Glycemic Control and Hypoglycemia
Is the loser the winner?
- 1Department of Psychology, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois
- 2Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois
- 3Department of Medicine, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois
- Corresponding author: Lawrence C. Perlmuter,
Glycemic control remains a delicate balancing act. The diabetic patient is tasked with maintaining euglycemic blood glucose levels, a goal requiring education, decision strategies, volitional control, and the wisdom to avoid hyper- and hypoglycemia, with the latter defined as plasma glucose less than ∼60 mg/dl. Glucose levels must be controlled continuously and without holidays. Failure to maintain euglycemia results from biological factors and psychosocial factors including overmedication and/or inappropriate choices regarding food, drink, and, in certain cases, exercise.
Diabetic patients, especially those treated with insulin, are at risk for developing hypoglycemia. Treatment, even with oral agents such as sulfonylureas, increases this risk. Asymptomatic episodes of hypoglycemia may constitute up to 10% of a 24-h period in diabetic patients (1,2). Individuals with type 1 diabetes average 43 symptomatic episodes annually; insulin-treated individuals with type 2 diabetes average 16 episodes (3). As for severe hypoglycemic episodes, patients with type 1 diabetes experience up to two episodes annually, whereas patients with type 2 diabetes experience about one episode over 5 years. The risk increases with a history of hypoglycemia and an increased number of years of insulin treatment (3,4).
Hypoglycemia deprives the brain of the constant supply of glucose needed for energy. Such low levels of blood glucose are sensed by the ventromedial hypothalamus (5). In turn, a counterregulatory hormonal cascade is activated to rapidly restore euglycemia that begins with inhibition of insulin secretion. Thereafter, the release of glucagon and epinephrine elevates endogenous glucose production through increased hepatic glycogenolysis and gluconeogenesis, as well as renal gluconeogenesis. Growth hormone and cortisol are slow-acting adjustments to prolonged hypoglycemia (6). Hypoglycemia may promote oxidative stress and neuronal cell death, primarily as a consequence of neuronal NADPH oxidase activation and extracellular zinc release during glucose reperfusion. Thus, heightened glucose concentrations during reperfusion …