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Search Results (143)

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20 pages, 994 KB  
Perspective
Endocrinology and the Lung: Exploring the Bidirectional Axis and Future Directions
by Pedro Iglesias
J. Clin. Med. 2025, 14(19), 6985; https://doi.org/10.3390/jcm14196985 - 2 Oct 2025
Viewed by 334
Abstract
The lung is increasingly recognized as an organ with dual endocrine and respiratory roles, participating in a complex bidirectional crosstalk with systemic hormones and local/paracrine activity. Endocrine and paracrine pathways regulate lung development, ventilation, immunity, and repair, while pulmonary cells express hormone receptors [...] Read more.
The lung is increasingly recognized as an organ with dual endocrine and respiratory roles, participating in a complex bidirectional crosstalk with systemic hormones and local/paracrine activity. Endocrine and paracrine pathways regulate lung development, ventilation, immunity, and repair, while pulmonary cells express hormone receptors and secrete mediators with both local and systemic effects, defining the concept of the “endocrine lung”. This narrative review summarizes current evidence on the endocrine–pulmonary axis. Thyroid hormones, glucocorticoids, sex steroids, and metabolic hormones (e.g., insulin, leptin, adiponectin) critically influence alveologenesis, surfactant production, ventilatory drive, airway mechanics, and immune responses. Conversely, the lung produces mediators such as serotonin, calcitonin gene-related peptide, endothelin-1, leptin, and keratinocyte growth factor, which regulate vascular tone, alveolar homeostasis, and immune modulation. We also describe the respiratory manifestations of major endocrine diseases, including obstructive sleep apnea and lung volume alterations in acromegaly, immunosuppression and myopathy in Cushing’s syndrome, hypoventilation in hypothyroidism, restrictive “diabetic lung”, and obesity-related phenotypes. In parallel, chronic pulmonary diseases such as chronic obstructive pulmonary disease, interstitial lung disease, and sleep apnea profoundly affect endocrine axes, promoting insulin resistance, hypogonadism, GH/IGF-1 suppression, and bone metabolism alterations. Pulmonary neuroendocrine tumors further highlight the interface, frequently presenting with paraneoplastic endocrine syndromes. Finally, therapeutic interactions are discussed, including the risks of hypothalamic–pituitary–adrenal axis suppression with inhaled corticosteroids, immunotherapy-induced endocrinopathies, and inhaled insulin. Future perspectives emphasize mapping pulmonary hormone networks, endocrine phenotyping of chronic respiratory diseases, and developing hormone-based interventions. Full article
(This article belongs to the Section Endocrinology & Metabolism)
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13 pages, 716 KB  
Article
Brain Monoamine Deficits in the CD Mouse Model of Williams–Beuren Syndrome
by Chloé Aman, Hélène Gréa, Alicia Rousseau, Anne-Emilie Allain, Susanna Pietropaolo, Philippe De Deurwaerdère and Valérie Lemaire
Biomolecules 2025, 15(10), 1382; https://doi.org/10.3390/biom15101382 - 28 Sep 2025
Viewed by 262
Abstract
Williams–Beuren Syndrome (WBS) is a rare neurodevelopmental disease caused by a microdeletion on chromosome 7 (7q11.23) and associated with behavioral disorders such as hypersociability, impaired visuospatial memory, anxiety, and motor disorders. The precise underlying neurobiological bases remain unknown. The CD mouse is a [...] Read more.
Williams–Beuren Syndrome (WBS) is a rare neurodevelopmental disease caused by a microdeletion on chromosome 7 (7q11.23) and associated with behavioral disorders such as hypersociability, impaired visuospatial memory, anxiety, and motor disorders. The precise underlying neurobiological bases remain unknown. The CD mouse is a genetic model that reproduces the deletion found in WBS patients on the equivalent mouse locus. Taking into account that monoaminergic systems are known to modulate behaviors that are altered in WBS, we hypothesized that CD mice could present quantitative and qualitative changes in brain noradrenaline, dopamine, and serotonin systems compared to wild-type (WT) littermates. We sampled 10 brain regions in female mice for quantifying monoamines and related compounds by high-performance liquid chromatography coupled to electrochemical detection. We found a decrease in dopamine in the nucleus accumbens and serotonin and its metabolites in the hypothalamus. Using correlative approaches of tissue content across the brain, we found that the relationships between neurotransmitters or their metabolic ratios (metabolite/neurotransmitter) changed in CD compared to WT. Notably, compared to WT, the ratios in CD mice showed striatal correlations for the serotonin/dopamine systems interaction, and cortical, thalamic, and hypothalamic correlations for the noradrenaline/dopamine systems interaction. The data suggest specific alterations of monoaminergic systems across the brain that could sustain the abnormal behavioral responses displayed by CD mice. Full article
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20 pages, 1331 KB  
Review
Sleep Disorders, Dysregulation of Circadian Rhythms, and Fatigue After Craniopharyngioma—A Narrative Review
by Hermann L. Müller
Biomedicines 2025, 13(10), 2356; https://doi.org/10.3390/biomedicines13102356 - 26 Sep 2025
Viewed by 361
Abstract
Introduction: Tumor- and/or treatment-associated hypothalamic damage results in reduced quality of life and increased morbidity due to sleep disorders in survivors of craniopharyngioma. Methods: The narrative review is based on a search of Web of Science, MEDLINE/PubMed, and Embase databases for [...] Read more.
Introduction: Tumor- and/or treatment-associated hypothalamic damage results in reduced quality of life and increased morbidity due to sleep disorders in survivors of craniopharyngioma. Methods: The narrative review is based on a search of Web of Science, MEDLINE/PubMed, and Embase databases for the identification of publications. The search terms craniopharyngioma, sleep disorders, fatigue, and daytime sleepiness were used. Selected English language papers published 1970–2025 were included. Results: Circadian rhythms (wakefulness and sleep) are controlled by hypothalamic suprachiasmatic nuclei and regulated by melatonin. A dysregulation of circadian rhythms due to altered melatonin secretion can be observed in craniopharyngioma with hypothalamic involvement. Furthermore, sleep quality is regulated by lateral hypothalamic areas, the ventrolateral preoptic nucleus, and monoaminergic nuclei which function as the arousal system. Flexible changes between sleep and wakefulness can be achieved through interaction of arousal and sleep-promoting systems named “flip–flop” switch. Insomnia can be the result of damage to the ventrolateral preoptic nucleus. Excessive daytime sleepiness and disrupted sleep patterns can be observed due to dysregulation of lateral hypothalamic areas. Obesity, chronic fatigue, headache, and excessive daytime sleepiness can be the result of poor sleep quality. “Primary” hypothalamic sleep dysfunction, including narcolepsy, dysregulated sleep–wake cycles, and hypersomnia, can be observed due to hypothalamic dysfunction. “Secondary” sleep disturbances including obstructive sleep apnea, insufficient substitution medication for arginine vasopressin deficiency (nocturia), or psychosocial factors are sequelae in patients with craniopharyngioma and hypothalamic lesions. Conclusions: Further research on novel treatment approaches for sleep disorders due to hypothalamic syndrome are warranted to improve the outcome after craniopharyngioma. Full article
(This article belongs to the Special Issue Pediatric Tumors: Diagnosis, Pathogenesis, Treatment, and Outcome)
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17 pages, 863 KB  
Review
When a Woman’s Heart Fails to Contain: Takotsubo Syndrome as a Gendered Collapse of Emotional Regulation
by Giuseppe Marano, Enrico Romagnoli, Giuseppe Biondi-Zoccai, Gianandrea Traversi, Osvaldo Mazza, Roberto Pola, Eleonora Gaetani and Marianna Mazza
Life 2025, 15(9), 1431; https://doi.org/10.3390/life15091431 - 12 Sep 2025
Viewed by 848
Abstract
Background: Takotsubo Syndrome (TTS), or stress-induced cardiomyopathy, is an acute and typically reversible cardiac condition that mimics acute coronary syndrome without obstructive coronary artery disease. Predominantly affecting postmenopausal women, TTS has been increasingly recognized as a psychobiological disorder involving neuroendocrine dysregulation, autonomic imbalance, [...] Read more.
Background: Takotsubo Syndrome (TTS), or stress-induced cardiomyopathy, is an acute and typically reversible cardiac condition that mimics acute coronary syndrome without obstructive coronary artery disease. Predominantly affecting postmenopausal women, TTS has been increasingly recognized as a psychobiological disorder involving neuroendocrine dysregulation, autonomic imbalance, psychosocial stress, and gendered patterns of emotional regulation. This review aimed to synthesize multidisciplinary evidence to propose an integrative, gender-informed model of TTS. Methods: A narrative literature review was conducted using PubMed/MEDLINE, Scopus, and Web of Science (2000–2025) to identify clinical, neurobiological, psychosocial, and psychoanalytic studies addressing sex/gender differences, psychiatric comorbidities, and emotional regulation in TTS. Results: Evidence indicates that catecholamine surge, hypothalamic–pituitary–adrenal axis dysregulation, estrogen deficiency, and autonomic imbalance provide a biological substrate for stress-induced myocardial stunning. Psychosocial factors, such as caregiving burden, chronic stress, and alexithymia, further decrease resilience. Gendered coping scripts and unconscious symbolic processes may amplify vulnerability and influence clinical presentation. The integrative model combines biological, psychological, and social mechanisms, highlighting the predominance of emotional triggers in women and worse in-hospital outcomes in men. Conclusions: TTS should be approached as both a cardiac and affective disorder. Gender-sensitive, multidisciplinary management, including psychiatric screening, psychocardiology interventions, and psychoanalytically informed care, may improve prevention, diagnosis, and patient outcomes. Full article
(This article belongs to the Special Issue Current and Future Perspectives of Takotsubo Syndrome)
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17 pages, 631 KB  
Review
Linking Psychological Stress to Epigenetic Regulation via the Gut–Liver–Brain Axis in Irritable Bowel Syndrome and Metabolic Dysfunction-Associated Fatty Liver Disease
by Annachiara Crocetta, Maria-Anna Giannelou, Agata Benfante, Lorys Castelli and Lemonica Koumbi
Livers 2025, 5(3), 43; https://doi.org/10.3390/livers5030043 - 5 Sep 2025
Viewed by 1702
Abstract
Irritable Bowel Syndrome (IBS) and Metabolic dysfunction-associated fatty liver disease (MAFLD) have traditionally been viewed as disorders of distinct organ systems. IBS is a gut–brain axis disorder characterized by abdominal pain, altered bowel habits, and psychological comorbidities. MAFLD, recently redefined to emphasize its [...] Read more.
Irritable Bowel Syndrome (IBS) and Metabolic dysfunction-associated fatty liver disease (MAFLD) have traditionally been viewed as disorders of distinct organ systems. IBS is a gut–brain axis disorder characterized by abdominal pain, altered bowel habits, and psychological comorbidities. MAFLD, recently redefined to emphasize its metabolic underpinnings, is the hepatic manifestation of systemic metabolic dysfunction. Growing evidence suggests that these conditions share overlapping pathophysiological mechanisms linked through disruption of the gut–liver–brain axis (GLBA), including psychological stress, gut dysbiosis, impaired intestinal permeability, systemic inflammation, and altered neuroendocrine signaling. Neuroimaging studies further reveal functional alterations in brain regions responsible for interoception, emotional regulation, and stress responsiveness in both disorders. This narrative review explores how psychological distress influences the onset and progression of IBS and MAFLD via GLBA dysfunction and stress-induced epigenetic reprogramming. A targeted literature search of major biomedical databases, supplemented by manual screening, identified relevant observational, clinical, neuroimaging, and molecular studies. Findings indicate that chronic psychological distress activates the hypothalamic–pituitary–adrenal (HPA) axis, elevates cortisol, disrupts gut microbiota, and reduces vagal tone; amplifying intestinal permeability and microbial translocation. These changes promote hepatic inflammation and gastrointestinal symptoms. Stress-related epigenetic modifications further impair GLBA communication, while psychological and lifestyle interventions may reverse some of these molecular imprints. Recognizing the shared neuromodulation and epigenetic mechanisms that link IBS and MAFLD opens promising avenues for integrated therapeutic strategies targeting the GLBA to improve outcomes across both conditions. Full article
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23 pages, 749 KB  
Review
The Hypothalamic Nuclei Implicated in the Regulation of Polycystic Ovary Syndrome: A Review of Its Clinical, Metabolic, and Endocrine Aspects
by Elizabeth Vieyra, Carlos-Camilo Silva, Rosa Linares, Gabriela Rosas, Julieta-Azucena Espinoza, Andrea Chaparro, Roberto Calderón, Belinda de la Peña and Leticia Morales-Ledesma
Molecules 2025, 30(16), 3407; https://doi.org/10.3390/molecules30163407 - 18 Aug 2025
Viewed by 1108
Abstract
Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by a clinical and/or biochemical hyperandrogenism. In addition, PCOS is also associated with the presence of ovarian cysts, anovulation, and menstrual abnormalities such as oligomenorrhea or amenorrhea. The aetiology of the syndrome [...] Read more.
Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by a clinical and/or biochemical hyperandrogenism. In addition, PCOS is also associated with the presence of ovarian cysts, anovulation, and menstrual abnormalities such as oligomenorrhea or amenorrhea. The aetiology of the syndrome is multifactorial and heterogeneous due to the interaction of genetic, hormonal, metabolic, and environmental factors, as well as the different phenotypes and responses to treatments exhibited by the patients. Considering this complex interaction, it is essential to continue with the research focused on the mechanisms involved in the development and maintenance of the pathology. The alteration in the pulsatile secretion of the gonadotropin-releasing hormone (GnRH) is considered to be one of the main causes that contributes to its onset. In this review, we discuss recent evidence about the role of the rostral periventricular area of the third ventricle (RP3V), the arcuate nucleus (ARC), and the ventromedial nucleus of the hypothalamus (VMH), key hypothalamic regions that regulate GnRH secretion, in the development of PCOS. In addition, we analyse the clinical, metabolic, and endocrine factors that interact in the patients with PCOS, offering a multifactorial perspective to improve our understanding of this disorder. Full article
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16 pages, 575 KB  
Article
Polycystic Ovary Syndrome Attenuates TSH-Lowering Effect of Metformin in Young Women with Subclinical Hypothyroidism
by Robert Krysiak, Karolina Kowalcze, Johannes Ott, Sofia Burgio, Simona Zaami and Bogusław Okopień
Pharmaceuticals 2025, 18(8), 1149; https://doi.org/10.3390/ph18081149 - 1 Aug 2025
Viewed by 1038
Abstract
Background/Objectives: The effect of metformin on the secretory function of thyrotropic cells is sex-dependent. The current study aimed to investigate whether the impact of this drug on activity of the hypothalamic–pituitary–thyroid axis in women is impacted by the androgen status of patients. Methods: [...] Read more.
Background/Objectives: The effect of metformin on the secretory function of thyrotropic cells is sex-dependent. The current study aimed to investigate whether the impact of this drug on activity of the hypothalamic–pituitary–thyroid axis in women is impacted by the androgen status of patients. Methods: The study population included 48 levothyroxine-naïve reproductive-aged women with subclinical hypothyroidism and prediabetes receiving 3.0 g of metformin daily. Women with (n = 24) and without (n = 24) polycystic ovary syndrome were matched for age, insulin sensitivity, TSH, and reasons for thyroid hypofunction. Circulating levels of glucose, glycated hemoglobin, insulin, TSH, thyroid hormones, gonadotropins, androgens, estradiol, SHBG, prolactin, ACTH, and IGF-1 were measured before metformin treatment and six months later. Results: At entry, women with and without polycystic ovary syndrome differed in LH, LH/FSH ratio, androgens, and estradiol. The decrease in TSH, fasting glucose and glycated hemoglobin, and the improvement in insulin sensitivity were less pronounced in women with than in women without polycystic ovary syndrome. In each group, there were no differences in the impact on TSH and thyroid hormones between patients with subclinical hypothyroidism of autoimmune and non-autoimmune origin. The changes in TSH inversely correlated with total testosterone and free androgen index. Only in women with coexisting polycystic ovary syndrome, did metformin slightly reduce LH, LH/FSH ratio, testosterone, and free androgen index. Conclusions: The results suggest that concurrent polycystic ovary syndrome attenuates metformin action on TSH secretion, which can be explained by increased androgen production. Moreover, the drug seems to alleviate PCOS-associated changes in the activity of the reproductive axis. Full article
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17 pages, 1772 KB  
Article
Exploration of the Possible Relationships Between Gut and Hypothalamic Inflammation and Allopregnanolone: Preclinical Findings in a Post-Finasteride Rat Model
by Silvia Diviccaro, Roberto Oleari, Federica Amoruso, Fabrizio Fontana, Lucia Cioffi, Gabriela Chrostek, Vera Abenante, Jacopo Troisi, Anna Cariboni, Silvia Giatti and Roberto Cosimo Melcangi
Biomolecules 2025, 15(7), 1044; https://doi.org/10.3390/biom15071044 - 18 Jul 2025
Viewed by 3503
Abstract
Background: Finasteride, a 5α-reductase inhibitor commonly prescribed for androgenetic alopecia, has been linked to persistent adverse effects after discontinuation, known as post-finasteride syndrome (PFS). Symptoms include neurological, psychiatric, sexual, and gastrointestinal disturbances. Emerging evidence suggests that PFS may involve disruption of sex steroid [...] Read more.
Background: Finasteride, a 5α-reductase inhibitor commonly prescribed for androgenetic alopecia, has been linked to persistent adverse effects after discontinuation, known as post-finasteride syndrome (PFS). Symptoms include neurological, psychiatric, sexual, and gastrointestinal disturbances. Emerging evidence suggests that PFS may involve disruption of sex steroid homeostasis, neuroactive steroid deficiency (notably allopregnanolone, ALLO), and gut–brain axis alterations. Objective: This study aimed to investigate the effects of finasteride withdrawal (FW) in a rat model and evaluate the potential protective effects of ALLO on gut and hypothalamic inflammation. Methods: Adult male Sprague Dawley rats were treated with finasteride for 20 days, followed by one month of drug withdrawal. A subgroup received ALLO treatment during the withdrawal. Histological, molecular, and biochemical analyses were performed on the colon and hypothalamus. Gut microbiota-derived metabolites and markers of neuroinflammation and blood–brain barrier (BBB) integrity were also assessed. Results: At FW, rats exhibited significant colonic inflammation, including a 4.3-fold increase in Mφ1 levels (p < 0.001), a 2.31-fold decrease in butyrate concentration (p < 0.01), and elevated hypothalamic GFAP and Iba-1 protein expression (+360%, p < 0.01 and +100%, p < 0.01, respectively). ALLO treatment rescued these parameters in both the colon and hypothalamus but only partially restored mucosal and BBB structural integrity, as well as the NF-κB/PPARγ pathway. Conclusions: This preclinical study shows that FW causes inflammation in both the gut and hypothalamus in rats. ALLO treatment helped reduce several of these effects. These results suggest ALLO could have a protective role and have potential as a treatment for PFS patients. Full article
(This article belongs to the Section Molecular Medicine)
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24 pages, 336 KB  
Review
Molecular Shadows of Per- and Polyfluoroalkyl Substances (PFASs): Unveiling the Impact of Perfluoroalkyl Substances on Ovarian Function, Polycystic Ovarian Syndrome (PCOS), and In Vitro Fertilization (IVF) Outcomes
by Charalampos Voros, Diamantis Athanasiou, Ioannis Papapanagiotou, Despoina Mavrogianni, Antonia Varthaliti, Kyriakos Bananis, Antonia Athanasiou, Aikaterini Athanasiou, Georgios Papadimas, Athanasios Gkirgkinoudis, Kyriaki Migklis, Dimitrios Vaitsis, Aristotelis-Marios Koulakmanidis, Charalampos Tsimpoukelis, Sofia Ivanidou, Anahit J. Stepanyan, Maria Anastasia Daskalaki, Marianna Theodora, Panagiotis Antsaklis, Dimitrios Loutradi and Georgios Daskalakisadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2025, 26(14), 6604; https://doi.org/10.3390/ijms26146604 - 10 Jul 2025
Cited by 1 | Viewed by 1424
Abstract
Per- and polyfluoroalkyl substances (PFASs) comprise a diverse array of synthetic chemicals that resist environmental degradation. They are increasingly recognised as endocrine-disrupting compounds (EDCs). These chemicals, found in non-stick cookware, food packaging, and industrial waste, accumulate in human tissues and fluids, raising substantial [...] Read more.
Per- and polyfluoroalkyl substances (PFASs) comprise a diverse array of synthetic chemicals that resist environmental degradation. They are increasingly recognised as endocrine-disrupting compounds (EDCs). These chemicals, found in non-stick cookware, food packaging, and industrial waste, accumulate in human tissues and fluids, raising substantial concerns regarding their impact on female reproductive health. Epidemiological studies have demonstrated associations between PFAS exposure and reduced fertility; nevertheless, the underlying molecular pathways remain inadequately understood. This narrative review investigates the multifaceted effects of PFASs on ovarian physiology, including its disruption of the hypothalamic–pituitary–ovarian (HPO) axis, alteration of anti-Müllerian hormone (AMH) levels, folliculogenesis, and gonadotropin receptor signalling. Significant attention is directed towards the emerging association between PFASs and polycystic ovarian syndrome (PCOS), wherein PFAS-induced hormonal disruption may exacerbate metabolic issues and elevated androgen levels. Furthermore, we analyse the current data regarding PFAS exposure in women undergoing treatment based on assisted reproductive technologies (ARTs), specifically in vitro fertilisation (IVF), highlighting possible associations with diminished oocyte quality, suboptimal embryo development, and implantation failure. We examine potential epigenetic and transgenerational alterations that may influence women’s reproductive capabilities over time. This study underscores the urgent need for further research and regulatory actions to tackle PFAS-related reproductive toxicity, particularly in vulnerable populations, such as women of reproductive age and those receiving fertility treatments. Full article
(This article belongs to the Special Issue Molecular Advances in Obstetrical and Gynaecological Disorders)
15 pages, 1361 KB  
Review
Gut Microbiome Dysbiosis and Its Impact on Reproductive Health: Mechanisms and Clinical Applications
by Efthalia Moustakli, Sofoklis Stavros, Periklis Katopodis, Anastasios Potiris, Peter Drakakis, Stefanos Dafopoulos, Athanasios Zachariou, Konstantinos Dafopoulos, Konstantinos Zikopoulos and Athanasios Zikopoulos
Metabolites 2025, 15(6), 390; https://doi.org/10.3390/metabo15060390 - 11 Jun 2025
Cited by 3 | Viewed by 2179
Abstract
The human gut microbiome is integral to maintaining systemic physiological balance, with accumulating evidence emphasizing its critical role in reproductive health. This review investigates the bidirectional interactions between the gut microbiota and the female reproductive system, mediated by neuroendocrine, immune, and metabolic pathways, [...] Read more.
The human gut microbiome is integral to maintaining systemic physiological balance, with accumulating evidence emphasizing its critical role in reproductive health. This review investigates the bidirectional interactions between the gut microbiota and the female reproductive system, mediated by neuroendocrine, immune, and metabolic pathways, constituting the gut–reproductive axis. Dysbiosis, characterized by microbial imbalance, has been linked to reproductive disorders such as polycystic ovary syndrome (PCOS), endometriosis, infertility, impaired spermatogenesis, and pregnancy complications. These associations can be explained by immunological dysregulation, systemic inflammation, altered sex hormone metabolism, and hypothalamic–pituitary–gonadal (HPG) axis disturbances. This review aims to clarify the molecular and cellular mechanisms underpinning gut–reproductive interactions and to evaluate the feasibility of microbiome-targeted therapies as clinical interventions for improving reproductive outcomes. Full article
(This article belongs to the Section Endocrinology and Clinical Metabolic Research)
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29 pages, 9570 KB  
Article
Neurotransmission Sex Dichotomy in the Rat Hypothalamic Paraventricular Nucleus in Healthy and Infantile Spasm Model
by Dumitru Andrei Iacobas, Jana Veliskova, Tamar Chachua, Chian-Ru Chern, Kayla Vieira, Sanda Iacobas and Libor Velíšek
Curr. Issues Mol. Biol. 2025, 47(5), 380; https://doi.org/10.3390/cimb47050380 - 21 May 2025
Cited by 2 | Viewed by 882
Abstract
We profiled the gene expressions in the hypothalamic paraventricular nuclei of 12 male and 12 female pups from a standard rat model of infantile spasms to determine the sex dichotomy of the neurotransmission genomic fabrics. Infantile spasms were triggered in rat pups prenatally [...] Read more.
We profiled the gene expressions in the hypothalamic paraventricular nuclei of 12 male and 12 female pups from a standard rat model of infantile spasms to determine the sex dichotomy of the neurotransmission genomic fabrics. Infantile spasms were triggered in rat pups prenatally primed with two doses of betamethasone followed by the postnatal repeated administration of N-methyl-D-aspartic acid to induce spasms. Publicly available microarray data were used to characterize each gene in each condition for both sexes by the independent transcriptomic features: average expression level, control of the transcript abundance, and expression correlation with every other gene. This study revealed substantial sex differences in the expression level, control, and inter-coordination of the investigated genes among the studied groups. The transcriptomic differences assist in providing a molecular explanation of the behavioral differences and development of infantile epilepsy spasm syndrome in the two sexes. Full article
(This article belongs to the Special Issue Molecules at Play in Neurological Diseases)
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18 pages, 1980 KB  
Review
Autoantibodies Targeting the Hypothalamic-Pituitary-Ovarian Axis in Polycystic Ovary Syndrome: Emerging Key Players in Pathogenesis?
by Nicole Akpang, Jakub Kwiatkowski, Lucja Zaborowska and Artur Ludwin
Int. J. Mol. Sci. 2025, 26(9), 4121; https://doi.org/10.3390/ijms26094121 - 26 Apr 2025
Cited by 4 | Viewed by 2297
Abstract
Polycystic ovary syndrome (PCOS) is a common female endocrinopathy associated with reproductive and metabolic abnormalities. PCOS is characterized by complex pathogenesis and pathophysiology. Its multifactorial etiology and heterogeneous presentation make effective treatment difficult. Endocrine abnormalities in PCOS create a vicious cycle of overriding [...] Read more.
Polycystic ovary syndrome (PCOS) is a common female endocrinopathy associated with reproductive and metabolic abnormalities. PCOS is characterized by complex pathogenesis and pathophysiology. Its multifactorial etiology and heterogeneous presentation make effective treatment difficult. Endocrine abnormalities in PCOS create a vicious cycle of overriding dysfunction involving the hypothalamic-pituitary-ovarian (HPO) axis. Most research has primarily focused on identifying genetic, epigenetic, or immunological factors underlying PCOS. In recent years, new reports have emerged on the possible involvement of antibodies directed against HPO axis components in the development of PCOS. Some of these have been shown to be able to interfere with hormone receptors or receptor binding by targeting the key domains for their function. However, the evidence is heterogeneous and challenging to interpret, given the overall predisposition to high levels of various autoantibodies found in women with PCOS. This review focuses on autoantibodies affecting the HPO axis in PCOS and their potential role in the pathogenesis of PCOS. The authors discuss PCOS as a potential antibody-mediated autoimmune disease in light of recent reports on its possible pathogenesis. Full article
(This article belongs to the Section Molecular Endocrinology and Metabolism)
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19 pages, 1804 KB  
Review
Management of Acquired Hypothalamic Obesity After Childhood-Onset Craniopharyngioma—A Narrative Review
by Hermann L. Müller
Biomedicines 2025, 13(5), 1016; https://doi.org/10.3390/biomedicines13051016 - 22 Apr 2025
Cited by 1 | Viewed by 2325
Abstract
Introduction: Craniopharyngiomas are rare sellar embryonic malformational tumors of low-grade histological malignancy. Despite high overall survival rates (92%), quality of life is frequently reduced due to adverse late effects caused by hypothalamic obesity. It is well known that morbid hypothalamic obesity is [...] Read more.
Introduction: Craniopharyngiomas are rare sellar embryonic malformational tumors of low-grade histological malignancy. Despite high overall survival rates (92%), quality of life is frequently reduced due to adverse late effects caused by hypothalamic obesity. It is well known that morbid hypothalamic obesity is associated with the grade of hypothalamic damage. Accordingly, craniopharyngioma should be considered a paradigmatic disease, reflecting challenges in the diagnosis and treatment of acquired hypothalamic obesity. Methods: A narrative review was performed after searching the MEDLINE/PubMed, Embase, and Web of Science databases for initial identifying articles. The search terms childhood-onset craniopharyngioma and hypothalamic obesity were used. Results: Despite the availability of promising therapeutic approaches, such as medication with central stimulating agents, antidiabetic drugs, glucagon-like peptide 1 (GLP1) receptor agonists, and Setmelanotide, it must be emphasized that there is currently no pharmaceutical treatment for hypothalamic obesity in craniopharyngioma proven to be effective in randomized controlled trials. For Setmelanotide, a prospective blinded randomized trial over a 12-month treatment period is ongoing. Bariatric interventions are effective, but non-reversible procedures such as bypass operations are controversial in the pediatric age group due to legal and ethical concerns. Recently, a treatment algorithm was introduced to improve the management of hypothalamic syndrome/obesity by offering more personalized treatment. Decisions on treatment strategies focusing on the preservation of visual, neuroendocrine, and hypothalamic integrity should be made by experienced multidisciplinary teams. Conclusions: Treatment approaches for hypothalamic obesity are limited. Further research on novel treatment approaches for hypothalamic obesity is warranted to improve the quality of life after childhood-onset craniopharyngioma. Full article
(This article belongs to the Special Issue Feature Reviews on Cardiovascular and Metabolic Diseases)
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14 pages, 316 KB  
Review
The Role of the Arcuate Nucleus in Regulating Hunger and Satiety in Prader-Willi Syndrome
by Charlotte Höybye and Maria Petersson
Curr. Issues Mol. Biol. 2025, 47(3), 192; https://doi.org/10.3390/cimb47030192 - 14 Mar 2025
Cited by 1 | Viewed by 2500
Abstract
Prader-Willi syndrome (PWS) is a rare genetic disorder. The main characteristics are muscular hypotonia, failure to thrive and feeding problems in infancy, which switch to hyperphagia in early childhood and continue into adulthood. Due to hyperphagia, the risk of developing morbid obesity is [...] Read more.
Prader-Willi syndrome (PWS) is a rare genetic disorder. The main characteristics are muscular hypotonia, failure to thrive and feeding problems in infancy, which switch to hyperphagia in early childhood and continue into adulthood. Due to hyperphagia, the risk of developing morbid obesity is high without treatment. PWS is considered a hypothalamic disease, and within the hypothalamus the arcuate nucleus (AC) is of central importance for controlling metabolism, hunger, and satiety. The AC has been studied in several animal models as well as in humans, including PWS. The function of AC is regulated by several neuropeptides and proteins produced within the central nervous system such as oxytocin, orexin, tachykinins as well as the hypothalamic hormones, regulating the adeno-hypophyseal hormones, also acting as neurotransmitters. Additionally, there are many peripheral hormones among which insulin, leptin, adiponectin, ghrelin, and glucagon-like peptide (GLP-1) are the most important. High levels of adiponectin and ghrelin have consistently been reported in PWS, but dysregulation and deviating levels of many other factors and hormones have also been demonstrated in both individuals with PWS and in animal models. In this review, we focus on the role of AC and peptides and proteins produced within the central nervous system in the regulation of hunger and satiety in PWS. Full article
(This article belongs to the Special Issue Current Advances in Oxytocin Research)
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18 pages, 682 KB  
Review
Trilostane: Beyond Cushing’s Syndrome
by Ali R. Olaimat, Parastoo Jafarzadehbalagafsheh, Mohammad Gol, Anna-Maria Costa, Giuseppe Biagini and Chiara Lucchi
Animals 2025, 15(3), 415; https://doi.org/10.3390/ani15030415 - 2 Feb 2025
Cited by 2 | Viewed by 3345
Abstract
Trilostane is a drug able to block the synthesis of progesterone from pregnenolone, dependent on the enzyme 3β-hydroxysteroid dehydrogenase/Δ5−4 isomerase. As a consequence of this effect, it is used to treat endocrinological diseases such as Cushing’s syndrome, especially in dogs. Because of [...] Read more.
Trilostane is a drug able to block the synthesis of progesterone from pregnenolone, dependent on the enzyme 3β-hydroxysteroid dehydrogenase/Δ5−4 isomerase. As a consequence of this effect, it is used to treat endocrinological diseases such as Cushing’s syndrome, especially in dogs. Because of the modulatory effects of trilostane on the hypothalamic–pituitary–adrenal axis, trilostane administration causes an increase in brain levels of neurosteroids with anticonvulsant properties, as in the case of allopregnanolone. Allopregnanolone is also of interest in curing depression, suggesting that trilostane might represent a tool to address neurological and psychiatric disorders. In this review, we investigated the historical development of this drug and its current use, mechanisms, and possible developments. By searching the literature from 1978 to 2025, we identified 101 papers describing studies with trilostane. Precisely, 55 were about dogs and trilostane, 3 were on cats, and 23 were with other animals. Some studies (15) were also designed with human patients. The main disease treatment with trilostane was hyperadrenocorticism. However, we also found two preclinical papers on trilostane’s potential use in psychiatric diseases and three on trilostane’s potential use in neurological disorders. Moreover, few clinical and preclinical studies suggested the involvement of neurosteroids modulated by trilostane in different neurological disorders, thus opening a possible new perspective for the use of this drug. Full article
(This article belongs to the Section Animal Welfare)
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