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Obesity is a major health concern, especially in the US and is closely linked to several medical conditions, such as heart disease, hypertension, type 2 diabetes, etc. A significant proportion of obese or overweight people look for ways to decrease their body mass and maintain a healthy weight. Although there are many diet pills, weight-loss methods and products employed for weight control, most are worthless. Dieting merely reduces the size of fat cells, which tend to remain more or less constant in number. These cells eventually regain their original size in most individuals. There are many weight loss pills/liquids in the market today, most of them based on little or no scientific research. So the fat cells get bigger again and you gain weight. Zyatonix actually kills the fat cells and removes them from your body just like liposuction
The Zyatonix Approach
We have identified and isolated several natural compounds that have strong inhibitory effects on adipogenesis, the process of generating adipocytes (fat cells) and have included them in the Zyatonix formula. This is the first time such technology has been used and the results have been nothing short of incredible. The synergistic combination of our proprietary compounds have an even greater effect on adipocytes. These compounds cause adipocytes to self-destruct, by a process called apoptosis. This causes a reduction in the number of fat cells, which is a long-term weight loss solution.
The photo above shows a fat cell being killed - never to return - thanks to the revolutionary new technology which causes Apoptosis - Fat Cell Death!
Apoptosis can be triggered in a cell through either the extrinsic pathway or the intrinsic pathway. The extrinsic pathway is initiated through the stimulation of the transmembrane death receptors, such as the Fas receptors, located on the cell membrane. In contrast, the intrinsic pathway is initiated through the release of signal factors by mitochondria within the cell.
The Extrinsic Pathway: In the extrinsic pathway, signal molecules known as ligands, which are released by other cells, bind to transmembrane death receptors on the target cell to induce apoptosis. For example, the immune system’s natural killer cells possess the Fas ligand (FasL) on their surface. The binding of the FasL to Fas receptors (a death receptor) on the target cell will trigger multiple receptors to aggregate together on the surface of the target cell. The aggregation of these receptors recruits an adaptor protein known as Fas-associated death domain protein (FADD) on the cytoplasmic side of the receptors. FADD, in turn, recruits caspase-8, an initiator protein, to form the death-inducing signal complex (DISC). Through the recruitment of caspase-8 to DISC, caspase-8 will be activated and it is now able to directly activate caspase-3, an effector protein, to initiate degradation of the cell. Active caspase-8 can also cleave BID protein to tBID, which acts as a signal on the membrane of mitochondria to facilitate the release of cytochrome c in the intrinsic pathway.
The Intrinsic Pathway: The intrinsic pathway is triggered by cellular stress, specifically mitochondrial stress caused by factors such as DNA damage and heat shock. Upon receiving the stress signal, the proapoptotic proteins in the cytoplasm, BAX and BID, bind to the outer membrane of the mitochondria to signal the release of the internal content. However, the signal of BAX and BID is not enough to trigger a full release. BAK, another proapoptotic protein that resides within the mitochondria, is also needed to fully promote the release of cytochrome c and the intramembrane content from the mitochondria. Following the release, cytochrome c forms a complex in the cytoplasm with adenosine triphosphate (ATP), an energy molecule, and Apaf-1, an enzyme. Following its formation, the complex will activate caspase-9, an initiator protein. In return, the activated caspase-9 works together with the complex of cytochrome c, ATP and Apaf-1 to form an apoptosome, which in turn activates caspase-3, the effector protein that initiates degradation. Besides the release of cytochrome c from the intramembrane space, the intramembrane content released also contains apoptosis inducing factor (AIF) to facilitate DNA fragmentation, and Smac/Diablo proteins to inhibit the inhibitor of apoptosis (IAP).
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