Lack of a Liver Molecule Skyrockets Blood Fat Levels in Type 2 Mice

More from the mouse front. German researchers noted a correlation between weight and the liver’s ability to produce LSR: the greater a mouse’s weight, the less able it is to produce a sufficiency of the molecule.

Feb 26, 2009

Too little production of a molecule called LSR (lipolysis-stimulated lipoprotein receptor) in the liver sends blood fat soaring to pathological levels in mice with type 2 diabetes and metabolic syndrome, say scientists at the German Cancer Research Center in Heidelberg.

The researchers also found, however, that when the mice were given leptin, a hormone that regulates hunger, their production of LSR was restored to normal levels. Additionally, they lost weight and their blood fat levels normalized. 

LSR, which is found primarily in the liver and the bowel, controls the removal of fat from the blood into the liver. It also controls fat breakdown in the liver itself. In overweight mice with type 2, LSR production is significantly reduced, meaning that little fat reaches the liver. Instead, it remains in the blood, making blood fat levels soar. Too much fat in the blood can lead to such ill effects as cardiovascular problems. 

The German researchers noted that there seems to be a direct correlation between weight and the liver's ability to produce LSR: the greater a mouse's weight, the less able it is to produce a sufficiency of the molecule. 

Future therapies based on this finding could involve administering LSR to type 2 patients who are deficient in it, in combination with leptin.

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Categories: Diabetes, Diabetes, Nutrition Research, Professional Issues, Type 2 Issues

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