{"title":"Hypoxia signaling in bone physiology and energy metabolism","authors":"Roger Valle-Tenney, Seppe Melis, Christa Maes","doi":"10.1016/j.coemr.2023.100473","DOIUrl":"10.1016/j.coemr.2023.100473","url":null,"abstract":"<div><p><span><span><span><span>Hypoxia-inducible factor (HIF) signaling activation in osteoblast lineage cells increases bone mass, likely through the combined actions of multiple key downstream effectors. These include the potent </span>angiogenesis<span> stimulator vascular endothelial growth factor (VEGF), which mediates coupled osteo-angiogenic responses in bone, among other non-cell-autonomous contributors. Additionally, local HIF activation in bone cells cell-intrinsically triggers increased glycolysis, which is associated with strongly enhanced osteoblastic glucose consumption. Strikingly, besides its local impact on bone mass, this boosting of cellular metabolism in the osteolineage has been linked to increased overall </span></span>glucose uptake by the </span>skeleton and concomitant effects on systemic </span>glucose homeostasis<span>. This review summarizes the cell-autonomous and non-cell-autonomous roles of the hypoxia signaling pathway in osteoblast lineage cells on bone physiology and the parallel systemic impact observed upon activation of the pathway in bone. New potential mechanisms extending the control of global energy metabolism by the skeleton will be discussed in light of the current evidence.</span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"32 ","pages":"Article 100473"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44998583","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":"Neoadjuvant therapy prior to surgery for advanced thyroid cancer","authors":"Curtis Hanba, Mark Zafereo","doi":"10.1016/j.coemr.2023.100469","DOIUrl":"10.1016/j.coemr.2023.100469","url":null,"abstract":"<div><p>This chapter aims to review historical perspective as well as detail recent progress in neoadjuvant systemic therapy prior to surgery for advanced thyroid cancer.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"32 ","pages":"Article 100469"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48245525","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}
Daniel Hägg , Per-Anders Jansson , Jakob Bellman , John-Olov Jansson , Claes Ohlsson
{"title":"Osteoblast-lineage cells regulate metabolism and fat mass","authors":"Daniel Hägg , Per-Anders Jansson , Jakob Bellman , John-Olov Jansson , Claes Ohlsson","doi":"10.1016/j.coemr.2023.100470","DOIUrl":"10.1016/j.coemr.2023.100470","url":null,"abstract":"<div><p>As energy depots in many circumstances have been limited during evolution, it is necessary to prioritize how to manage energy resources. In this review we summarize data from the last 15 years indicating that osteoblast-lineage cells are regulators of whole-body energy metabolism and fat mass. We focus mainly on three factors, osteocalcin, lipocalin-2 and sclerostin, that are released by osteoblast-lineage cells and proposed to exert endocrine effects on metabolism. In addition, we present a hypothesis on why osteoblast-lineage cells during evolution have developed a function to regulate metabolism and fat mass. We propose that osteoblast-lineage cells through the osteocyte network in bone are sensors of gravitational forces induced by body mass and gravity on land-living species. By sensing the body weight, the osteoblastlineage cells may then feed-back this information on the whole-body nutritional status via osteoblast-derived endocrine factors or via the nervous system to regulate energy metabolism and fat mass.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"31 ","pages":"Article 100470"},"PeriodicalIF":0.0,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45656773","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":"Evidence in humans for bone as an endocrine organ regulating energy metabolism","authors":"Sundeep Khosla","doi":"10.1016/j.coemr.2023.100471","DOIUrl":"10.1016/j.coemr.2023.100471","url":null,"abstract":"<div><p><span>There is increasing evidence from animal models that bone, in addition to its traditional function of providing structural support for the organism, has a rich network of interactions with multiple other tissues. This perspective focuses on evidence from human studies demonstrating that bone is an endocrine organ regulating energy metabolism, with the specific examples being </span>osteocalcin<span><span><span>, lipocalin 2<span>, RANKL, and sclerostin. Conversely, animal studies have also demonstrated that a key hormone regulating energy metabolism, leptin, regulates </span></span>bone metabolism via the </span>sympathetic nervous system<span><span>. Studies in humans have established a role for the sympathetic nervous system in regulating bone turnover; indeed, the potential therapeutic benefit of targeting this pathway in humans to prevent postmenopausal </span>bone loss is currently being evaluated.</span></span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"31 ","pages":"Article 100471"},"PeriodicalIF":0.0,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10417886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10003016","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":"Anxiety and depression in midlife transition and beyond: The role of estrogens","authors":"Claudio N. Soares","doi":"10.1016/j.coemr.2023.100457","DOIUrl":"https://doi.org/10.1016/j.coemr.2023.100457","url":null,"abstract":"<div><p>Depression and anxiety are amongst the most prevalent and disabling conditions worldwide, imposing significant burden to individuals, families, and their communities. It is now known that both conditions affect females more often than males, and that some can be particularly more vulnerable to symptoms (new, recurrent) during reproductive-related windows of vulnerability, including the menopause transition and early postmenopausal years.</p><p><span><span>As estrogen exerts neuro-modulatory effects on mood, cognition, and behaviour through </span>monoaminergic systems<span> (e.g., 5-HT, NE), rapid fluctuations of estradiol (E2) levels seem to be associated with heightened risk for/emergency of anxiety and depression during midlife years, along with other menopause-associated complaints such as </span></span>vasomotor symptoms and sleep disturbances.</p><p><span>Psychopharmacologic and behavioural interventions remain the first-line treatment for depression and anxiety across the life span; however, estrogen-based therapies, particularly </span>transdermal estradiol, should be considered as part of the treatment armamentarium for symptomatic, midlife women.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"31 ","pages":"Article 100457"},"PeriodicalIF":0.0,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50172066","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":"Thyroid cancer incidence differences between men and women","authors":"Quynh-Lam Tran , Louise Davies","doi":"10.1016/j.coemr.2023.100472","DOIUrl":"10.1016/j.coemr.2023.100472","url":null,"abstract":"<div><p><span>Early-stage thyroid<span><span> cancer is about 4 times more common in women than men, but the underlying subclinical prevalence is the same between the two sexes. As the lethality<span><span> of the cancer type increases, the ratio in incidence for women compared to men approaches 1:1. These facts suggest that differences in healthcare utilization may be a major reason </span>thyroid cancer is diagnosed more in women than men. Physiological elements could also contribute, as women have a higher prevalence of thyroid nodularity compared to men. Current research suggests estrogen does not play a major role, but </span></span>genetics may be a potential reason for increased rates of thyroid cancer in women compared to men. </span></span>Immune surveillance is greater in women and currently is thought to be protective against thyroid cancer development. This review summarizes recent evidence examining the role of these factors in modulating the sex-disparity observed in thyroid cancer incidence.</p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"31 ","pages":"Article 100472"},"PeriodicalIF":0.0,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45055264","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":"Menopause research: Looking back to move forward","authors":"Chrisandra Shufelt, Stephanie Faubion","doi":"10.1016/j.coemr.2023.100459","DOIUrl":"10.1016/j.coemr.2023.100459","url":null,"abstract":"","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"30 ","pages":"Article 100459"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47966023","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":"InTERTwined: How TERT promoter mutations impact BRAFV600E-driven thyroid cancers","authors":"Iñigo Landa","doi":"10.1016/j.coemr.2023.100460","DOIUrl":"https://doi.org/10.1016/j.coemr.2023.100460","url":null,"abstract":"<div><p><span>Thyroid cancers are often initiated by the acquisition of a BRAF</span><sup>V600E</sup> mutation. BRAF<sup>V600E</sup><span><span><span>-driven thyroid tumors display a wide range of </span>behaviors, from the slow-growing </span>papillary carcinomas to the highly aggressive anaplastic. Mutations in the promoter of </span><em>TERT</em> (telomerase reverse transcriptase) gene were discovered a decade ago and identified as prevalent events in thyroid cancers. Multiple studies showed that <em>TERT</em> promoter mutations, particularly when co-occurring with BRAF<sup>V600E</sup>, are markers of poor prognosis across thyroid cancer subtypes, and can be implemented for routine clinical stratification. Mechanistically, <em>TERT</em><span> promoter mutations reactivate telomerase<span> expression via the differential recruitment of transcriptional complexes. Re-expression of TERT impacts tumor biology, plausibly via both the well-known function of telomerase maintaining telomeres and by affecting other cancer-relevant processes.</span></span></p></div>","PeriodicalId":52218,"journal":{"name":"Current Opinion in Endocrine and Metabolic Research","volume":"30 ","pages":"Article 100460"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50173240","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}