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Shedding light on nonalcoholic fatty liver disease: gene mutationlinked to accumulation of fat, oth by 123wert sdfsf
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Shedding light on nonalcoholic fatty liver disease: gene mutationlinked to accumulation of fat, oth by 123WERT SDFSF
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| Article Posted: 03/23/2013 |
| Article Views: 106 |
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Shedding light on nonalcoholic fatty liver disease: gene mutationlinked to accumulation of fat, oth |
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Business,Business News,Business Opportunities
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A team of scientists from the University of Utah and the Universityof California at San Francisco has discovered that the mutation ofa gene encoding a ketone body transporter triggers accumulation offat and other lipids in the livers of zebrafish. This discovery,published in the Feb. 1, 2012, issue of Genes & Development , reveals that transport of ketone bodies out of the liver is acritical step in energy metabolism during fasting. It also providesa new approach for studying the development of fatty liver diseasein humans.
Nonalcoholic fatty liver disease (NAFLD), or abnormally highaccumulation of lipids in the liver, is the most common cause ofchronic liver disease worldwide. Lipids are a broad group ofmolecules that include fats, triglycerides, and cholesterol . In some people, NAFLD causes no complications, but in others,excess fat in the liver can lead to inflammation or development ofscar tissue, resulting in permanent liver damage or even liverfailure. NAFLD may also increase the risk of heart disease in people who are overweight or obese.
The increasing prevalenceof NAFLD in the United States is due, in large part, to the obesity epidemic and it is estimated that more than 6 million U.S.children already have fatty liver disease. "Currently, there are a limited number of treatment options fordecreasing excess fat in the liver and there are no methods forreversing damage to liver tissue due to NAFLD," says AmnonSchlegel, M.D., Ph.D., investigator in the University of UtahMolecular Medicine program, assistant professor of internalmedicine at the University of Utah School of Medicine, and seniorauthor on the study. "By identifying and characterizing novel genesthat regulate accumulation of lipids in the liver, we may be ableto gain new insight into the physiological processes that lead toNAFLD." Previous research has shown that many of the proteins known tocontrol lipid metabolism in humans are also present in zebrafish.Schlegel and his colleagues began by identifying a zebrafish mutantknown as red moon (rmn), which developed abnormal lipidaccumulation in liver cells, without evidence of associated liverinflammation or liver damage, when exposed to fasting conditions.Schlegel and his colleagues then used a molecular genetic techniquecalled positional cloning to isolate the gene disrupted by the rmnmutation. They found that the rmn mutation inactivated slc16a6a, agene thought to encode a protein required in the transport ofnutrients during fasting. "Until now, the activity of the Slc16a6a protein has not beenfunctionally characterized in any organism," says Schlegel, who'salso an adjunct assistant professor of biochemistry at the Umedical school.
"Our studies indicate that Slc16a6a is a proteininvolved in the transport of -hydroxybutyrate." -hydroxybutyrate is a ketone body, a compound that is produced inthe liver when blood glucose is low and fatty acids are broken downfor energy. During periods of fasting, most body tissues can usefatty acids as an energy source, but the brain relies on -hydroxybutyrate and other ketone bodies for fuel. Schlegel andhis colleagues discovered that, in rmn mutants deprived of nutrition , loss of Slc16a6a function disabled secretion of ketone bodiesfrom liver cells and increased lipid accumulation in the liver.They also found that introducing the human form of the SLC16A6protein into rmn mutant livers restored ketone body secretion. "Our research has uncovered a previously unrecognized, but criticalstep, in the complicated physiology of fasting," says Schlegel. "Westill don't know whether altered fasting liver metabolisminfluences the development of NAFLD, but knowing that Slc16a6a isrequired for secretion of ketone bodies from liver cells duringfasting may have implications for our understanding and treatmentof other medical conditions where ketone bodies play a role.
Theseinclude uncontrolled type 1 diabetes , obesity, and childhood metabolic disorders caused by defects infatty acid metabolism." Additional References Citations. I am an expert from Business Services, usually analyzes all kind of industries situation, such as forward freight agreement , acrylic display units.
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