To fully comprehend the difference between type 1 and type 2 diabetes mellitus it is important to understand how the body regulates glucose and what goes wrong with each disease. The main difference between the two is in the pathophysiology. Most of the other differences are a spinoff of it.
What is diabetes mellitus?
Diabetes mellitus is a disorder of blood glucose homeostasis. Its mechanisms are deficient insulin production and/or a blunted response of cells to insulin. The effect it has on the maintenance of equilibrium causes glucose in the blood to be elevated. Other than gestational diabetes there are two main types of diabetes mellitus.
An expert panel, with input from the American Diabetic Association (AMA) and World Health Organization (WHO), made changes to the system for classifying and naming diabetes in 1997. It eliminated confusing terms and replaced Roman numerals with regular numbers.
As a result of the changes type 1 diabetes mellitus is now the accepted term for what used to be termed type I, juvenile-onset, or insulin-dependent diabetes mellitus (IDDM). By the same token, type 2 diabetes mellitus is now the approved term for type II, adult-onset, or non-insulin-dependent diabetes mellitus (NIDDM).
Glucose homeostasis is the body’s functions and processes that maintain a balance of glucose in the blood and in cells and tissues. Glycemic control is an indicator of how well this mechanism is working. It is also a measuring stick of how effective treatment of diabetes is. Glycemic means pertaining to the level of glucose in the blood. Therefore, glycemic control denotes the degree to which the level of glucose in the blood is within the normal range.
Proper regulation of the pendulum keeps glucose in blood from being too high or too low. The balance is important because glucose is the main source of energy for all cells; yet it must be in the blood for delivery to appropriate cells at the right time. Critical to this balance is the role of insulin.
The source of blood sugar is directly from the diet or from the conversion of more complex compounds by means of chemical reactions within the body. Glucose can be absorbed directly into the bloodstream via the small intestine or following digestion of more complex sugars or starches. In the fasting state the liver produces glucose from protein and fat subunits. Those subunits are amino acids and glycerol respectively. Gluconeogenesis is the name of this process. Additionally, in the fasting state, the liver produces glucose from the breakdown of glycogen – a storage form of carbohydrate in liver and muscle tissue. The name for this process is glycogenolysis. The glucose is then absorbed into the blood.
The function of insulin in glucose homeostasis is to make sure that the level of glucose in blood is not too high and to drive it into cells. Insulin stimulates the entry of glucose into muscle, fat, brain and all cells of the body that need it for energy and survival. It also stimulates the synthesis of glycogen in the liver and inhibits the process of gluconeogenesis. All of these phenomena tend to lower blood glucose when it tends to rise.
Pathophysiology of diabetes mellitus
In type 1 disease there is an absolute deficiency or absence of insulin production. The cause is a decrease in the number of beta islet cells – the structures in the pancreas that produce insulin. Researchers have found circulating autoantibodies against islet cells and insulin in most but not all individuals with type 1 disease. Additionally, there is research evidence of destruction of islet cells by various expressions of the immune system. For these reasons, type 1 diabetes mellitus is amongst the list of autoimmune diseases.
With type 2 diabetes mellitus there is a relative deficiency of insulin along with a blunted response of tissue cells to the insulin the pancreas produces. The islet cells still function and are able to increase insulin production in response to rises in blood glucose, but the response is less than normal.
It is not clear if the abnormal response is strictly functional, due to a decrease in the number of beta islet cells, or both. The uncertainty is due to the fact that researchers have also detected beta cell loss in persons with type 2 disease, although the decrease in the number of cells is less than with type 1 disease.
One study showed that at the time of diagnosis beta cell loss with type 1 disease was between 70% and 80% compared to 25% and 50% when the disease is type 2. In contrast to type 1 diabetes, autoantibodies are not present with type 2 disease. Neither is there any evidence of the immune system playing a role in beta cell destruction. Thus, type 2 diabetes is not among the group of autoimmune diseases.
The party line used to be that insulin resistance – the decreased response of various cells in the body to the effects of insulin was the earliest defect in type 1 diabetes. But in recent years it has become evident that the beta cell defect and insulin resistance coexist early in the disease.
Conventional wisdom is that insulin resistance is the hallmark of type 2 disease and that it is not a feature of type 1 diabetes at all. To the contrary though, although it is far more common with type 2 disease, there are research findings which prove its existence in some patients with type 1 disease as well.
As is the case with the main difference, other differences between type 1 and type 2 diabetes are not absolute. They are relative with respect to their comparative frequencies. The table to the right is a summary of the main differences.
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