In the case of hypoprolactinemia, the inadequately low PRL levels necessary for metabolic homeostasis do not affect food intake but promote adipocyte enlargement and adipose tissue hypertrophy, particularly at visceral level, together with a reduced expression of adipocyte markers such as adiponectin and GLUT-4, thus leading to insulin resistance [69], and foster the increase in fasting glucose and insulin levels, HbA1c, LDH-cholesterol and triglycerides, and the decrease in HDL-cholesterol [73, 74], thus facilitating the development of type 2 diabetes mellitus and metabolic syndrome. This evidence concerns the gene PRL and Insulin resistance.