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A B 3.2.1 Mechanism of Action of LLLT on Fat Reduction: AdiposeCelMembrane PoreFormationontheCelMembrane Adipocytes Fat Droplets ShrinkageofAdipocytes Figure 4: Formation of transitory micropores and shrinkage of adipocytes following LLLT. A. Formation of a transitory pore forming in the bi-lipid membrane of an adipose cell causing fatty contents of the cell to evacuate [48]. B. Secretion of triglycerides and fatty acids and shrinkage of adipocytes [48]. In the original paper published by Neira et al. the fat liberating effects of LLLT on adipocytes were attributed to its ability to induce transitioning micropores which were visualized with the help of SEM (Figure 4) [48].Furthermore, it was postulated that this stimulated the release of intracellular lipids from the adipocytes. Based on this, it was formulated that up to 99% of the fat stored within the adipocytes could be released and subsequently removed with the help of LLLT (635 nm, 10W intensity, 6 minutes irradiation time) [48]. Re-cultured adipocytes exhibited a tendency to attain their native cellular conformation which was further confirmed by Caruso-Davis et al. utilizing a live-dead assay to assess the viability of these adipocytes following irradiation [61]. Increase in ROS following LLLT has been proposed to bring about lipid peroxidation within the cell membrane which may cause damage and may present as the transitory pores. This may cause temporary damage that presents as transitory micropores. [30, 62-64]. However, when Brown et al. attempted to replicate Neira et al’s findings [48], they failed to visualize any transitory micropores via SEM [59]. No further SEM studies have documented these pores, but many publications have reported findings that indirectly support the transitory micropore formation theory. Another proposed mechanism that explains the release of intracellular lipids form adipocytes, suggests the activation of the compliment cascade which is responsible for induction of adipocyte apoptosis and subsequent release of intracellular lipid components [61]. To test the feasibility of this theory Caruso-Davis et al. exposed differentiated human adipocytes to plasma and exposed one group of cells to laser, while the control group received no laser intervention [61]. Other evidence is suggestive of LLLT’s ability to stimulate an increase in cAMP levels [65, 66]. cAMP is accountable for activation of certain protein kinases which further activate certain enzymes and these enzymes are responsible for the breakdown of triglycerides into fatty acids and glycerol both of which can penetrate the adipocyte membrane [67, 68]. However, findings from Caruso-Davis et al’s studies on in vitro cell cultures of human adipocytes treated with LLLT (635-680 nm for 10 min) did not exhibit any increase in glycerol and fatty acid levels suggesting that fat liberation from adipocytes in response to LLLT is not due to lypolytic stimulation of the adipose tissue. Interestingly enough, as the cellular components were being examined, the presence of triglycerides in the supernatant seemed to support the theory involving transient pore formation in adipocytes [61]. Although these mechanisms have been worked out independently, the mechanism by which triglycerides would traverse the adipocyte lipid membrane remains the most enigmatic. Following the initial results that Neira et al. obtained [48], they extracted samples of adipose tissue from lipectomy Proc. of SPIE Vol. 8932 89320X-8PDF Image | Low-level light therapy (LLLT) for cosmetics and dermatology
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