Summary. This review seeks to supply the arguments which support or deny the relationship between the quality of control of blood glucose levels and the course of diabetic microangiopathy. The ideal study is impossible to do in man but most prospective studies suggest that the better the control the slower the rate of progression and severity of lesions. "Scientific" but indirect arguments from biochemical, enzymatic and functional studies have shown that insulin and/or blood glucose control reverse some early diabetic changes that are probably related to the late events. Recent studies suggest that observations on animals that have shown the beneficial effect of treatment are relevant to the problem of diabetic microvascular lesions in man. Heredity influences the development of diabetic microangiopathy in diabetics but retinal and/or glomerular lesions -which are definitely not pathognomonic for diabetes -do not appear in the absence of hyperglycaemia. Muscle capillary basement membrane thickening that seems not to be a specific abnormality was not observed by several investigators in recently diagnosed diabetics. Therefore most of the arguments that have been given to support the point of view that tight control is not justified may be rejected. The opinion of the author is that strict control of diabetes is worthwile in patients with long life expectancy and no psychological, social or cultural handicaps.

The glycemic index concept neglects the insulin secretion factor and has not been systematically studied during mixed meals. Six starch-rich foods were tested alone and in an isoglucido-lipido-protidic meal in 18 NIDDs and compared with a glucose challenge. These test meals were randomly assigned using a three factor experiment design. All three tests contained 50 g carbohydrate; mixed meals were adjusted to bring the same amount of fat (20 g), protein (24 g), water (300 mL), and calories (475 kcal) but not the same amount of fiber. Whatever the tested meals, foods elicited a growing glycemic index hierarchy from beans to lentils, rice, spaghetti, potato, and bread (mean range: 0.21 +/- 0.12-92 +/- 0.12, p less than 0.001). Mixing the meals significantly increased the insulinemic indexes (p less than 0.05) and introduced a positive correlation between glycemic and insulinemic indexes (n = 6, r = 0.903; p less than 0.05). The glycemic index concept remains discriminating, even in the context of an iso-glucido-lipido-protidic meal. Insulinemic indexes do not improve discrimination between foods taken alone in type 2 diabetics: they only discriminate between foods during mixed meals, similarly to glycemic indexes.

Early-onset symptomatic polyneuropathy in patients with diabetes mellitus is characterized by the loss of both myelinated and unmyelinated nerve fibers. Spontaneous axonal regeneration is remarkably frequent, even when neuropathy is severe.

The effects of a daily intake of 30 g fructose on blood glucose regulation, erythrocyte insulin receptors, and lipid metabolism have been studied in type II (non-insulin-dependent) diabetic subjects. Eight well-controlled patients received, in a randomly assigned crossover design over two 2-mo study periods, 30 g of fructose in exchange for an isocaloric amount of starch. Fructose could be taken at any time during the day as part of the 1400-1600 kcal allowed diet (50% carbohydrate, 30% fat, 20% protein). No significant difference was observed concerning body weight, HbA1c, fasting plasma glucose, fasting plasma insulin, uric acid, total cholesterol, high-density lipoprotein cholesterol, and triglycerides, nor was there any change in insulin binding to erythrocytes between the fructose and the control starch period. However, the mean plasma triglyceride levels after the fructose period, although still in the normal range, were significantly higher than baseline values (P less than .05). We conclude that moderate amounts of fructose incorporated into the diet of well-controlled type II diabetic subjects have no significant deleterious effect on glycemic control, insulin receptors of erythrocytes, or lipid metabolism.

The aim of this study was to discover the frequency, severity and causes of hypoglycaemic reactions in Type 1 (insulin-dependent) diabetes. One hundred and seventy-two outpatients answered a questionnaire which also inquired about their feelings, opinions and fears with respect to insulin reactions. Hypoglycaemic reactions were common: a mild episode occurred at least once a month in 58% of patients, and at least one severe reaction (defined by the need of assistance) during the past year was described by 26%. Both were positively related to the duration of the disease. However, the occurrence of mild and severe attacks was not related. In addition, patients prone to mild hypoglycaemia seem to be somewhat different from patients prone to severe attacks in their attitudes towards the disease. For example, mild reactions are more fie-quent in patients devoted to 'perfect' control, whereas severe episodes were observed more frequently in those who did not think that controlling diabetes is a difficult task. The social consequences of any reaction, even mild, were important in 30% of the patients. Twenty-one percent of the patients said that the short-term risks of a hypoglycaemic reaction, even if correctly treated, were high and 6% said that the fear of having a reaction was unbearable. In addition to rational explanations, emotional factors were given as a cause of hypoglycaemia (14%), but 11% of cases felt that attacks occured without any obvious reason in spite of correct management.