Dipartimento di Medicina Clinica e Chirurgia, Sezione di Endocrinologia, University of Naples Federico II, Naples, Italy.
Unesco Chair for Health Education and Sustainable Development, "Federico II" University, Naples, Italy.
Front Endocrinol (Lausanne). 2022 Sep 27;13:1015520. doi: 10.3389/fendo.2022.1015520. eCollection 2022.
Over the last years, the metabolic role of PRL has emerged. PRL excess is known to promote weight gain, obesity, metabolic syndrome, and impairment in gluco-insulinemic and lipid profiles, likely due to the suppression of physiologic dopaminergic tone. Prolactin receptors and dopamine receptors type 2 have been demonstrated to be expressed on both human pancreatic β- cell and adipocytes, supporting a key role of prolactin and dopamine in peripheral metabolic regulation. Medical treatment with the dopamine agonists bromocriptine and cabergoline has been demonstrated to decrease the prevalence of metabolic syndrome and obesity, and significantly improve gluco-insulinemic and lipid profiles. In hyperprolactinemic men with concomitant hypogonadism, correction of hyperprolactinaemia and testosterone replacement has been proven to restore metabolic impairment. In turn, low prolactin levels have also been demonstrated to exert a detrimental effect on weight gain, glucose and lipid metabolism, thus leading to an increased prevalence of metabolic syndrome. Therefore, PRL values ranging from 25 to 100 mg/L, in absence of other recognizable pathological causes, have been proposed to represent a physiological response to the request for an increase in metabolic activity, and nowadays classify the so-called HomeoFIT- PRL as a promoter of metabolic homeostasis. The current review focuses mainly on the effects of hyperprolactinemia and its control by medical treatment with DAs on the modulation of food intake, body weight, gluco-insulinemic and lipid profile. Furthermore, it provides the latest knowledge about the metabolic impact of hypoprolactinemia.
在过去的几年中，PRL 的代谢作用已经显现出来。已知 PRL 过多会导致体重增加、肥胖、代谢综合征，并损害糖胰岛素和脂质谱，这可能是由于生理性多巴胺能张力的抑制。已经证明催乳素受体和多巴胺受体 2 型在人胰腺β细胞和脂肪细胞上均有表达，这支持了催乳素和多巴胺在周围代谢调节中的关键作用。用多巴胺激动剂溴隐亭和卡麦角林进行医学治疗已被证明可降低代谢综合征和肥胖的患病率，并显著改善糖胰岛素和脂质谱。在伴有性腺功能减退的高催乳素血症男性中，纠正高催乳素血症和睾酮替代治疗已被证明可恢复代谢损伤。反过来，低催乳素水平也已被证明对体重增加、葡萄糖和脂质代谢有不利影响，从而导致代谢综合征的患病率增加。因此，在没有其他可识别的病理原因的情况下，提出 25 至 100mg/L 的 PRL 值代表对代谢活性增加的生理反应，并且现在将所谓的 HomeoFIT-PRL 归类为代谢稳态的促进剂。目前的综述主要集中在高催乳素血症及其通过 DAs 治疗控制对食物摄入、体重、糖胰岛素和脂质谱的调节作用。此外，它还提供了关于低催乳素血症代谢影响的最新知识。
