Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver conditions in the United States, affecting 30 percent of the population, and increasing — and likely to catch up in prevalence with obesity and diabetes. In NAFLD, fat content of the liver is elevated to 6 percent or more in people who drink in moderation or not at all. Patients will first present with elevated liver enzyme values in blood tests, but then an imaging test or tissue biopsy may be ordered to evaluate the extent of the damage. NAFLD is mostly asymptomatic and is variable in severity; a majority of those afflicted do not need drug treatments. However, NAFLD is thought to be a preliminary condition that can eventually progress to severe manifestations, such as cirrhosis, hepatocellular carcinoma, and end stage liver failure.
Progression of liver disease, from NIDDK.
This is a guest post from Kristina Bargeron Clark, a MMG graduate student at Emory and communications chair for Women in Bio-Atlanta. Her website is www.inkcetera.org.
At Emory, Frank Anania, director of the Department of Medicineâ€™s Division of Digestive Diseases, and his colleagues are developing a tool to treat liver disease. A recent publication in the FASEB Journal describes their investigation into the potential for the hormone adiponectin to modulate liver fibrosis.
Adiponectin is produced by adipose tissue, but is known to decrease in overweight people with metabolic disease. Research by others indicates that it may prevent heart and kidney fibrosis. The Emory teamâ€™s studies were conducted to determine if adiponectin could also reduce liver fibrosis.
For a May explainer, weâ€™d like to spotlight liver fibrosis. Two recent papers from Emory research teams in the journal Hepatology focus on this process.
Liver fibrosis is an accumulation of scar tissue and proteins outside cells that occurs as a result of chronic damage to the liver. It involves inflammation and immune cells, as well as activation of a type of cell in the liver (hepatic stellate cells), which usually stores fat and vitamin A.Â Fibrosis and cirrhosis are not the same. Think of it this way: cirrhosis is the late stage of the disease, but fibrosis is how someone can get there.
The liver has a remarkable, even mythical, ability to regenerate, but there is a long list of ways that someone can injure this most vital organ. Quickly – take too much acetaminophen (the most common cause of acute liver failure in the United States). More slowly – develop a hepatitis C infection. Drink large quantities of alcohol. Or something with more subtle effects: consume a diet high in sugar, which can lead to fatty liver. The relationship between fatty liver and more serious liver diseaseÂ is currently underÂ investigation.
One of the Hepatology papers comes at liver fibrosis from a malaria angle. Patrice Mimche, Tracey Lamb and colleagues show the involvement of EphB2 tyrosine kinase, a signaling molecule not previously known to be involved in liver fibrosis.
Malaria parasites have a complex life cycle, growing in the liver and then in the blood. Lamb says an important part of her paper was the finding that in mouse malaria infection, EphB2 is activated during the blood stageÂ on immune cells infiltrating intoÂ the liver. EphB2 (an active drug discovery target)Â may be acting as a tissue-specific adhesion molecule, she says.