Through a variety of mechanisms, pregnancy causes insulin resistance, which suppresses the intracellular transport of glucose and increases blood glucose concentrations. In the extreme, gestational diabetes (GDM) mellitus may develop. In addition to insulin resistance, pregnant bitches have decreased ability to produce glucose via gluconeogenesis, glycogenolysis and lipolysis, because the normal multi-factorial responses to hypoglycemia are blunted late in pregnancy. Simply fasting late-pregnant bitches is sufficient to cause blood glucose and insulin concentrations to decrease and ketones to increase. The purpose of this paper is to review the clinical implications of pregnancy-associated changes in glucose homeostasis in bitches.