Type 2 diabetes is a term to be used for idiopathic forms of diabetes with insulin resistance and without severe insulin deficiency or dramatic loss of beta cells. It has recently been appreciated that approximately 5–25% of patients initially diagnosed with type 2 diabetes actually have type 1 diabetes. Very little research can be done in medicine without a thorough knowledge of the patho-genesis and the pathophysiology of the disease pro¬cess. Figure 4 depicts pathophysiology and metabolic abnormalities).
A. Insulin Secretion
Regulation of insulin secretion is influenced by plasma levels of glucose. This level is the most important stimulus for insulin secretion (see Fig. 5). Glucagon secretion and amino acids are also important. Neural influences, gut insulinogenic hormones, and other factors appear to be of minor importance.
B. Underlying Mechanisms
The great majority of patients with type 2 diabetes have four major defects (see Fig. 4):
1. Insulin deficiency caused by a decline in pancreatic beta cell function
2. Insulin resistance because of a deficiency of cell surface insulin receptors (see Fig. 4)
3. Increased hepatic glucose production (see Fig. 4)
4. Glucagon secretion is increased

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