Antiobesity mechanisms of action of conjugated linoleic acid. J Nutr Biochem

Department of Nutrition, University of North Carolina Greensboro, PO Box 26170, Greensboro, NC 27402-6170, USA.
The Journal of nutritional biochemistry (Impact Factor: 3.79). 11/2009; 21(3):171-9. DOI: 10.1016/j.jnutbio.2009.08.003
Source: PubMed


Conjugated linoleic acid (CLA), a family of fatty acids found in beef, dairy foods and dietary supplements, reduces adiposity in several animal models of obesity and some human studies. However, the isomer-specific antiobesity mechanisms of action of CLA are unclear, and its use in humans is controversial. This review will summarize in vivo and in vitro findings from the literature regarding potential mechanisms by which CLA reduces adiposity, including its impact on (a) energy metabolism, (b) adipogenesis, (c) inflammation, (d) lipid metabolism and (e) apoptosis.

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    • "In contrast to the chain structure of the linoleic acid, in CLA the double bonds are separated by only one single bond and occur most frequently at carbons 9 and 11 as well as 10 and 12 forming c9t11 and t10c12-CLA isomers [7]. Studies have shown that CLA isomers actively inhibit carcinogenesis [8] and prevent atherosclerosis [9], diabetes [10] [11] [12], obesity [13] [14], and osteoporosis [15] [16] [17]. Recently, it has been shown that CLA can prevent NAFLD induced by a high-fat diet [18] and influence endothelium-mediated vascular homeostasis, by reducing the release of proinflammatory mediators, such as prostaglandin E 2 and the vasoconstrictive agent thromboxane A 2 , within vascular endothelial cells [19] [20]. "
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    ABSTRACT: This study assessed the effects of individual conjugated linoleic acid isomers, c9t11-CLA and t10c12-CLA, on nonalcoholic fatty liver disease (NAFLD) and systemic endothelial dysfunction in rats fed for four weeks with control or high-fructose diet. The high-fructose diet hampered body weight gain (without influencing food intake), increased liver weight and glycogen storage in hepatocytes, upregulated expression of fatty acid synthase (FAS) and stearoyl-CoA desaturase-1 (SCD-1), and increased saturated fatty acid (SFA) content in the liver. Both CLA isomers prevented excessive accumulation of glycogen in the liver. Specifically, t10c12-CLA decreased concentration of serum triacylglycerols and LDL + VLDL cholesterol, increased HDL cholesterol, and affected liver lipid content and fatty acid composition by downregulation of liver SCD-1 and FAS expression. In turn, the c9t11-CLA decreased LDL+VLDL cholesterol in the control group and downregulated liver expression of FAS without significant effects on liver weight, lipid content, and fatty acid composition. In summary, feeding rats with a high-fructose diet resulted in increased liver glycogen storage, indicating the induction of gluconeogenesis despite simultaneous upregulation of genes involved in de novo lipogenesis. Although both CLA isomers (c9t11 and t10c12) display hepatoprotective activity, the hypolipemic action of the t10c12-CLA isomer proved to be more pronounced than that of c9t11-CLA.
    06/2015; 2015:1-10. DOI:10.1155/2015/535982
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    • "McIntosh). (reviewed in Ref. [4]). Studies have linked 10,12 CLA-mediated inflammatory signaling to the suppression of adipogenesis [5] [6], lipogenesis [5] [6] [7], insulin sensitivity [5] [6] [8], and induction of lipolysis [5] and apoptosis [9]. "
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    ABSTRACT: The objective of this study was to determine the extent to which a low level of trans-10, cis-12 (10,12) conjugated linoleic acid (CLA) decreases adiposity and increases browning in overweight mice, its dependence on inflammatory signaling and potential synergistic effects of daily exercise. Young, Sv129 male mice were fed a high-fat diet for 5 weeks to make them fat and glucose intolerant and then switch them to a low-fat diet with or without 0.1% 10,12 CLA, sodium salicylate or exercise for another 7 weeks. 10,12 CLA decreased white adipose tissue (WAT) and brown adipose tissue mass, and increased the messenger RNA and protein levels, and activities of enzymes associated with thermogenesis or fatty acid oxidation in WAT. Mice fed 10,12 CLA had lower body temperatures compared to controls during cold exposure, which coincided with decreased adiposity. Although sodium salicylate decreased 10,12 CLA-mediated increases in markers of inflammation in WAT, it did not affect other outcomes. Exercise had no further effect on the outcomes measured. Collectively, these data indicate that 10,12 CLA-mediated reduction of adiposity is independent of inflammatory signaling, and possibly due to up-regulation of fatty acid oxidation and heat production in order to regulate body temperature. Although this low level of 10,12 CLA reduced adiposity in overweight mice, hepatomegaly and inflammation are major health concerns. Copyright © 2015. Published by Elsevier Inc.
    The Journal of nutritional biochemistry 02/2015; 26(6). DOI:10.1016/j.jnutbio.2014.12.016 · 3.79 Impact Factor
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    • "In addition, fat accumulation is an important health issue in humans and animals. Previous reports have proposed mechanisms to reduce fat accumulation through energy intake, energy expenditure, preadipocyte differentiation and proliferation, lipogenesis, lipolysis and fat oxidation (Wang and Jones, 2004; Kennedy et al., 2010). Among these, adipogenesis regulates preadipocyte differentiation into adipocytes. "
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    ABSTRACT: Capsaicin is a major constituent of hot chili peppers that influences lipid metabolism in animals. In this study, we explored the effects of capsaicin on adipogenic differentiation of bovine bone marrow mesenchymal stem cells (BMSCs) in a dose- and time-dependent manner. The BMSCs were treated with various concentrations of capsaicin (0, 0.1, 1, 5, and 10 μM) for 2, 4, and 6 days. Capsaicin suppressed fat deposition significantly during adipogenic differentiation. Peroxisome proliferator-activated receptor gamma, cytosine-cytosine-adenosine-adenosine-thymidine/enhancer binding protein alpha, fatty acid binding protein 4, and stearoyl-CoA desaturase expression decreased after capsaicin treatment. We showed that the number of apoptotic cells increased in dose- and time-dependent manners. Furthermore, we found that capsaicin increased the expression levels of apoptotic genes, such as B-cell lymphoma 2-associated X protein and caspase 3. Overall, capsaicin inhibits fat deposition by triggering apoptosis.
    Asian Australasian Journal of Animal Sciences 12/2014; 27(12):1783-93. DOI:10.5713/ajas.2014.14720 · 0.54 Impact Factor
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