking down lipids or fats, causing them to build up in the organ. Doctors are not sure what causes this to happen, but if more than 5-10 percent of the liver’s weight is fat, that person has the disease. It tends to develop in those who are overweight or obese, or have diabetes, high cholesterol or high triglycerides.

Non-alcoholic fatty liver disease, Wikipedia Commons
This image illustrates nonalcoholic fatty liver disease. The white/clear/oval spaces represent fat accumulation that is so large it distorts the cell’s nucleus.

This is a common disease (about 30 percent of the U.S. population has it) and for most people, it causes no signs and symptoms and no complications. But at its most severe, it can progress to liver failure.

The liver is also the central organ for maintaining proper levels of copper, an essential metal nutrient we get through diet. Too much copper is lethal. Too little copper has been linked to the development of non-alcoholic fatty liver disease.

Jason Burkhead was recently awarded INNOVATE seed money to develop a mouse model to investigate the role of copper in non-alcoholic liver disease.

“We know that copper deficiency causes changes in liver lipid metabolism, but we do not know why deficiency induces these changes, or the changes in gene expression and cell machinery that lead to pathology, “ Burkhead said.

His main questions are:
  • What is the copper handling machinery in cells and how is it regulated?
  • What are the molecular-level changes due to copper excess or deficiency?
  • How do these changes lead to disease?
Looking forward, he says he’s excited about moving from basic to translational research, and developing collaborations with clinicians who specialize in liver disease, including the Alaska Native Tribal Health Consortium.


Jason Burkhead is an assistant professor of Biology and researcher at UAA affiliated with INBRE (IDeA Network of Biomedial Research Excellence) and ENRI (Environment and Natural Resources Institute). He came to UAA after earning a Ph.D. in biology from Colorado State University in Fort Collins, CO and doing postdoctoral work at the Oregon Health & Science University in Portland, OR. His research focuses on understanding the molecular machinery that regulates cellular copper levels and what goes wrong when those levels aren’t maintained.


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  2. Is this still in process or was there an outcome to his research?

  3. Copper has a role in antioxidant defense, lipid peroxidation, and mitochondrial function, and copper deficiency has been linked to atherogenic dyslipidemia. We aimed to investigate the potential role of copper availability in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). abogado españa veterinario por internet medico online abogado online consulta online veterinario online psicologo por internet ginecologo online dermatologo online pediatra online doctor por internet medico por internet abogado por internet abogado online psicologo online doctor online Reduced hepatic copper concentrations are found in human NAFLD and are associated with more pronounced hepatic steatosis, NASH, and components of the MetS. The development of hepatic steatosis and IR in response to dietary copper restriction in rats suggests that copper availability may be involved in the development of NAFLD.