4. Derangement Of Function
There are several major areas where functional derangement is especially evident in diabetes.
A partial or absolute lack of insulin secretion results in excess glucose in the blood. Glucose is the primary fuel for all body tissues. The brain utilizes 25% of the total body glucose. Because brain energy stores are very small, a constant supply of glucose must always be available to maintain adequate brain function. It is, therefore, imperative that the blood glucose level be maintained in the 60 to 120 mg/dl (deciliter) range to prevent central nervous system impairment. The body has special homeostatic devices to maintain this required range.
Insulin is the primary hormone for regulating blood glucose levels and does so by controlling the rate that blood glucose is taken in by muscle, fat and liver cells. Each of these three types of cells utilizes glucose in a different way, as determined by specific enzyme systems.
The primary function of the fat cell is providing storage. It contains unique enzymes that convert glucose into triglycerides as well as enzymes that convert triglycerides to fatty acids. These fatty acids are released and converted to ketones in the liver, when needed.
The conversion of glucose to triglycerides and the breakdown of triglycerides to free fatty acids take place continuously and simultaneously within the same fat cell, and both processes are regulated by insulin. High blood insulin levels stimulate the uptake of glucose by fat cells to form triglycerides; thus there is a net gain of storage fat. During low blood insulin levels, glucose uptake into the fat cell is poor; thus less triglyceride is formed. Triglyceride breakdown then exceeds formation, resulting in a net loss of the storage fat. Thus, by regulating glucose uptake into fat cells, insulin can influence net fat metabolism.
Insulin also inhibits the enzyme lipase, which breaks down storage fat into fatty acids and glycerol. When insulin is high and lipase is inhibited, there is also a net increase in storage fat. There is a net decrease in storage fat when insulin is low, because lipase becomes activated and a fat is then broken down.
The muscle cell has two primary functions: it converts glucose into energy needed for muscle function, and it serves as a reservoir for protein and glycogen. During starvation, the protein of the muscle itself can be made available in the form of amino acids. These amino acids can then be converted in the liver into glucose in order to maintain blood glucose at an adequate concentration for brain function.
In the muscle cell, as in the fat cell, insulin promotes the uptake of glucose. The muscle cell, however, has different enzymes that control two metabolic pathways for glucose. First, glucose can be converted into “contractile energy.” Second, glucose can be converted to glycogen, a storage form of glucose that is more readily available than triglycerides in times of glucose insufficiency.
When blood glucose levels are normal, insulin also affects the enzymes of the muscle cell to maintain muscle mass by promoting the uptake of amino acids and preventing the breakdown of protein.
Liver glycogen is another storage form of glucose. Glycogen is more readily available for use than are triglycerides, which first have to be converted to free fatty acids and then converted to ketones. The liver monitors these conversions and also converts amino acids to glucose when necessary. The conversion of amino acids to glucose is called gluconeogenesis.
Although insulin is not required for the transport of glucose into the liver, insulin directly affects the liver to promote the uptake of glucose by reducing the rate of glycogen breakdown, increasing glycogen synthesis, and decreasing the rate of gluconeogenesis.
4.1.2 Beta Cell
Insulin is secreted by the beta cells of the pancreas. The beta cells function first as a sensor of blood glucose levels. The beta cells then secrete enough insulin to regulate the carbohydrate load, maintaining the blood glucose level within a very narrow range. A feedback system exists whereby a small amount of carbohydrate stimulates a small amount of insulin release. The liver responds to increased insulin secretion by suppressing glycogen release (glycogenolysis). The formation of new glucose is likewise suppressed. A large carbohydrate intake stimulates a greater insulin response, and the peripheral and liver cells take up glucose. When glucose levels are low, insulin release is suppressed and glycogenolysis and gluconeo-genesis occur in order to feed glucose into the system and maintain the blood glucose levels.
When the body is enervated and a state of toxicosis exists, all bodily functions will be impaired. This may effect the pancreas and its secretion of insulin. When insulin secretion is abnormally diminished, glucose will not be utilized by the fat and muscle cells and the liver will continue to break down glycogen to glucose to further add to the blood glucose levels. Hyperglycemia is then present.
Other hormones contribute to the release of glucose in the blood and further complicate the situation when insulin secretion is diminished. Stress stimulates epinephrine release and the hormone then serves to mobilize glycogen to yield a higher blood glucose level. Epinephrine also suppresses insulin release to further enhance blood glucose levels. Glucagon and cortisol also increase levels of blood glucose.
4.2 Large Vessel Disease
Diabetics have an increased incidence, earlier onset and increased severity of atherosclerosis and calcification of the arterial wall. Peripheral vascular disease is 50 to 100 times more common in diabetics than in healthy individuals. More fat is broken down when insulin is low and enters the bloodstream. Excess fat in the blood may then accumulate in the large vessels of the heart or elsewhere.
It is likely, however, that there is already some arteriosclerosis in diabetic patients, not because of the diabetes, but it is due to the same conditions that resulted in the diabetes in the first place. That is, a diet too high in fats and sugars, lack of exercise, and a generally unhealthful lifestyle.
4.3 Microvascular Disease
Many diabetics demonstrate a thickening of the capillary membrane in major areas of skin and skeletal muscles. This is most obvious in the retina of the eye and the renal glomeruli of the kidney and this situation may eventually lead to blindness or kidney failure. It becomes clear that diabetes is not a “one-organ disease” but does indeed involve the entire system. Suppressing one symptom, such as hyperglycemia, certainly does not produce health.
Neuropathy involves injury to nerves, associated with destruction of the myelin sheath of nerve tissue and nerve cell degeneration. This involves sensory and motor nerves, nerve roots, the spinal cord, and the autonomic nervous system. Affected nerves show basal membrane thickening similar to the capillary abnormalities.
Did the diabetes cause this nerve degeneration? No, diabetes is merely a symptom of a systemic disorder. Again, this “disease” that is associated with diabetes is another indication of systemic involvement.
The fat cell attempts to provide fuel in the absence of insulin by mobilizing fat stores. The free fatty acids are initially utilized for energy production, but the majority reach the liver where three strong acids are found: acetoacetic acid, beta-hydroxybutyric acid and acetone. The keto-acids are ultimately excreted by the kidneys along with sodium bicarbonate. The combination ketoacid accumulation and bicarbonate excretion causes a fall in plasma pH, resulting in acidosis.
A diet high in acid-forming foods further complicates this problem. This would include such foods as meat, dairy products, dry beans, most cereals (especially wheat) and all refined sugars.
- Part I – Diabetes Mellitus
- Part II – Diabetes Insipidus
- Part III – Hypoglycemia
- Questions & Answers
- Article #1: Diabetes Mellitus By Dr. Herbert M. Shelton
- Article #2: Diabetes