Supplementation of Coconut Oil from Different Sources to the Diet Induces Cellular Damage and Rapid Changes in Fatty Acid Composition of Chick Liver and Hepatic Mitochondria

Abstract

Supplementation of 20% coconut oil from two commercial sources, pharmaceutical (“Pharmacy”) and cooking (“Pastry”) use, to the chick diet for 14 days produced a clear damage to the hepatic mitochondria, accompanied by an accumulation of glycogen and lipid droplets in the hepatocyte cytoplasm. These effects may be accounted for the high proportion of fat supplemented to the diets (20%). Pharmacy coconut oil induced a high percentage of cellular death when administered for 14 days. Fatty acid profiles in liver and hepatic mitochondria rapidly changed (24 hr) after both coconut oils supplementation to the diet. The accumulation of shorter chain fatty acids (12:0 and 14:0) was always higher after Pharmacy than after Pastry diet feeding. This fact may contribute, at least in part, to the cellular damage mentioned above especially after Pharmacy diet feeding. Mitochondrial ratios of saturated/unsaturated and saturated/polyunsaturated fatty acids rapidly changed in parallel to these ratios in both diets. Most of the mitochondrial parameters measured tend to recuperate the control values when diets were supplied for 5–14 days. Nevertheless, the maintenance of the mentioned ratios after 14-days Pharmacy diet feeding at significantly higher levels than those observed in control, seems to suggest the lack of the homeostatic mechanism in these membranes and could be also related with the high percentage of cellular death observed after this dietary manipulation.