Wolfberry Supplements Prevent the Development of Hepatic Steatosis

Objective To determine if wolfberry supplements prevent the development of hepatic steatosis. Methods Male C57BL/6J mice, at 6 weeks of age, were fed 45 kcal % fat diets (high fat diets) for up to 28 weeks (10 mice for each group). Two groups of mice had their diets supplemented with either 1 % or 5 % (w/w) wolfberry fruits; and there was a high fat diet control group without any added fruit. In addition, there was a group of mice fed 10 kcal % fat diets only as a low fat diet control. Body weight and food consumption were monitored weekly. Development of hepatic steatosis and cellular biochemical alterations were determined at 8, 18, and 28 weeks of dietary treatments. Western blotting was used to determined activation of AMP‐activated protein kinase (AMPK), sirtuin 1 (SIRT1), acetyl‐CoA carboxylase (ACC), and endoplasmic reticulum (ER) stress in the liver tissues. Results Mice fed high fat diets (45 kcal % fat) developed obesity and hepatic steatosis as early as 8 weeks of treatment. Wolfberry supplements, at both levels, completely prevented hepatic steatosis occurring, whereas it was present in high fat diet controls, but not in low fat diet controls. Wolfberry supplements activated AMPK, inhibited ACC, but SIRT1 level was not altered. Wolfberry addition prevented high fat diet‐triggered ER stress through inhibition of GRP78/BiP and protein kinase‐like endoplasmic reticulum kinase (PERK). Conclusions Wolfberry fruits prevent high fat diet‐induced hepatic steatosis most likely through a rebalance of cellular energy homeostasis, control of fatty acid synthesis, and diminishing cellular ER stress. Support: National Institutes of Health COBRE Grant P20‐RR‐017686 to D. L. Grant Funding Source: National Institutes of Health COBRE Grant P20‐RR‐017686