Prolactin has evolved from being viewed solely as a lactogenic hormone to being recognized as a key regulator of maternal metabolic adaptation during pregnancy. However, clinical studies have reported apparently conflicting associations between circulating prolactin and gestational diabetes, maternal adiposity and metabolic health, limiting its clinical interpretation despite compelling experimental evidence for its metabolic effects. Experimental models demonstrate that prolactin receptor (Prlr) signalling regulates pregnancy-induced β-cell expansion and insulin secretion, adipose tissue remodelling and maternal energy allocation, while also contributing to the endocrine network governing calcium homeostasis and skeletal adaptation. By contrast, human studies show heterogeneous relationships between circulating prolactin and glucose homeostasis, gestational diabetes, adiposity and lipid metabolism, with limited evidence linking physiological prolactin concentrations to maternal bone remodelling. These discrepancies may partly reflect dynamic changes in prolactin across gestation and differences in maternal metabolic phenotype. Accounting for gestational timing and metabolic context may therefore improve the interpretation of circulating prolactin and help define its contribution to maternal metabolic adaptation across pregnancy and lactation.
Previous research suggests a possible association between obesity and behavioral addictions; however, findings remain inconsistent and the psychological mechanisms underlying this relationship remain poorly understood. This study examined the prevalence of overweight and obesity across different behavioral addictions (gambling disorder, internet gaming disorder, and compulsive buying-shopping disorder), compared sociodemographic, clinical, and psychological characteristics according to weight status, and explored pathways between personality, psychological distress, emotion dysregulation, food addiction, and body mass index (BMI). This cross-sectional study included 1,265 adults seeking treatment for behavioral addictions at a specialized public hospital. Sociodemographic variables, psychopathology, impulsivity, emotion regulation, personality features, and food addiction were assessed using validated psychometric instruments. Overweight and obesity were prevalent across behavioral addictions. Compared to participants without obesity, those with obesity were older, more frequently women, reported higher somatization and harm avoidance, lower sensation seeking, and greater food addiction symptomatology. Structural equation modeling showed that food addiction was the only direct statistical predictor of BMI, mediating indirect effects of impulsivity, harm avoidance, psychological distress, and emotion dysregulation. These findings suggest that features of food addiction may act as a link between emotional vulnerability and obesity across behavioral addictions, highlighting the importance of assessing food addiction symptomatology in clinical contexts .
Lysosomal storage diseases are inherited multisystem disorders caused by defects in lysosomal enzymes, transporters, or associated proteins, leading to intracellular substrate accumulation and progressive organ dysfunction. The thyroid gland may be particularly vulnerable because hormone release depends on thyroglobulin endocytosis, endosomal trafficking, lysosomal proteolysis, iodide recycling, and cellular proteostasis. This review summarizes current evidence on thyroid involvement in lysosomal storage diseases, with emphasis on clinical manifestations, pathophysiological mechanisms, diagnostic evaluation, and management. A literature search was performed in PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar from database inception through August 31, 2026. Eligible clinical, review, and experimental studies addressing thyroid function, morphology, autoimmunity, treatment effects, or bidirectional thyroid–lysosomal mechanisms were descriptively synthesized. The strongest association is observed in nephropathic cystinosis, in which progressive primary hypothyroidism is frequent and may be delayed by early cysteamine therapy. Thyroid abnormalities have also been reported in Fabry disease, Gaucher disease, Hurler syndrome, and Pompe disease, although evidence is less consistent and often based on small cohorts, isolated reports, or animal models. Proposed mechanisms include direct substrate accumulation, impaired thyroglobulin processing, altered autophagy and proteostasis, oxidative and inflammatory injury, microvascular dysfunction, and indirect effects of chronic systemic disease. Experimental evidence also suggests that thyroid hormones can modulate lysosomal activity, although clinical relevance remains unproven. Routine disease-specific surveillance is best supported in nephropathic cystinosis; in other lysosomal storage diseases, thyroid assessment should be individualized. Prospective multicenter studies and standardized screening protocols are needed to clarify prevalence, natural history, reversibility, and optimal management.
Glucose-dependent insulinotropic polypeptide is one of the principal incretin hormones involved in the regulation of glucose homeostasis, lipid metabolism, and adipocyte function. Increasing evidence indicates that its biological actions differ substantially between adipose tissue depots. The aim of this narrative review with a structured literature search was to summarize current evidence on the role of GIP in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), incorporating preclinical, clinical, and genetic data. Animal studies have demonstrated that VAT is characterized by higher expression of the GIP receptor (GIPR) and greater sensitivity to the lipogenic and proinflammatory effects of GIP. Activation of GIPR in VAT promotes lipid accumulation, inflammation, and insulin resistance. Conversely, pharmacological blockade or genetic deletion of GIPR confers protection against diet-induced obesity and leads to improvements in metabolic parameters. In SAT, GIP exerts more heterogeneous and metabolically context-dependent effects that differ according to insulin sensitivity and obesity status. Moreover, under specific conditions, GIP may promote lipolysis in SAT, distinguishing its actions in this depot from those observed in VAT. These observations may help explain the efficacy of dual and triple incretin receptor agonists, including tirzepatide and retatrutide, which produce significant improvements in body weight and metabolic outcomes. Collectively, current evidence supports a depot-specific and context-dependent role of GIP in adipose tissue biology and underscores the therapeutic potential of targeting the GIP/GIPR axis in obesity and metabolic disease.
Dysregulated eating in obesity and eating disorders (ED) is associated with complex relationships between peripheral hormonal signals and neurobehavioral characteristics. Ghrelin and its endogenous antagonist liver-expressed antimicrobial peptide–2 (LEAP2) have been implicated in the regulation of energy homeostasis and food intake, while trait impulsivity has been proposed as a transdiagnostic characteristic associated with dysregulated eating. This study aimed to integrate narrative evidence with exploratory empirical data to examine associations between ghrelin, LEAP2, and trait impulsivity in women with obesity, with and without ED, and to explore their associations with food addiction (FA) and eating psychopathology. A total of 164 adult women (67 with obesity, 35 with obesity + ED, 62 healthy controls) completed anthropometric assessments, fasting ghrelin and LEAP2 determinations, and psychometric measures of trait impulsivity, FA, and eating psychopathology. Group comparisons and exploratory structural equation modeling (SEM) were used to explore associations between endocrine and behavioral variables. Women with obesity (with or without ED) showed significantly lower ghrelin levels than controls, while LEAP2 concentrations did not differ between groups. Trait impulsivity and FA scores were higher in the obesity + ED group. Within this subgroup, SEM analyses identified positive associations of trait impulsivity and FA with eating psychopathology, while LEAP2 was positively associated with trait impulsivity and FA scores. Previous research has pointed to potential associations of ghrelin and LEAP2 with obesity and ED, as well as with behavioral characteristics related to dysregulated eating, although the available evidence remains limited and heterogeneous. In our study, ghrelin was lower in women with obesity, whereas LEAP2 did not differ between groups. The observed associations involving LEAP2 emerged only in the exploratory SEM analysis and should therefore be interpreted cautiously. These findings are hypothesis-generating and do not provide evidence of mechanistic or causal relationships. Further research in larger and longitudinal samples is needed to replicate these findings and clarify the relationships among endocrine and behavioral factors.
