Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
Cabergoline counteracts adipose and skeletal muscle lipid accumulation: A novel therapeutic approach to obesity?
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Negri Mariarosaria, Pivonello Claudia, Auriemma Renata Simona, Amatrudo Feliciana, Provvisiero Donatella Paola, Patalano Roberta, Marciano Maria Anna, Vecchio Guendalina Del, Rinaldi Laura, Menafra Davide, Feliciello Antonio, Colao Annamaria, Crescenzo Raffaella, Pivonello Rosario
Аннотация
OBJECTIVE: Obesity represents a global health problem with large costs for public health. Cabergoline (CAB), a potent dopamine agonist with a high affinity for type 2 dopamine receptor (D2R), usually used in clinical practice for hyperprolactinemia management, has been reported to significantly decrease metabolic syndrome prevalence and visceral adiposity associated with improved insulin sensitivity in prolactinoma patients. Nevertheless, scant data are reported about CAB effects on obesity condition.
METHODS: The current preclinical study investigated the in vivo chronic effects of CAB on obese rat models by exploring energy homeostasis and tissue molecular modifications. Simultaneously, the current study evaluated the in vitro chronic effects of CAB on adipocyte and myocyte models by investigating cellular lipid accumulation, respiration and glucose internalization.
RESULTS: The in vivo study demonstrated for the first time that CAB, chronically administered to an obese rat model, positively impacts body composition, energy balance, insulin secretion, and sensitivity and lipid profile, while outlining the molecular mechanisms fundamentally based on the reduction of the expression of the main markers of lipid accumulation and on the activation of the proteins classically involved in fat oxidation, PKA-Cα and pAMPKα Thr172. The in vitro study further demonstrated that the treatment with CAB, alone or in combination with insulin, significantly reduces lipid accumulation both in adipocytes and myocytes, confirming the in vivo results, by activating catabolic pathways, enhancing respiration in adipocytes and promoting glucose uptake in myocytes.
CONCLUSIONS: The current preclinical study demonstrated that chronic treatment with CAB improves obesity-associated metabolic disorders such as dyslipidemia and hyperinsulinemia, by regulating the expression of lipid accumulation markers and reducing skeletal muscle ectopic lipid accumulation.
METHODS: The current preclinical study investigated the in vivo chronic effects of CAB on obese rat models by exploring energy homeostasis and tissue molecular modifications. Simultaneously, the current study evaluated the in vitro chronic effects of CAB on adipocyte and myocyte models by investigating cellular lipid accumulation, respiration and glucose internalization.
RESULTS: The in vivo study demonstrated for the first time that CAB, chronically administered to an obese rat model, positively impacts body composition, energy balance, insulin secretion, and sensitivity and lipid profile, while outlining the molecular mechanisms fundamentally based on the reduction of the expression of the main markers of lipid accumulation and on the activation of the proteins classically involved in fat oxidation, PKA-Cα and pAMPKα Thr172. The in vitro study further demonstrated that the treatment with CAB, alone or in combination with insulin, significantly reduces lipid accumulation both in adipocytes and myocytes, confirming the in vivo results, by activating catabolic pathways, enhancing respiration in adipocytes and promoting glucose uptake in myocytes.
CONCLUSIONS: The current preclinical study demonstrated that chronic treatment with CAB improves obesity-associated metabolic disorders such as dyslipidemia and hyperinsulinemia, by regulating the expression of lipid accumulation markers and reducing skeletal muscle ectopic lipid accumulation.