Diabetes type 2

Diabetes is classically diagnosed as a failure of the body to properly metabolize Carbohydrates. Its defining symptom is a high blood Glucose level. Type 1 Diabetes is caused by "insufficient Insulin" production by the pancreas. Type 2 Diabetes, which constitutes about 95% of all the cases, is caused by normal, or sometimes excessive production of "ineffective Insulin". In both types, the blood Glucose level remains elevated. Neither insufficient Insulin nor ineffective Insulin can limit post prandial (after eating) blood sugar to the normal range; in established cases of Type 2 Diabetes, these elevated blood sugar levels often result in chronically elevated Insulin levels.

The ineffective insulin is no different from normal insulin. Its ineffectiveness lies in the failure of our cell population to respond to it not in any biochemical change in the insulin itself. Therefore it is appropriate to note that this disease is a disease that affects almost every cell in our body. The biochemistry of our cellular metabolism is changed from the normal.

The classification of Diabetes as a failure to metabolize Carbohydrates is a traditional classification that originated in the early 19th century when little was known about metabolic diseases or about metabolic processes. Today, with our increased knowledge of metabolic processes, it would appear quite appropriate to define Type 2 Diabetes more fundamentally as a failure of the body to properly metabolize Fats and Oils as well as carbohydrates. This failure results in a loss of effectiveness of Insulin and in the consequent failure to metabolize Carbohydrates. Unfortunately, much medical insight into this matter, except at the research level, remains hampered by its 19th century legacy.

The Type II diabetes and the Hyperinsulinemic symptoms that occur are system wide symptoms of a basic cellular failure to properly metabolize Glucose. Each cell of our body, for reasons which are becoming clearer, find themselves unable to transport Glucose from the blood stream to their interior. The glucose then either remains in the blood stream or is stored as body fat, or otherwise disposed of in the Urine.

Until quite recently it was believed that Insulin molecules bound themselves to Glucose molecules to form a sort of "lock and key" configuration at the cellular Membrane interface. These two molecules together sort of fit the Membrane Receptor and allowed the Glucose to be transported into the cell where it was used for fuel. Many doctors practicing today were taught this concept in medical school. While this theory is descriptive and attractive in its simplicity and while it may be adequate for some purposes, the true picture that is emerging is much more complex and much more revealing.

It appears that when Insulin binds to a Membrane receptor it initiates a complex cascade of biochemical reactions inside the cell. One of these reactions causes Glucose transporters known as GLUT4 molecules to leave their parking area inside the cell and travel to the inside surface of the cell Plasma Membrane. When in the Membrane, they migrate through the Membrane to special areas of the Membrane called Caveolae areas. There, by another series of biochemical reactions they identify and "hook up" with Glucose molecules and transport them into the interior of the cell by a process called endocytosis. Within the cells interior, this Glucose is burned for fuel by the Mitochondria to produce ATP and waste products. The ATP provides energy to power the cellular activity and the waste products are excreted by other metabolic cellular pathways.

These GLUT4 transporters are responsible for transporting glucose from the blood stream into all of our peripheral cells. Of the seven glucose transporters so far identified they have, by far, the greatest ability to quickly reduce our blood borne post prandial glucose. GLUT1 and GLUT3 are glucose transporters that facilitate the transport of glucose from the blood stream across the blood brain barrier to the neuronal cells of the brain. Remember that the brain uses glucose as a primary fuel almost exclusively. GLUT2 facilitates transport of glucose from our liver and intestines into the blood stream; it also regulates insulin release from the pancreatic beta cells. GLUT5 functions in the absorption of Glucose from the intestine into the blood stream and also in the reabsorption of glucose from the kidneys back into systemic circulation when we are in a glucose sparing mode of operation.. Two additional glucose transporters have been identified but not yet characterized as to their function; they are, as you might expect, GLUT6 and GLUT7.

Each of the glucose transporters operate most efficiently at different levels of blood glucose. GLUT4 swiftly reduces very high levels of glucose. GLUT3 operates efficiently at low blood glucose concentrations in order to keep the brain supplied when blood sugar is low. GLUT2, in its regulatory function, has an activity that is linear across a wide range of blood glucose concentrations. It can thus provide an insulin demand signal to the pancreatic beta cells that is proportional to the blood borne concentration of glucose. Since our BSCS functions as a type 0 control system we would expect to find a proportional sensor somewhere and this seems to be it.

Type 2 Diabetics, perhaps because of the high average Insulin levels, typically have only about 1200 Insulin Receptors, or less, per cell Membrane. This is about half of the norm. This appears to be one of the issues involved in the high average Insulin levels often encountered in Type 2 Diabetes.

Many of the molecules involved in these Glucose and Insulin mediated pathways are Lipids, that is they are Fatty Acids. A healthy Plasma Membrane, now known as an active player in the Glucose scenario, contains a complement of Cis type w=3 unsaturated fatty acids. This makes the Membrane relatively fluid and slippery. When these Cis fatty acids are chronically unavailable because of our diet, Trans fatty acids and short and medium chain Saturated Fatty Acids are substituted in the cell Membrane. These substitutions make the cellular Membrane stiffer and more sticky and inhibit the Glucose transport mechanism. The mobility of the GLUT4 transporters is diminished, the interior biochemistry of the cell is changed and the number of Insulin Receptors on the cell surface is reduced. Although there remains much work to be done to fully elucidate all of the steps in these pathways, this clearly marks the beginning of a biochemical explanation for the known epidemiological relationship between fat metabolism and the onset of Type 2 Diabetes.

There exists another phenomena peculiar to Type II Diabetes that operates to keep the blood sugar elevated. It works like this. Remember that normally the liver stores glucose as glycogen and inhibits the release of glucose when glucose stimulated insulin levels are high. You may recall from our earlier discussion that this mechanism keeps our short term, rapidly accessed supply of glucose replenished. In Type II Diabetes the elevated glucose levels do not seem to inhibit glucogenesis in the liver as it does in normal systems. Although all of the evidence is not yet clear, this can quite likely be due to the same impaired cellular glucose transport at the liver similar to that observed in the peripheral cells. Also when the system is stressed, the Catacholamines that are released stimulate additional glucose release by the liver. Sometimes this effect can be noted by observing a fasting blood sugar in the morning that is higher than the blood sugar of the previous evening, several hours after the last meal of the day. Such unexpected over night elevation of the blood sugar cannot be explained by a meal in the middle of the night when there wasn't one.

It is fashionable for pop medical science to blame "trans fats" for the failure of the plasma cell membranes in our 67 or so trillion cells to facilitate the operation of our GLUT 4 transporters to haul glucose into the cell. To the extent that these trans fats are responsible for stiffening the cell membrane and reducing its fluidity when they are used in place of the Cis type w=3 unsaturated acids, trans fats are indeed a culprit. However, if we didn't eat transfats and ate only "good" short and medium chain saturated fats, we would still get Type II diabetes. The body limits its use of either these transfats or saturated fats in cell membrane repair only when adequate Cis w=3 unsaturated fatty acids are present in the diet. It is only when these Cis w=3 fats are chronically unavailable to the body that Trans fats and Saturated fats appear in excess in the membranes. These important membranes then stiffen and become sticky, and systemic disease, including Type 2 Diabetes, manifests.

All of these Cis w=3 unsaturated fatty acids have been completely removed from our food chain and replaced by their trans isomer counterparts. This was done because Cis w=3 oils require refrigeration and typically have a fairly short shelf life. This makes them incompatible with the economics of modern food distribution. Our convenient grocery store availablity of these Cis type essential fatty acids ended in 1950 when Archer Daniels Midland, the last supplier, decided to stop producing this valuable oil and concentrate on processing flour. Our diet now consists only of saturated fats, transfats and some of the hardier Cis w=6 and w=9 fats. All of the delicate w=3 Cis fats, uniquely needed by our cell membranes, because of their poor room temperature shelf life, have completely disappeared from the local grocery store.

Two of the w=3 Cis fats are called essential because without them our bodies develop chronic disease and because our bodies cannot synthesize them from any other food that we eat. These two are: Linoleic acid (LA) and Alpha Linolenic acid (LNA). A third fatty acid, Arachidonic Acid (AA), was once thought to be essential. However, recently it has been discovered that a healthy body can convert LA into AA, so it is no longer believed to be essential for healthy people.

A major reason for discontinuing the production of the Cis w=3 oils is that they rapidly become rancid when placed in a transparent bottle on a room temperature grocery store shelf. The resulting manufacturing and distribution problems that would ensue would seriously impact the bottom line of profitability. The trans isomer counterpart to the essential fatty acid we need and do not get has a very long shelf life. Trans fatty acids present few manufacturing or distribution problems for the oil makers; this substitution of the trans isomers for the needed Cis type oils causes Hyperinsulinemia and results in the many other symptoms of the disease that are curently killing us. This outrageous fraud is often accompanied by advertising that informs us of the "monounsaturated" or "polyunsaturated" value of these worthless and damaging trans oils. The law does not require the oil sellers to state that their oil is a trans isomer and not the Cis isomer that we desperately need; and, this is their reason for not doing so.

For more information about these poisonous fats and oils, please visit our fats page.

This story started to come to light in 1950 when serum Insulin assays became available to the medical community. It has been actively suppressed since then; the careers of many ethical scientists have been damaged by trying to bring this story to the light of day. Many others have been cowed into politically correct silence. Now the evidence is so overwhelming and the number of people becoming knowlegable about the matter is so large that it cannot remain hidden in industry funded, politically correct ivory towers any longer. For additional information on the effect of these fats and oils, including how to protect ourselves from the damage they are believed to cause, see our page on Hyperinsulinemia .

For those that prefer more information in hard copy form, this is available in our special report. Please visit this page to see if this is something you would like to know more about.

References:

  1. Le Marchand-Brusted Y, et al, "From insulin receptor signalling to GLUT 4 translocation abnormalities in obesity and insulin resistance.", J Recept Signal Transduct es. 1999 Jan-Jul; 19(1-4):217-228
  2. Dresner A, et al, "Effects of free fatty acids on glucose transport and IRS-1 associated phosphatidylinositol 3-kinase activity.", J Clin Invest 1999 Jan;103(2):253-9
  3. Gustavsson J, et al, "Insulin-stimulated glucose uptake involves the transition glucose transporters to a caveolae-rich fraction within the plasma membrane: implications for type 2 diabetes.", Mol Med 1996 May;2(3):367-72
  4. Farese RV, "Phospholipid signalling systems in insulin action.", Am J Med 1988 Nov;28;85(5A):36-43
  5. Katan MB, et al, "Trans fatty acids and their effects on lipoproteins in humans.", Annu Rev Nutr 1995;15:473-493
  6. Hjelte L. et al, "Pancreatic function in the essential fatty acid deficient rat.", Metabolism 1990 Aug;39(8):871-875
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