Heart failure (HF) is associated with a significant risk for either concurrently having diabetes or subsequently developing diabetes. Medications that block the sympathetic nervous system (SNS) have been shown to improve clinical outcomes in patients with chronic HF but may be associated with the development of new-onset diabetes. Depending on the receptor specificity of the individual agent, beta-blockers have different effects on glucose and lipid metabolism as well as on the risk for developing new-onset diabetes. Although SNS modulation with beta-blockade reduces mortality in patients with chronic HF, certain beta-blockers may actually worsen glucose and lipid metabolism and increase the risk for new-onset diabetes. The use of vasodilating beta-blockers, on the other hand, has not produced these harmful metabolic effects.