Geanina Maria Bud

Hepatocrinology is an emerging interdisciplinary field that examines the bidirectional interactions between the liver and the endocrine system, emphasizing how hepatic dysfunction influences hormonal regulation and how endocrine disorders, in turn, shape liver metabolism, inflammation, and disease progression. This review summarizes current theoretical frameworks, including hepato-endocrine axes, hepatokine signaling, and multi-organ communication models, highlighting the liver’s role as a central endocrine hub. Key hepatic hormones, transport proteins, and hepatokines such as fetuin-A, fibroblast growth factor 21, and selenoprotein P are discussed in relation to metabolic disorders including metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction-associated steatohepatitis, polycystic ovary syndrome, diabetes, and advanced chronic liver disease. The review further explores hormonal axes involving the thyroid, pancreas, adrenal glands, parathyroids, and gonads, illustrating their complex interplay with hepatic physiology. Current challenges, such as limited long-term studies and therapeutic controversies, are examined alongside emerging directions involving hepatokine-targeted therapies, precision medicine, and microbiome-driven modulation. Understanding these interconnected pathways is essential for improving diagnostic accuracy, risk stratification, and therapeutic strategies in hepato-endocrine disorders.

Purpose: Obesity is a chronic multifactorial disease whose increasing prevalence cannot be fully explained by excessive caloric intake and sedentary behaviour alone. This review aimed to synthesize current evidence on the role of endocrine-disrupting chemicals (EDCs), particularly obesogenic EDCs, as potential environmental contributors to obesity-related phenotypes, with emphasis on their main classes, etiopathogenetic mechanisms and clinical implications. Methods: A structured literature analysis was conducted using PubMed, Web of Science and additional relevant scientific reports and governmental publications. Eligible sources included original research articles, systematic reviews, meta-analyses and authoritative reports addressing endocrine disruption, obesogens, obesity, metabolic dysfunction and related molecular mechanisms. Results: The review identified several major classes of obesogenic EDCs, including organotins, bisphenols, phthalates and persistent organic pollutants. These compounds have been linked to obesity-related phenotypes through overlapping mechanisms, including disruption of adipogenesis via estrogen receptor-dependent and independent pathways, PPARγ/RXR activation, altered adipokine signalling, neuroendocrine dysregulation across developmental stages, oxidative stress and pro-inflammatory activation, genetic and epigenetic alterations, gut microbiota-mediated effects and impaired thermoregulation through brown and beige adipose tissue dysfunction. EDC-associated obesity may contribute to metabolic, endocrine, cardiovascular, hepatic and reproductive complications. Conclusion: Obesogenic EDCs should be regarded as environmental contributors to obesity that act through interconnected molecular, cellular and systemic pathways. Their biological effects support the need for further mechanistic and epidemiological research, preventive strategies, public education and regulatory measures aimed at reducing exposure.