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The old concept of insulin deficiency as the basic mechanism in the development of diabetes in man has, in recent years, seen a revival. It has been amply demonstrated that not only the ketosis-prone juvenile but also the mild mature-onset diabetics and even latent diabetics (with decreased glucose tolerance only) respond to glucose with a subnormal elevation of plasma insulin (Yalow and Berson, 1960; Cerasi and Luft, 1967 a; Seltzer et al., 1967; Parker et al., 1968). For this reason we presented some years ago the working hypothesis that a diminished insulin response to glucose is the basic pathogenic factor on which foundation the different stages of the diabetic syndrome develop (Cerasi and Luft, 1967 b). The presence of low insulin response in healthy monozygotic twins of diabetic patients indicates that this insulin deficiency is inherited and precedes the appearance of decreased glucose tolerance (Cerasi and Luft, 1967 c; Pyke et al., 1970). We therefore concluded that the combination of normal glucose tolerance and decreased insulin response to glucose characterizes the so called prediabetic state (Fig. 1). With this definition, the frequency of prediabetes in normal adults (Cerasi and Luft, 1967 a) and children (Cerasi and Luft, 1970 a) was found to be about 20 per cent. Since the frequency of manifest diabetes is much lower, it is obvious that not all prediabetics will eventually develope diabetes. The term is used in order to designate the group of subjects in which diabetes mellitus may develop. "Low insulin responder" might be a more appropriate term in this connection. The term "low responder" or "low response" refers to the promptness and the degree of insulin secretion in relation to the height of the glycemic stimulus. In our studies, insulin response to glucose was evaluated with the aid of an analogue computer model, which measures the response as a function of the intensity of stimulation used (Cerasi, 1967). Four major questions emanate from these basic observations A. What is the mechanism for the deficient insulin secretion in prediabetes and diabetes? B. Which mechanisms contribute to the maintenance of a normal glucose tolerance in subjects with deficient insulin secretion, and which are the factors that precipitate clinical diabetes in low insulin responders? C. Does the deficient insulin secretion bring about any metabolic derangements in low insulin responders? These problems have been dealt with by our group during the last five years, and some of the results will be discussed in the following.

Pathogenesis of Genetic Diabetes Mellitus Further Development of a Hypothesis