Patients with Type I, i.e., insulin-deficient diabetes, Type II or non-insulin-deficient diabetes, and impaired glucose tolerance or so-called chemical diabetes are variably predisposed to develop macroangiopathy, i.e., atherosclerosis, microangiopathy or basement membrane thickening, and neuropathy. Once these morphologic changes appear, they in all probability will remain irreversible even when precise regulation is attained. Hence prevention is the only realistic goal.
Glycosuria can be a misleading indicator of blood or plasma glucose levels. Thus glycosuria may be present when blood glucose levels are within the normal fasting or postprandial range, and it may be absent when the blood glucose is distinctly above normal. In such patients the blood glucose must be measured, preferably by the patient, as a guide to insulin and other therapy. However, urine glucose tests are valid indicators in a minority of patients and are essential in all patients for the detection of acetone.
Optimal control of diabetes should achieve not only euglycemia and normal levels of glycosylated hemoglobin but also absence of the reversible concomitants of diabetes such as red cell rigidity, hyperlipidemia, increased capillary permeability, enlargement of the kidneys, proteinuria, etc. Unfortunately, in most patients consistent euglycemia cannot be assured even with two daily injections of insulin. However, self-measurement of blood glucose as a guide to insulin taken before each meal and at bedtime can, in selected patients, increase the frequency of normal glucose levels without undue hypoglycemia.
The intravenous glucose tolerance and insulin response to glucose infusion was studied in two large families with diabetic mothers in the first generation, 42 family members in all. Manifest diabetes occurred in only one subject who belonged to generation 11, while decreased glucose tolerance was much more common. Delayed and decreased initial insulin response to glucose was observed in the majority of the family members including thosc with normal glucose tolerance. The frequency of low insulin response diminished with each generation. These findings, together with previous ones on healthy monozygotic twin sibs of diabetic patients, indicate that a decreased initial insulin response to glucose may be an inherited and predisposing factor in diabetes mellitus. The present material is insufficient to aHow any conclusions regarding the inheritance of this factor. However, it emphasizes the necessity of studying the pattern of insulin secretion when investigating the mode of inheritance of.diabetes.
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