Disfunction of the dopamine-prolactin axis in the development of NAFLD.

Abstract

NAFLD is currently recognized as the hepatic manifestation of metabolic syndrome and is the leading cause of liver-related morbidity and mortality. Risk factors for NAFLD include obesity, diabetes, insulin resistance, and hypertriglyceridemia [1]. These studies suggest that endocrine dysfunction may play an important role in the development, progression, and severity of NAFLD [2,3,4,5]. Chronic prolactin excess is associated with increased food intake and weight gain, leading to obesity [6,7]. This is due to the functional blockade of dopaminergic tone caused by hyperprolactinemia. Abnormal lipid profile is a common feature in patients with prolactin excess. Physiologically, dopaminergic tone plays a key role in reducing food intake and increasing energy expenditure, which supports the hypothesis of dopamine involvement in body weight regulation [8]. Preclinical studies using rats with hyperprolactinemia showed that dopamine reduction led to obesity.