Journal of endocrinological investigation · 2026
Neuroendocrine regulation of adipose partitioning in polyendocrine metabolic ovarian syndrome: the gut-brain-adipose axis.
СтатьяОбзорНазвание 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.
Gunesli Irmak, Aksun Seren, Yildiz Bulent Okan
Аннотация
PURPOSE: Polyendocrine Metabolic Ovarian Syndrome (PMOS), formerly polycystic ovary syndrome (PCOS), is a common, complex, and heterogeneous endocrine disorder characterized by reproductive and metabolic dysregulation that significantly increases long-term cardiometabolic risk. Growing evidence indicates that dysregulated adipose tissue partitioning, resulting in preferential visceral and ectopic fat accumulation, is a major determinant of metabolic dysfunction in PMOS. The presence of metabolic abnormalities in lean women with PMOS further suggests that mechanisms beyond obesity and total fat mass contribute to disease pathophysiology. This review aims to examine the potential role of gut-brain-adipose signaling in adipose tissue distribution and insulin resistance in PMOS.
METHODS: This narrative review synthesizes current evidence on the gut-brain-adipose axis and its potential role in adipose tissue distribution and metabolic dysfunction in PMOS, with particular emphasis on oxytocin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), leptin, and other gut- and adipose-derived mediators.
RESULTS: The gut-brain-adipose axis represents a neuroendocrine network regulating appetite, energy homeostasis, and adipose tissue function. Within this framework, oxytocin and glucagon-like peptide-1 (GLP-1), alongside gut- and adipose-derived mediators including glucose-dependent insulinotropic polypeptide (GIP), leptin, and other adipokines, may also contribute to these processes. Evidence demonstrating altered fasting and postprandial oxytocin and GLP-1 responses in women with PMOS suggests that impaired neuroendocrine signaling may be associated with dysregulated adipose partitioning and could contribute to visceral and ectopic fat accumulation and increasing metabolic risk.
CONCLUSION: This review discusses the gut-brain-adipose axis as a conceptual framework for understanding how neuroendocrine signaling influences adipose tissue distribution and insulin resistance in PMOS. Further understanding of the gut-brain-adipose axis may help identify potential therapeutic targets for improving metabolic health in women with PMOS.
METHODS: This narrative review synthesizes current evidence on the gut-brain-adipose axis and its potential role in adipose tissue distribution and metabolic dysfunction in PMOS, with particular emphasis on oxytocin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), leptin, and other gut- and adipose-derived mediators.
RESULTS: The gut-brain-adipose axis represents a neuroendocrine network regulating appetite, energy homeostasis, and adipose tissue function. Within this framework, oxytocin and glucagon-like peptide-1 (GLP-1), alongside gut- and adipose-derived mediators including glucose-dependent insulinotropic polypeptide (GIP), leptin, and other adipokines, may also contribute to these processes. Evidence demonstrating altered fasting and postprandial oxytocin and GLP-1 responses in women with PMOS suggests that impaired neuroendocrine signaling may be associated with dysregulated adipose partitioning and could contribute to visceral and ectopic fat accumulation and increasing metabolic risk.
CONCLUSION: This review discusses the gut-brain-adipose axis as a conceptual framework for understanding how neuroendocrine signaling influences adipose tissue distribution and insulin resistance in PMOS. Further understanding of the gut-brain-adipose axis may help identify potential therapeutic targets for improving metabolic health in women with PMOS.