PubMed · 14836668
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S GREIF, E MORO. 1951-04-20. [Functional hypoglycemia].. https://pubmed.ncbi.nlm.nih.gov/14836668/
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The prevalence of diabetes mellitus has been increasing dramatically in recent decades. This trend closely follows the marked increase in the prevalence of obesity in the United States. As the proportion of the population with diabetes increases, the need for prevention and therapy to reduce cardiovascular events in these patients becomes critically important. Although plasma glucose control is important in reducing microvascular complications due to diabetes, lipid management is essential in these patients to reduce the incidence of cardiovascular events. Adult patients with type 2 diabetes, in the absence of known coronary artery disease (CAD), have a similar 10-year risk for cardiac events as do patients without diabetes with established coronary disease. Recent clinical trials have highlighted the importance of aggressive plasma lipid lowering for both the primary and secondary prevention of atherosclerotic events in patients with diabetes. The likelihood of an ever-increasing diabetic patient population requires new systematic approaches to prevention as well as therapy for these patients and further development of a team approach by the medical community to optimize care despite limited resources.
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Short-term exercise training improves insulin action, but the impact of replacing the energy expended during exercise to prevent energy deficit is unclear. The purpose of this study was to establish the role of an energy deficit in mediating improved insulin action after short-term exercise training. Two groups of previously sedentary, overweight/obese subjects performed 6 consecutive days of moderate-intensity walking to expend approximately 500 kcal/day. In one group, energy and carbohydrate expended during exercise was replaced [balance group (BAL), n = 8] and in the other group, energy was not replaced [deficit group (DEF), n = 8]. Insulin action (blood glucose uptake during glucose infusion) and selected lipids and adipokines were measured pre- and posttraining. Training increased estimated daily energy expenditure by approximately 500 kcal/day (DEF = 469 +/- 45, BAL = 521 +/- 48), generating an energy deficit in DEF (-481 +/- 24 kcal/day) but not BAL (+8 +/- 20 kcal/day). Insulin action increased 40% in DEF (P = 0.032) but not BAL (-8.4%, P = 0.107). Hepatic glucose production was suppressed during glucose infusion in DEF (30.2 +/- 9.5%, P = 0.037) but not BAL (-10.0 +/- 7.4%, P = 0.417). Fasting leptin concentrations declined in DEF but not BAL. Six days of exercise training without energy replacement significantly increased insulin action. Restoring energy balance by refeeding the energy and carbohydrate expended during exercise resulted in no change in insulin action. These findings suggest that changes in short-term energy and/or carbohydrate balance play a key role in mediating the beneficial effects of exercise on whole body and hepatic insulin action.