GLP-1 Receptor Analogs: Evidence Linking to Effect on Metabolic and Reproductive Functions in Patients with PCOS and Obesity.
Аннотация
<p>
Background
Polycystic ovary syndrome (PCOS) is a multifaceted hormonal disorder that impacts both metabolic functions and reproductive health in women. PCOS pathophysiology is characterized by insulin resistance and chronic inflammation, which contribute to disrupted gonadotropin secretion, elevated androgen levels, and irregular ovulation. There is a bidirectional relationship between obesity and PCOS. Obesity contributes to the pathophysiology of PCOS, particularly by exacerbating insulin resistance - a core feature of the condition. Insulin resistance can lead to further weight gain and hinder successful weight loss. Summary: According to the latest international guidelines, improving insulin sensitivity and promoting weight loss are key strategies in the effective management of PCOS. GLP-1 receptor analogs (GLP-1 RAs) are a group of agents that are used in type 2 diabetes mellitus to regulate blood glucose levels, in addition to being indicated for weight loss in obesity. Thus, GLP-1 RAs may play a role in the management of PCOS, both due to weight loss effect and through pleiotropic effects like ameliorating insulin resistance, decreasing inflammation, and modulation of adiposity. Key Messages: In light of these effects, this review aimed to perform a systematic search and narrative synthesis on the impact of GLP-1 receptor agonists (GLP-1 RAs) on the metabolic and reproductive outcomes in PCOS, with the goal of elucidating the mechanistic link between the action of GLP-1 RAs and the underlying pathophysiology of the condition. </p>.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
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.
Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.