Multiple mechanisms have been postulated to explain drug-induced diabetes (6). Some of these mechanisms have been confirmed while others are conflicting. It is important to remember that a drug can act through more than one mechanism. In general, these mechanisms can be classified into four categories: effects on insulin release, effects on insulin sensitivity, effects on liver, and effects on peripheral blood flow (Figure 1).
i. Inhibition of insulin release will result in hyperglycemia, and medications that result in destruction of beta cells like pentamidine (7) or beta-blockers (8) which have long been considered to inhibit insulin release through pancreatic beta-cell blockade. Diuretics have also been associated with impaired insulin release through depletion of serum potassium (9).
ii. Insulin sensitivity can be altered through effects on insulin receptors or post-receptor disturbance of signaling. Hypokalemia has been linked to reduced insulin-receptor sensitivity. Various medications are involved in the alteration of glucose transport proteins (GLUT-1 and GLUT-4), tyrosine kinase activity or insulin receptor-binding affinity (10).
Finally, medications that reduce peripheral blood flow could direct blood flow away from the sites of glucose uptake, reducing glucose disposal (12). Non-selective beta-blockers are known to act via this mechanism as well (8). This mechanism is documented by reduced capillary density in skeletal muscles and increased risk of beta-blocker-induced hyperglycemia.
This chapter reviews commonly used prescribing agents that are associated with hyperglycemia (Table 1).
Was this article helpful?
Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...