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This article briefly summarizes the “Pre-Diabetes Detection and Intervention Symposium” that described ongoing and past pre-diabetes interventions, and outlined some considerations when deciding to target specific populations with pre-diabetes. The success of type 2 diabetes (T2D) prevention clinical trials provides clear evidence that healthy lifestyle change can prevent the development of T2D in a cost effective manner in high risk individuals. However, who to target and what cut-points should be used to identify individuals who would qualify for these T2D prevention programs are not simple questions. More stringent cut-offs are more efficient in preventing T2D, but less equitable. Interventions will likely need to be adapted and made more economical for local communities and health care centers if they are to be adopted universally. Further, they may need to be adapted to meet the specific needs of certain high-risk populations such as ethnic minorities. The Chronic Disease Management & Prevention Program for Diverse Populations in Alberta and the Pre-diabetes Detection and Physical Activity Intervention Delivery project in Toronto represent 2 examples of specialized interventions that are targeted at certain high risk populations. To reverse the current T2D trends will require continued efforts to develop and refine T2D prevention interventions.

Exercise and metformin may prevent or delay Type 2 diabetes by, in part, raising the capacity for fat oxidation. Whether the addition of metformin has additive effects on fat oxidation during and after exercise is unknown. Therefore, the purpose of this study was to evaluate the effect of metformin on substrate oxidation during and after exercise. Using a double-blind, counter-balanced crossover design, substrate oxidation was assessed by indirect calorimetry in 15 individuals taking metformin (2,000 mg/d) and placebo for 8–10 d. Measurements were made during cycle exercise at 5 submaximal cycle workloads, starting at 30% peak work (W_peak) and increasing by 10% every 8 min to 70% W_peak. Substrate oxidation was also measured for 50 min postexercise. Differences between conditions were assessed using analysis of variance with repeated measures, and values are reported as M ± SE. During exercise, fat oxidation (0.19 ± 0.03 vs. 0.15 ± 0.01 g/min, p < .01) and percentage of energy from fat (32% ± 3% vs. 28% ± 3%, p < .01) were higher with metformin than with placebo. Postexercise, metformin slightly lowered fat oxidation (0.12 ± 0.02 to 0.10 ± 0.02 g/min, p < .01) compared with placebo. There was an inverse relationship between postexercise fat oxidation and the rate of fat oxidation during exercise (r = –.68, p < .05). In healthy individuals, metformin has opposing actions on fat oxidation during and after exercise. Whether the same effects are evident in insulin-resistant individuals remains to be determined.

The concept that participation in exercise/physical activity reduces the risk for a host of chronic diseases is undisputed. Along with adaptations to habitual activity, each bout of exercise induces beneficial changes that last for a finite period of time, requiring subsequent exercise bouts to sustain the benefits. In this respect, exercise/physical activity is similar to other “medications” and the idea of “Exercise as Medicine” is becoming embedded in the popular lexicon. Like other medications, exercise has an optimal dose and frequency of application specific to each health outcome, as well as interactions with food and other medications. Using the prevention of type-2 diabetes as an exemplar, the application of exercise/physical activity as a medication for metabolic “rehabilitation” is considered in these terms. Some recommendations that are specific to diabetes prevention emerge, showing the process by which exercise can be prescribed to achieve health goals tailored to individual disease prevention outcomes.