Abstract
BackgroundThe individual genetic variations, as a response to diet, have recently caught the attention of several researchers. In addition, there is also a trend to assume food containing beneficial substances, or to supplement food with specific compounds. Among these, there is the conjugated linoleic acid (CLA), which has been demonstrated to reduce fat mass and to increase lean mass, even though its mechanism of action is still not known. We investigated the effect of CLA isomers (CLA c9,t11 and CLA t10,c12) on the proteomic profile of liver, adipose tissue, and muscle of mouse, with the aim of verifying the presence of a modification in fat and lean mass, and to explore the mechanism of action.MethodsC57/BL6 mice were fed for 2 months with different diets: (1) standard chow, (2) CLA c9,t11 diet, (3) CLA t10,c11 diet, (4) CLA isomers mixture diet, and (5) linoleic acid diet. The proteomic profile of liver, white adipose tissue, and muscle was investigated. Statistical significance of the spots with an intensity higher than twofold in expression compared to the control was tested using student’s t test (two-tail).ResultsWe found that both isomers modulate the proteomic profiles of liver, adipose tissue, and muscle by different mechanisms of action. Liver steatosis is mostly due to the isomer CLA t10,c12, since it alters the expression of lipogenetic proteins; it acts also reducing the adipose tissue and increasing fatty acid oxidation in muscle. Conversely, CLA c9,t11 has no relevant effects on liver and adipose tissue, but acts mostly on muscle, where it enhances muscular cell differentiation.ConclusionsAdministration of CLA in humans has to be carefully personalized, since even considering the presence of a species-specific effect, adverse effects might occur on long-term supplementation. Here we demonstrated that, in mouse, CLA is effective in reducing fat mass, but it also induces liver steatosis. The increase of lean mass is linked to an induction of cell proliferation, which, on long-term supplementation, might also lead to adverse effects.
Highlights
The individual genetic variations, as a response to diet, have recently caught the attention of several researchers
Steatosis was mild in mice fed with conjugated linoleic acid (CLA) c9,t11 diet, moderate in mice fed with CLA mix diet, and severe in mice fed with CLA t10,c12 diet: this latter was pale in comparison to all the other livers
We found the down-regulation of six proteins: major urinary protein 6 (MUP6, spot # 3), major urinary protein 2 (MUP2, spot # 4 and 5), glutathione S-transferase
Summary
The individual genetic variations, as a response to diet, have recently caught the attention of several researchers. There is a trend to assume food containing beneficial substances, or to supplement food with specific compounds. The individual genetic variations, as a response to diet, have recently caught the attention of several researchers leading to an impressive growth of the nutrigenomic field. The. In the last 10 years, there is a trend to assume food directly containing beneficial substances or to supplement food with specific compounds that naturally occur in milk and meat and, among these, conjugated linoleic acid (CLA) plays an important role. CLA originates from two sources: one source is CLA formed during ruminal biohydrogenation of linoleic acid; the other source is CLA synthesized by the animal’s tissues from vaccenic acid, another intermediate in the biohydrogenation of unsaturated fatty acids
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