LIPOCLASERXL
I- COMBINED MECHANISM of action of the LIPOCLASERXL®
LIPOCLASERXL® has been developed and designed to perform reduction treatment of adipose areas and cellulites. It has visible and durable results that can almost be compared to liposuction without the disadvantage of an invasive intervention. The Lipoclaser-XL uniqueness is based on the following three combined mechanisms of action: I-Lipolisis LIPOCLASERXL® initially act over the triglycerides (TGs) inside fat cells by breaking down the bond of TGs into free fatty acids and glycerol. The free fatty acids, relatively insoluble in water, are bound to albumin and are slowly carried to the liver or to other tissues in need of these molecules as building blocks or energy. In other words, free fatty acids released from treated fat cell are being processed in normal pathways that nature has evolved for the transport of fat. II-Lipoclasia A second mechanism of action is by cavitation. LIPOCLASERXL® disrupts fat cells, breaking down the cell membranes causing the release of TGs from the cells. A large portion of TGs is probably broken down into the free fatty acids and glycerol that follow the pathway described before. In case the released TGs is not broken down, it may bind to very low density lipoprotein particles (VLDL) found in the lymph system. VLDL is further processed to other lipoprotein classes (IDL, LDL) and ultimately transported to the liver for recycling back to free glycerol and free fatty acids. III-Lipoinduccion Finally, there is a third mechanism of action which is produced by the alteration in some membranes of fat cells by cavitation effect of the LIPOCLASERXL®; The membranes lose some of its properties during the process without reaching breakage, but neither is it capable of regenerating and it is detected by the immune system and marked in order, finally, to be absorbed by the macrophages (induced apoptosis).
In conclusion, the released TGs or its derivatives are processed by known metabolic pathways. No unnatural or new metabolic pathways are required for the body to process the released TGs or cells. In addition, TGs from adipocytes treated by LIPOCLASERXL® ultimately travels to the liver, where it is recycled to meet the continuing demands of the body. These mechanisms stress the importance of the necessary drainage and evacuation process following each session with the LIPOCLASERXL®.
II- HOW FAT IS AFFECTED BY THE LIPOCLASERXL
Fat is nature’s way of storing excess energy. Fat is very efficient at storing energy as it takes up very little space and does not require a lot of water when stored in a cell.
What appear as empty cells are in fact fat-filled cells. Up to 75% of the volume of fat cells is occupied with what we call fat (triglycerides).
When fatty tissue is treated by the LIPOCLASERXL device, the mechanical growth of the bubbles causes mechanical disruption of the membranes of the fat cells sparing the blood vessels, peripheral sensory nerves and connective tissue. Since the effect is localized to a specific depth, overlying skin is not damaged.
The most common question that arises is the fate of the fat previously contained in the adipose cells, after the cell membrane is broken. This article aims to describe the mechanism of fat absorption following cell disruption by LIPOCLASERXL treatment.
FAT CLEARANCE MECHANISM
Fat, inside fat cells, exists in the form of triglycerides. A triglyceride molecule is composed of three fatty acids attached to a glycerol backbone. When the fat cell membrane is destroyed, triglycerides are released into the interstitial fluid between the cells.
The presence of large amounts of triglycerides, in interstitial fluid compartments, has no natural correlate. When outside the fat cell, triglycerides are normally packaged in discrete lipoprotein particles – a combination of apolipoproteins and lipids, cholesterol, triglycerides, and cholesteryl esters. A series of metabolic pathways direct the trafficking of water-insoluble molecules of cholesterol and triglycerides through the water-based circulatory system and to the interstitial fluid space.
During the passage through the arteries and interstitial space, lipoprotein-bound triglycerides are catabolised to free fatty acids and glycerol molecules.
There are few or no animal or clinical data describing the distribution and temporal processing of free triglycerides released from traumatized adipocytes. The only clinical correlate may be trauma cases of massive areas of soft tissues (car accidents, burns, etc).
This discussion focuses on the interstitial compartment and the metabolism of triglycerides, free fatty acids and glycerol. It is well established that interstitial fluid compartments contain lipoproteins, biological signals and chemical analysis that all interact and engage cells through cell surface membrane receptors or processes (phagocytes, etc). The kinetic features of the interstitial compartment are now being understood for normal analysis, as about 42% of total body water is extracellular.
Are triglyceride molecules present in the interstitial fluid metabolized to free fatty acids and glycerol?
According to the literature, it seems very reasonable to assume that triglycerides are immediately (4 hours) processed by lipoprotein lipase (LPL), an enzyme bound to adipocytes.
In vitro studies have shown that triglycerides presented as emulsions and not in lipoprotein particles are readily hydrolyzed by LPL to glycerol and free fatty acids.
Glycerol is a water-soluble molecule and requires no chaperone or carrier through interstitial fluids or the circulatory system.
A short-term increase in glycerol concentration following LIPOCLASERXL treatment appears reasonable but has not been directly measured. However, interstitial levels of glycerol are similar to plasma levels.
To date, no clinically significant elevation of plasma glycerol levels has been reported in any subject treated with the LIPOCLASERXL. One may extrapolate that interstitial glycerol levels were not significantly elevated in this compartment or sequestered subsequent to LIPOCLASERXL treatments.
Free fatty acids are not readily immiscible in water, and the transport of these molecules is accomplished by albumin. Albumin, present in interstitial fluid and circulation, has the capacity to bind 2-3 molecules of free fatty acid per molecule.
Recently, a differentially radiolabelled triglyceride was injected into the circulatory system of eight subjects. The glycerol and fatty acid moieties had different radiolabels which allowed the kinetic examination of the fate of glycerol and fatty acids.
In the forearm, systemic clearance and forearm fractional extraction of glycerol
(59%) was greater than that of oleate (14%). Equal systemic and forearm fractional release levels of LPL-generated were observed, again validating the equilibrium that exists between these two water compartments for glycerol. This study suggested that LPL-mediated fatty acid uptake is an inefficient process, and that muscle is more effective than adipose tissue.
Free fatty acids released during the treatment will eventually be delivered to the liver.
In the liver, there is no distinction between fatty acids that originate from disrupted adipocytes, those taken from adipocytes due to physiological needs or those originating from a meal consumed several hours previously. In other words, free fatty acids released from the LIPOCLASERXL-treated fat cell are being processed in normal pathways that nature has evolved for the transport of fat.
Simplified way of describing the normal transport of cholesterol and triglycerides in our circulatory system.
Triglycerides (TG) are primarily ingested during the dietary processes [stomach and intestine] and transported by chylomicrons through the capillaries and lymph system where a large portion is broken down into free fatty acids and glycerol. Any unprocessed TG in chylomicrons is taken up by the liver. A second source of triglycerides is through production in the liver from excess free fatty acids and glycerol. The important cell type that stores TG as an energy bank or depot is the fat cell, or in more scientific terms – adipocyte.
The LIPOCLASERXL disrupts fat cells by breaking down the cell membranes, causing the release of TG from the cells. A large portion of TG is probably broken down into the free fatty acids and glycerol because of the enzyme, lipoprotein lipase, on the fat cell membrane walls.
Since the free fatty acids are relatively insoluble in water, they bind to albumin and are slowly transported to the liver or other tissues that require these molecules as building blocks or energy.
Glycerol is soluble in water and is transported to the liver or to other cells that could use this molecule. The free glycerol equilibrates among both the interstitial fluid compartment (tissue fluids) and systemic (blood) fluid compartments.
If the released TG is not broken down, it may bind to very low density lipoprotein (VLDL) particles found in the lymph system. VLDL is further processed to other lipoprotein classes (IDL, LDL) and ultimately transported to the liver for recycling back to free glycerol and free fatty acids.
All of these pathways have a huge capacity and fast response times in terms of handling TG, as witnessed in the removal of TG in 3-4 hrs after digesting a 2000 calorie milkshake.
SUMMARY
In conclusion, the released TG or derivatives are processed by known metabolic pathways. No unnatural or new metabolic pathways are required for the body to process the released TG. In addition, TG from adipocytes treated by LIPOCLASERXL ultimately travel to the liver, where they are recycled to meet the continuing demands of the body.
LIPOCLASERXL is therefore superior to the previous Ultrasound generation based on high frequencies of 3 Mhz and also the very aggressive high intensity focused ultrasound (HIFU).
LIPOCLASERXL operates at 38 Khz in either continuous or pulsed mode, dynamically generating a range of frequencies of +/- 2 Khz which increase the resonance effect on the fat cells.
