Experimental Biology 2014: Non-alcoholic fatty liver disease

I learned something at poster session 1116. Alcoholic and Nonalcoholic Fatty Liver Disease
Tue, Apr 29, 7:30 AM – 4:00 PM.

Tue, Apr 29, 12:45 – 3:00 PM 1116.11/A601 – Low copper and dietary sucrose drive fibrosis pathways in a rat model of non-alcoholic fatty-liver disease

Tallino and Burkhead presented a poster studying non-alcoholic fatty liver disease in a rodent model. I’m most used to considering similar damage in the context of alcohol exposure, given that abused drugs are my focus. So it was interesting to learn that some 20-25% of those on a Western diet may exhibit some signs of fatty liver disease that has nothing to do with alcohol.

The study Tallino and Burkhead conducted was based on evidence that steatosis may be related to copper (Cu) deficiency and that this may interact with sucrose in the diet.

The study consisted of four groups of Wistar rats, exposed to different dietary conditions for 12 weeks. The factors were a diet either sufficient or deficient in Cu and a 10% or 30% sucrose addition.

The authors show that low Cu diet works, serum Cu was significantly lowered in these groups. Interestingly there was an interaction whereby the group with low Cu and 30% sucrose diet was further depleted in serum Cu. As expected, serum glucose was elevated with 30% sucrose but this was only out of the normal range with the low Cu / 30% sucrose group.

Interestingly, these dietary conditions resulted in no change in free fatty acids and no change in body weight. Remember that now.

The low Cu diet increased liver steatosis significantly with an interaction with the sucrose treatment to increase this sign of non-alcoholic fatty-liver disease. So Cu deficiency can combine with high sucrose in the diet to produce liver damage in the absence of other indications of a fatty diet (weight gain, high circulating triglycerides).

The study then went on to find that the high sucrose, low Cu diet was associated with alterations in gene transcripts related to fibrosis progression, hepatic stellate cell activation and a few other things related to the hypothesized model of damage.