No abstract

The aim of the present study was to verify the validity of diagnostic criteria developed by the NDDG for the diagnosis of diabetes mellitus in old age. One hundred and fifty-one ambulatory old (range: 66-77 years) subjects (group A) underwent OGTT showing the following results: 33% normal, 12% non-diagnostic, 23% impaired glucose tolerance (IGT), 32% diabetic-type tolerance (DT). In addition, 84 subjects (group B) selected from 1978 to 1982 (42 aged 51-60 years, 30 aged 61-70, and 12 aged 71-80) with abnormalities of glucose tolerance during OGTT (IGT or DT) were asked to control their fasting plasma glucose every month during 1984. In group B a significant correlation between DT and subsequent development of fasting hyperglycemia was observed only in the subjects of the 6th and 7th decades of age. On the contrary, no subjects aged 71-80 years developed fasting hyperglycemia. The authors suggest that a high prevalence of abnormalities in glucose tolerance according to NDDG exists in old age which cannot be considered evidence of a true diabetes mellitus being unpredictive of a progression towards fasting hyperglycemia.

The usual practice of considering type I diabetes synonymous with insulin-dependent diabetes has been criticized. Since type I diabetes can have a non-insulin-dependent phase (pre-type I diabetes and/or honeymoon) the differentiation of two main types of diabetes according to insulin-dependency is not absolute. We studied the insulin, C-peptide and glucagon responses to various tests (OGTT, IVGTT, glibenclamide test, mixed meal tolerance test and ITT) performed during the non-insulin-dependent phase of 3 young patients (range 8-18 years) who developed ketosis 12-24 months after the discovery of fasting hyperglycemia, and in 6 patients (age 15-23 years) who presented a remission phase 4-6 months after the sudden clinical onset of type I diabetes. An insignificant insulin and C-peptide increase following i.v. glucose was observed in all patients, whereas the B-cell response to both oral glucose and other secretagogues was preserved, although at a subnormal level. In the three hyperglycemic and preketoacidotic patients the basal levels of glucagon were low and no significant increase after secretagogues was seen. Sensitivity to exogenous insulin in all patients was good. Thus, B-cell response in our patients was reminiscent of the differential responsiveness to various stimulants in the early stage of type II (non-insulin-dependent) diabetes. These results suggest that type I and type II diabetes can be characterized by the same functional B-cell defect during a period of their natural history.

Oxygen-release capacity of the red blood cells was investigated in non-acidotic insulin-dependent diabetics before and after the achievement of strict metabolic control with the aid of the artificial pancreas. P50std (oxygen tension at 50% oxygen saturation) values were low in basal condition and returned to normal after the 24-h treatment period. No significant changes were observed in the content of red cell 2,3-diphosphoglycerate nor in the acid-base balance. Only the labile form of glycosylated hemoglobin showed significant decreases after treatment. These results suggest that insulin-dependent diabetics may have a state of relative tissue hypoxia which can be easily overcome by the achievement of strict metabolic control.