ABSTRACT
Conjugated linoleic acid (CLA) strongly prevents fat accumulation in adipose tissue of mice, even if hepatic fat deposition and insulin resistance are concomitantly observed. This study investigated the possibility of maintaining the antiadiposity properties of CLA while preventing adverse effects such as liver steatosis and hyperinsulinemia. To this end, mice were divided into three groups and fed a standard diet (control) or a diet supplemented with 1% CLA (CLA) or a mixture of 1% CLA plus 7.5% pine nut oil (CLA + P). The combination of CLA + P preserved the CLA-mediated antiadiposity properties (70% fat reduction), preventing hepatic steatosis and a sharp increase in plasmatic insulin starting from the eighth week of CLA treatment. The assay of both fatty acid synthesis and oxidation in the CLA + P mice revealed a time-dependent biphasic behavior of the corresponding enzymatic activities. A sudden change in these metabolic events was indeed found at the eighth week. A strong correlation between the changes in key enzymes of lipid metabolism and in insulin levels apparently exists in CLA-fed mice. Furthermore, lower levels of lipids, in comparison to values found in CLA-fed mice, were observed in the liver and plasma of CLA + P-fed animals.
Subject(s)
Dietary Fats, Unsaturated/administration & dosage , Fatty Liver/prevention & control , Linoleic Acids, Conjugated/administration & dosage , Pinus/chemistry , Plant Oils/administration & dosage , Seeds/chemistry , Animals , Drug Interactions , Fatty Acids/metabolism , Fatty Liver/chemically induced , Insulin/blood , Lipid Metabolism/drug effects , Liver/metabolism , Male , Mice , Mice, Inbred ICR , Oxidation-ReductionABSTRACT
Diet supplementation with olive oil exerts beneficial effects on an organism, even if an increase in the level of hepatic lipids has been concomitantly observed. This study was therefore designed to investigate whether the stimulation of lipogenesis was responsible for the olive oil-induced hepatic fat accumulation. In mice fed for 8 weeks with an olive oil-enriched diet, an increase of about 2.6 fold in the level of liver triglycerides was found in comparison to animals fed with a corn oil-containing diet. Despite that, no increase in the activities of cytosolic lipogenic enzymes or of the mitochondrial tricarboxylate carrier was found; on the contrary, a decrease in the activity of carnitine palmitoyltransferase I was observed. This impairment of fatty acid oxidation, which was not apparent in corn oil-fed animals, may have had a role in the increase of hepatic lipid content found in the olive oil-fed mice.
Subject(s)
Fatty Acids/metabolism , Liver/metabolism , Plant Oils/pharmacology , Triglycerides/metabolism , Animal Feed , Animals , Body Weight/drug effects , Cholesterol/blood , Corn Oil/pharmacology , Dietary Supplements , Energy Intake , Fatty Acids/biosynthesis , Kinetics , Liver/anatomy & histology , Liver/drug effects , Male , Mice , Mice, Inbred ICR , Olive Oil , Organ Size/drug effects , Oxidation-Reduction , Phospholipids/blood , Triglycerides/bloodABSTRACT
Conjugated linoleic acid (CLA) is able to reduce adiposity by affecting lipid metabolism. In particular, CLA administration to mice reduces body fat mass with a concomitant lipid accumulation in the liver. We investigated the effects of CLA on the activity of the mitochondrial citrate carrier (CIC), which is implicated in hepatic lipogenesis. The transport activity of the CIC, measured both in intact mitochondria and in the proteoliposomes, progressively increased with the duration of CLA feeding. An increase in the CIC activity of approximately 1.7-fold was found in 16 week CLA-treated mice with respect to control animals. A kinetic analysis showed a 1.6-fold increase in the V(max) of citrate transport but no change in the K(m) value. Western blot experiments revealed an increase of approximately 1.7-fold in the expression of CIC after CLA treatment. A strict correlation between the increase in CIC activity and the stimulation of the cytosolic lipogenic enzymes was also found. These data indicate that the CIC may play a role in the onset of hepatic steatosis in CLA-fed mice by supplying the carbon source for de novo fatty acid synthesis.
