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Diabetes simulators: ready for prime time?

55 D IABETES IS A DISEASE OF COMPROMISES. Irrefutable evidence demonstrates that good glycemic control significantly reduces the risk for developing many of the devastating longterm complications of diabetes. Conversely, limitations inherent in the current methods for providing insulin replacement make euglycemia a very dangerous proposition for most type 1 diabetics because of the risk of severe hypoglycemia. Normal beta cells within the pancreas modulate insulin secretion, responding in minutes to small changes in blood glucose concentrations. This tight feedback loop maintains blood glucose concentrations within a narrow range. Current clinical insulin regimes pale in comparison. Patients, and often their families, face a substantial challenge as they tread the narrow path between lowand high-glucose concentrations each day. Using a handful of glucose determinations each day, they must integrate diet and activity with a bewildering array of possible exogenous insulin preparations and doses to forge a reasonable level of glycemic control. Given this complexity, patients and providers alike seek a clear-cut set of rules to guide them to euglycemia. Given our increasing understanding of physiology and the massive computing capability on our desktops, an algorithm to predict glucose concentrations does not seem, at first blush, an unreasonable request. With some patient-specific information, shouldn’t we be able to accurately predict the glucose concentrations resulting from various dietary and insulin regimens? In the article elsewhere in this issue, Dr. E.D. Lehmann discusses one such glucose simulator, AIDA v4.0. This program is freely available via the Internet. A DOS program, it ran reasonably well in a Windows 95 environment. The user interface is a bit cumbersome. The program uses a physiology-based, single glucose compartment model to integrate the actions of carbohydrates and exogenous insulin. Glucose enters the compartment by intestinal absorption and liver gluconeogenesis. Glucose leaves the compartment via insulin-independent and insulin-dependent pathways. Hepatic and peripheral glucose utilization are modeled separately so that different insulin sensitivities may be assigned to each. Renal glucose losses occur when the renal threshold is exceeded. Insulin concentrations (from virtual subcutaneous injections) are derived using a two-compartment model. Counterregulatory hormones, exercise, stress, and circadian variations in insulin sensitivity are not included within this model. The technical guide that is included in the program contains a complete description of the equations involved in the model. The author has done some evaluation of the potential clinical utility of this model using patient specific parameters derived from actual historical glucose concentrations. Reasonably large differences were found between predicted and actual glucose concentrations.