Dr Gerald Reaven of Stanford Medicine, may be my new hero. Dr Reaven:
Jerry is credited with developing the insulin suppression test, the first quantitative method to measure insulin-mediated glucose uptake in humans. Using this technique, he established the importance of insulin resistance in human disease, and importantly, in type 2 diabetes.
[Added 2017-11-30]: Dr Reaven delivered the seminal paper on the subject of Insulin Resistance at the Banting Lecture in 1988 (Role of Insulin Resistance in Human Disease).
Dr. Reaven challenged the then prevailing theory that defective insulin secretion adequately explained the hyperglycemia of T2DM, postulating that insulin resistance might be as, or more, important.
He is a prolific writer of studies. Here’s just one (All obese individuals are not created equal: insulin resistance is the major determinant of cardiovascular disease in overweight/obese individuals) of his papers.
[Added 2017-11-30]: Another hero is Dr Kraft.
Related to the Kraft Test (Kristine Faerch, Adam Hulman, Thomas P.J. Solomon. Heterogeneity of Pre-diabetes and Type 2 Diabetes: Implications for Prediction, Prevention and Treatment Responsiveness. Current Diabetes Reviews, Volume 12 , Issue 1 , 2016).
We aimed to examine heterogeneity in glucose response curves during an oral glucose tolerance test with multiple measurements and to compare cardiometabolic risk profiles between identified glucose response curve groups. We analyzed data from 1,267 individuals without diabetes from five studies in Denmark, the Netherlands and the USA. Each study included between 5 and 11 measurements at different time points during a 2-h oral glucose tolerance test, resulting in 9,602 plasma glucose measurements. Latent class trajectories with a cubic specification for time were fitted to identify different patterns of plasma glucose change during the oral glucose tolerance test. Cardiometabolic risk factor profiles were compared between the identified groups. Using latent class trajectory analysis, five glucose response curves were identified. Despite similar fasting and 2-h values, glucose peaks and peak times varied greatly between groups, ranging from 7–12 mmol/L, and 35–70 min. The group with the lowest and earliest plasma glucose peak had the lowest estimated cardiovascular risk, while the group with the most delayed plasma glucose peak and the highest 2-h value had the highest estimated risk. One group, with normal fasting and 2-h values, exhibited an unusual profile, with the highest glucose peak and the highest proportion of smokers and men. The heterogeneity in glucose response curves and the distinct cardiometabolic risk profiles may reflect different underlying physiologies. Our results warrant more detailed studies to identify the source of the heterogeneity across the different phenotypes and whether these differences play a role in the development of type 2 diabetes and cardiovascular disease.