Similarly, Protein Kinases, (enzymes of which there are over 2,000 identified up to this point in time), are the catalysts required for the initiation of cellular communication and connexin functionability. Cellular communication can follow the route of providing information for cells to be either directed normally, (i.e., to purposefully provide the correct information codes in order to manufacture “healthy cells”), or to be directed abnormally, (i.e., to purposefully provide misinformation [codes] in order to “misdirect” the otherwise normal production of healthy cells). The latter scenario of “misdirection” can cause unwanted metabolic changes; these are known as “mutations”. Mutations can be overtly presented as “dysplastic”, (i.e., abnormal in structure). The more abnormal and primitive, (or unlike the healthy cell structure), these dysplastic cells become, the less control our normal GJIC has in directing healthy metabolism and proper cellular response (7-9). Over time, this loss of normal GJIC control will allow more cells to replicate, grow, and function in an uncontrolled, “wild-type”, exponential manner, which can, (and many times will), lead to non-reversible malignant cellular development. What normally follows is what we normally “label” as cancer . Whether we are looking at tissues from liver, kidney, heart, muscle, brain, or those of the entire G.I. tract, the cells which comprise these tissues are all protected by cell membranes. Basically, the cell membrane itself, is composed of a lipid, (fat), bilayer which is held together by weak electrostatic interactions of “dipole-to-dipole” chemistry; i.e., in layman’s terms; positive and negative magnetic forces are what hold these bilayers together. These electrostatic forces, (i.e., bonds), are nowhere as strong as either covalent or even ionic bonds, but are strong enough to keep the lipid layers in contact with each other, (i.e., so to maintain their cellular membrane structure), yet “loose” enough to allow substances to travel through/across them in order to get them into the cell matrices. The rational of this “structural science” is simple; the roles of the cell membrane are to protect the cell, to regulate the transport of substances in and out of it, and to control “cell recognition”; thus, keeping the cell functioning properly requires that the cell membrane maintain its physical shape/appearance, as retaining the integrity of the cell matrix has the most impact on cellular function . Permeability factors, and the cellular membrane’s control over these factors, whether focusing on the cells which line the intestinal tract, those that line the pancreas, cardiac tissue cells, or hepatocytes, (liver cells), are most important here regardless of cellular origin. The ability to transport nutrients and vital substances, and transfer information via the required chemicals and electrolytes from cell to cell, is accomplished only by proper anatomical maintenance of the cellular membrane . Cell membranes generally possess receptor/recognition sites which identify whether a foreign substance is one that has entered the body either through the GI tract, (i.e., is from an external source), or is a product/metabolite of an indigenous nature, (i.e., is a xenotoxin or xenoestrogen that has been metabolically transformed by one’s own Cytochrome P450 system). This way, the receptor will be able to provide information to the body on how this substance should be handled, and whether it should be recognized as benign or potentially lethal. An example of cell membrane receptor identification, is the working of a fat cell, (adipocytye), cell membrane in a Type II (NIDDM) diabetic. Because the Beta-cells of the pancreas usually still produce insulin in Adult-Onset Type II Diabetes Mellitus, insulin receptor sites are usually still present, (and presumably active in most cases), on cell membranes of the cells that are normally responsive to glucose. http://truthaboutcellulite.plays-guitar.com/
Type II diabetics, although they usually do produce insulin, frequently present insulin resistance; this may be due to a number of reasons, with the most acceptable ones concluding that insulin receptors on fat and muscle tissue cells have “sunken” below the cell membrane, and/or that the receptors themselves have been anatomically or structurally altered, changed, or deformed, so they no longer efficiently recognize the Insulin structure . This, in fact, does constitute a change/modification of the cell membrane itself. The example above explains how a change in the cellular membrane will affect cellular membrane mechanics. What we do know, is that stress, regardless of its origin, in most cases, will most likely be either the primary, secondary, or even the tertiary culprit somewhere along the line. We are aware of the negative effects that stress has upon our immune system, as well as upon our overall health in general, and many times we tend to overlook the basics; that our health and longevity is completely dependent upon proper, functioning Cell communication. In its relation to cell membrane health, we also know that stress is a disruptor, and any disruption of membrane anatomy will negatively affect the regulatory flow of ions, (both into and out of the cell), interfere with cellular communication processes, (due to membrane protein disruption and possible denaturization), and will activate the inflammatory response .
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