Recently, increasing evidences relate left ventricular mass (LVM) and plasma glucose concentrations in hypertensive patients. In this respect, it has been described a positive and significant relation between LVM and Hemoglobin A1c in essential hypertension. Moreover, hypertensive individuals with diabetes have higher LVM than nondiabetic hypertensive patients with similar blood pressure. It has been also described that an improvement of glycemic control contributes to left ventricular hypertrophy regression in hypertensive patients with type 2 diabetes, and that these changes occurred independently of variation in blood pressure. Finally, we have recently published that "glucose effectiveness" (that represents the ability of glucose per se to effect its own disappearance from plasma independent of dynamic changes from basal insulin) is strongly related to left ventricular mass in subjects with stage 1 hypertension or high-normal blood pressure. The mechanisms by which glucose in itself can induce proliferation and hypertrophy seem to be mainly related to the activation of protein Kinase C pathways. However, it has been also shown that glucose increases intracellular calcium "in vitro" and this increase directly stimulates vascular proliferation and hypertrophy. In the present paper we will review different clinical studies and in vitro experiments, showing that glucose in itself, independently of insulin, can induce vascular proliferation,and cardiac hypertrophy.