{"title":"Bone mineralisation and glucose metabolism","authors":"Fiona L. Roberts , Vicky E. MacRae","doi":"10.1016/j.coemr.2023.100446","DOIUrl":"10.1016/j.coemr.2023.100446","url":null,"abstract":"<div><p>Recent advancements in the bone biology field have identified a novel bone-metabolism axis. In this review, we highlight several novel studies that further our knowledge of new endocrine functions of bone; explore remaining unanswered questions; and discuss translational challenges in this complex era of bone biology research.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"29 ","pages":"Article 100446"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41390103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Giulia Lanzolla , Mohd Parvez Khan , Elena Sabini , Amato Giaccia , Ernestina Schipani
{"title":"Erythropoietin and skeletal cells crosstalks in physiology and disease","authors":"Giulia Lanzolla , Mohd Parvez Khan , Elena Sabini , Amato Giaccia , Ernestina Schipani","doi":"10.1016/j.coemr.2023.100436","DOIUrl":"10.1016/j.coemr.2023.100436","url":null,"abstract":"<div><p><span>The hypoxia-inducible factor 2alpha (HIF-2), which is a member of the HIF family of transcription factors and a critical component of the hypoxia-driven pathway, regulates adult erythropoiesis through the renal production and secretion of </span>erythropoietin<span><span> (EPO). Notably, circulating EPO also affects bone mass through either direct or indirect actions on osteoblastic and osteoclastic cells. Adding complexity to the picture, we have recently reported that osteoblastic cells produce and secrete EPO upon activation of HIF-2. Although physiological role of osteoblastic EPO in controlling hematopoiesis remains to be determined, our findings could have translational implications for the </span>treatment of anemia.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"29 ","pages":"Article 100436"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43327511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recent basic and clinical findings concerning FGF23: A bone-derived hormone","authors":"Seiji Fukumoto","doi":"10.1016/j.coemr.2023.100445","DOIUrl":"10.1016/j.coemr.2023.100445","url":null,"abstract":"<div><p><span>FGF23<span> is essential for the regulation of serum phosphate level and the aberrant actions of FGF23 cause hypophosphatemic or hyperphosphatemic </span></span>diseases<span>. The objective of this review is to provide a current and relevant summary of the recent basic and clinical findings concerning FGF23. Recent findings: Many factors have been shown to affect FGF23 production while the precise roles of these factors in phosphate metabolism are largely unknown. Anti-FGF23 antibody has become clinically available, and the efficacy of this antibody has been reported in several hypophosphatemic diseases caused by excessive actions of FGF23.Summary: The identification of FGF23 came to the development of a new therapy for hypophosphatemic diseases. Still, there are many unanswered questions concerning FGF23.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"29 ","pages":"Article 100445"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45932922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Endocrine functions of sclerostin","authors":"Ryan C. Riddle","doi":"10.1016/j.coemr.2022.100433","DOIUrl":"10.1016/j.coemr.2022.100433","url":null,"abstract":"<div><p>Sclerostin, the product of the <em>SOST</em> gene has primarily been studied for its profound impact on bone mass. By interacting with LRP5 and LRP6, the glycoprotein suppresses the propagation of Wnt signals to β-catenin and thereby suppresses new bone formation. In this review, we discuss emerging data which suggest that sclerostin also acts outside the skeleton to influence metabolism. In humans, serum sclerostin levels are associated with body mass index and indices of metabolic function. Likewise, genetic mouse models of <em>Sost</em> gene deficiency indicate sclerostin influences adipocyte development and insulin signaling. These data raise the possibility that sclerostin neutralization may be effective at treating two epidemic conditions: osteoporosis and obesity.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"28 ","pages":"Article 100433"},"PeriodicalIF":0.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9881182/pdf/nihms-1859916.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9169542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Premature ovarian insufficiency","authors":"Ekta Kapoor","doi":"10.1016/j.coemr.2023.100435","DOIUrl":"10.1016/j.coemr.2023.100435","url":null,"abstract":"<div><p><span>Natural menopause typically occurs between the ages of 46–55 years. Premature ovarian insufficiency<span> or premature menopause<span> results from compromised ovarian follicular activity, occurring spontaneously or because of medical interventions, prior to the age of 40 years. The premature loss of estrogen leads to bothersome menopause symptoms and predisposes the women to multiple long-term health risks including a higher mortality risk. Hormone replacement therapy used until the natural age of menopause can help manage the symptoms effectively, and can mitigate the long-term risk of estrogen deprivation. However, hormone replacement therapy is underutilized in this population due to the inappropriate extrapolation of potential risks observed with </span></span></span>hormone therapy use in women after natural menopause. There is a large unmet need for educating patients and providers regarding the impact of premature ovarian insufficiency and its appropriate management.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"28 ","pages":"Article 100435"},"PeriodicalIF":0.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10022589/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9145858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"How preclinical models of menopause can inform clinical care: A focus on midlife and reciprocal communication between clinical and preclinical science","authors":"Heather A. Bimonte-Nelson , Victoria E. Bernaud","doi":"10.1016/j.coemr.2023.100434","DOIUrl":"10.1016/j.coemr.2023.100434","url":null,"abstract":"<div><p>Midlife in women typically includes the menopausal transition<span>, a time of hormonal transformation, adaptation, and reorganization. Coincident with this dynamic period of physiological change, there are putatively modifiable factors that influence disease, short-term and long-term health outcomes, symptom emergence, and longevity. The menopause transition could be considered a window of vulnerability; however, it is also a window of opportunity for intervention. Thus, the menopause transition is a critical sensitive window whereby there is opportunity for turning points for healthy aging trajectories. Preclinical research can aid in this pursuit of scientific discovery for modifiable factors and treatments, and their particular parameters. Rodent menopause models include surgical and transitional variations, allowing detection of precise determinants impacting menopause-related outcomes. These models permit systematic manipulation of endogenous and exogenous hormone exposures across the lifespan, with infinite outcome measurements ranging from molecular to behavioral. This research is uniquely poised to address complex, interactive hypotheses with extensive control in a relatively short timeframe, including dissociation of age and menopause effects. To understand the many dynamic changes with menopause, iterative and reciprocal communication between clinical and preclinical domains of science is key.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"28 ","pages":"Article 100434"},"PeriodicalIF":0.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46112513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Glucocorticoid action in osteoblasts and systemic energy metabolism","authors":"Hong Zhou , Markus J. Seibel","doi":"10.1016/j.coemr.2022.100432","DOIUrl":"10.1016/j.coemr.2022.100432","url":null,"abstract":"<div><p><span><span>Glucocorticoids are pleiotropic hormones with potent regulatory roles in tissue </span>homeostasis<span><span>, electrolyte balance, immune defence, central nervous function, stress response, </span>growth and development, as well as fuel metabolism. Clinically, glucocorticoids are widely used for their unsurpassed anti-inflammatory and immunomodulatory effects. However, chronic exposure to excessive levels of endogenous or exogenous glucocorticoids causes insulin resistance, glucose intolerance, </span></span>dyslipidaemia<span>, central obesity, muscle wasting<span><span> and bone loss. Topical studies in rodents have demonstrated that the effects of chronic </span>hypercortisolism<span><span> on systemic fuel metabolism and body composition are in part mediated through their actions on osteoblasts. Interestingly, targeted abrogation of glucocorticoid signalling in osteoblasts also attenuates the effects of high </span>fat intake<span> as well as ageing on body composition and systemic fuel metabolism. Here we briefly review the physiology of glucocorticoid action and discuss emerging concepts regarding the molecular mechanisms underlying the adverse effects of glucocorticoid excess.</span></span></span></span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"28 ","pages":"Article 100432"},"PeriodicalIF":0.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49172988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Modelling KNDy neurons and gonadotropin-releasing hormone pulse generation","authors":"Zoe Plain , Margaritis Voliotis , Craig A. McArdle , Krasimira Tsaneva-Atanasova","doi":"10.1016/j.coemr.2022.100407","DOIUrl":"10.1016/j.coemr.2022.100407","url":null,"abstract":"<div><p>The pulsatile release of gonadotropin-releasing hormone (GnRH) and its frequency are crucial for healthy reproductive function. To understand what drives GnRH pulses, a combination of experimental and mathematical modelling approaches has been used. Early work focussed on the possibility that GnRH pulse generation is an intrinsic feature of GnRH neurons, with autocrine feedback generating pulsatility. However, there is now ample evidence suggesting that a network of upstream neurons secreting kisspeptin, neurokinin-B and dynorphin are the source of this GnRH pulse generator. The interplay of slow positive and negative feedback via neurokinin-B and dynorphin, respectively, allows the network to act as a relaxation oscillator, driving pulsatile secretion of kisspeptin, and consequently, of GnRH and LH. Here, we review the mathematical modelling approaches exploring both scenarios and suggest that with pulsatile GnRH secretion driven by the KNDy pulse generator, autocrine feedback still has the potential to modulate GnRH output.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"27 ","pages":"Article 100407"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9823092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9072199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Maria G. Grammatikopoulou , Meletios P. Nigdelis , Dimitrios G. Goulis
{"title":"Weight gain in midlife women: Understanding drivers and underlying mechanisms","authors":"Maria G. Grammatikopoulou , Meletios P. Nigdelis , Dimitrios G. Goulis","doi":"10.1016/j.coemr.2022.100406","DOIUrl":"10.1016/j.coemr.2022.100406","url":null,"abstract":"<div><p><span><span><span>Overweight and obesity patterns demonstrate a sexual dimorphism, with women being more prone to weight gain and overweight/obesity compared to men. As a result, weight gain is an important concern in women, particularly during midlife, when reproductive and physiological aging coincide, altering body composition. During this time, multiple factors contribute to the accumulation of body weight and adipose tissue, inducing a decrease in lean mass. These factors include hormonal changes -mainly hypoestrogenism-, </span>genetic<span> and exogenous factors, poor nutritional intake and physical inactivity<span><span>, all of which might act synergistically to promote weight gain. Basal metabolic rate is also reduced due to aging, muscle mass loss, and the reduction in brown tissue activity. Impairments of the circadian system are associated with reduced endogenous </span>melatonin secretion, altered sleep–wake cycles and metabolic inflexibility. </span></span></span>Inflammaging<span>, gut dysbiosis and physical inactivity further promote weight gain and the loss of lean </span></span>skeletal muscle<span>, leading to sarcopenic obesity.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"27 ","pages":"Article 100406"},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43247028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}