|Image 1: Most commercially available |
products still have a mixture of the active
10,12 CLA and the inactive 9,11 CLA.
Thomas Obsen and his colleagues found that incubation of cultured human adipocytes (human fat cells) with 30 μM 10,12 CLA, but not 9,11 CLA (the other of the two most abundant CLA isomers,
decreased de novo synthesis of triglyceride, free FA, diacylglycerol, cholesterol esters, cardiolipin, phospholipids and ceramides [fromWith regard to the underlying mechanism, the scientists are quite certain that it was not "due to a 'structural trans effect'", because several other trans FA, the scientists used as controls "did not delipidate adipocytes or alter the MUFA/SFA ratio to the extent of 10,12 CLA".
[14C]-acetic acid and [14C]-pyruvic acid as substrates] within 3–24 h. [It also] decreased total cellular lipids within 3 days and the ratio of monounsaturated FA (MUFA) to saturated FA, and increased C18:0 acyl-CoA levels within 24 h.
|Figure 1: Relative changes in de novo lipogenesis of triglycerides and free fatty acids in adipocytes incubated with either 9,11 or 10,12 CLA vs. control (data adapted from Obson. 2011)|
These and previously published data suggest that 10,12 CLA lowers the lipid content of adipocytes by (1) rapidly decreasing SCD-1 [enzyme responsible for mono unsatuarated fatty acid = MUFA synthesis] activity, thereby reducing the MUFA needed for neutral and compound lipid synthesis (reviewed in Ref. ); (2) decreasing PPARγ activity, thereby reducing the expression of adipogenic and lipogenic proteins needed for lipid biosynthesis; or (3) increasing inflammatory lipid metabolites or signals that antagonize glucose and FA uptake and subsequent metabolism.In that, the results confirm the pro-inflammatory nature of CLA (whenever it "works") I have mentioned in previous blogpost. Chung et al. (Chung. 2005) and Kennedy et al. (Kennedy. 2010) have analyzed the inflammatory effect of CLA before and Obson et al. speculate that the "activation of inflammatory signals such as NFκB that antagonize LXRα, PPARγ and possibly also SREBP-1" could be the underlying mechanism which leads to "decreased activity of lipogenic enzymes essential for FA desaturation and incorporation into neutral and compound lipids within 3–24 h." This is of particular interest, because despite its effect on weight loss, the inflammatory component 10,12 CLA has could eventually turn against you, once overall inflammation passes a certain "healthy" threshold.
|Figure 2: Rleative changes in adipocyte fatty acid composition after 3, 24, 72 and 216h of incubation with 9,11 CLA & 10,12 CLA vs. control (data adapted from Obson. 2011)|