{"title":"Pulling the trigger: Noncoding RNAs in white adipose tissue browning","authors":"","doi":"10.1007/s11154-023-09866-6","DOIUrl":"https://doi.org/10.1007/s11154-023-09866-6","url":null,"abstract":"<h3>Abstract</h3> <p>White adipose tissue (WAT) serves as the primary site for energy storage and endocrine regulation in mammals, while brown adipose tissue (BAT) is specialized for thermogenesis and energy expenditure. The conversion of white adipocytes to brown-like fat cells, known as browning, has emerged as a promising therapeutic strategy for reversing obesity and its associated co-morbidities. Noncoding RNAs (ncRNAs) are a class of transcripts that do not encode proteins but exert regulatory functions on gene expression at various levels. Recent studies have shed light on the involvement of ncRNAs in adipose tissue development, differentiation, and function. In this review, we aim to summarize the current understanding of ncRNAs in adipose biology, with a focus on their role and intricate mechanisms in WAT browning. Also, we discuss the potential applications and challenges of ncRNA-based therapies for overweight and its metabolic disorders, so as to combat the obesity epidemic in the future.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"56 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139067847","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}
Rodolfo A. Rey, Ignacio Bergadá, María Gabriela Ballerini, Débora Braslavsky, Ana Chiesa, Analía Freire, Romina P. Grinspon, Ana Keselman, Andrea Arcari
{"title":"Diagnosing and treating anterior pituitary hormone deficiency in pediatric patients","authors":"Rodolfo A. Rey, Ignacio Bergadá, María Gabriela Ballerini, Débora Braslavsky, Ana Chiesa, Analía Freire, Romina P. Grinspon, Ana Keselman, Andrea Arcari","doi":"10.1007/s11154-023-09868-4","DOIUrl":"https://doi.org/10.1007/s11154-023-09868-4","url":null,"abstract":"<p>Hypopituitarism, or the failure to secrete hormones produced by the anterior pituitary (adenohypophysis) and/or to release hormones from the posterior pituitary (neurohypophysis), can be congenital or acquired. When more than one pituitary hormone axis is impaired, the condition is known as combined pituitary hormone deficiency (CPHD). The deficiency may be primarily due to a hypothalamic or to a pituitary disorder, or concomitantly both, and has a negative impact on target organ function. This review focuses on the pathophysiology, diagnosis and management of anterior pituitary hormone deficiency in the pediatric age. Congenital hypopituitarism is generally due to genetic disorders and requires early medical attention. Exposure to toxicants or intrauterine infections should also be considered as potential etiologies. The molecular mechanisms underlying the fetal development of the hypothalamus and the pituitary are well characterized, and variants in the genes involved therein may explain the pathophysiology of congenital hypopituitarism: mutations in the genes expressed in the earliest stages are usually associated with syndromic forms whereas variants in genes involved in later stages of pituitary development result in non-syndromic forms with more specific hormone deficiencies. Tumors or lesions of the (peri)sellar region, cranial radiation therapy, traumatic brain injury and, more rarely, other inflammatory or infectious lesions represent the etiologies of acquired hypopituitarism. Hormone replacement is the general strategy, with critical periods of postnatal life requiring specific attention.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"198 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138745930","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":"The genetics of Graves’ disease","authors":"Lydia Grixti, Laura C. Lane, Simon H Pearce","doi":"10.1007/s11154-023-09848-8","DOIUrl":"https://doi.org/10.1007/s11154-023-09848-8","url":null,"abstract":"<p>Graves’ disease (GD) is the commonest cause of hyperthyroidism and has a strong female preponderance. Everyday clinical practice suggests strong aggregation within families and twin studies demonstrate that genetic factors account for 60-80% of risk of developing GD. In this review, we collate numerous genetic studies and outline the discoveries over the years, starting with historic candidate gene studies and then exploring more recent genome-wide linkage and association studies, which have involved substantial cohorts of East Asian patients as well as those of European descent. Variants in genes including <i>HLA</i>, <i>CTLA4</i>, and <i>PTPN22</i> have been shown to have substantial individual effects on disease susceptibility. In addition, we examine emerging evidence concerning the possibility that genetic variants may correlate with relevant clinical phenotypes including age of onset of GD, severity of thyrotoxicosis, goitre size and relapse of hyperthyroidism following antithyroid drug therapy, as well as thyroid eye disease. This review supports the inheritance of GD as a complex genetic trait, with a growing number of more than 80 susceptibility loci identified so far. Future implementation of more targeted clinical therapies requires larger studies investigating the influence of these genetic variants on the various phenotypes and different outcomes of conventional treatments.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138715867","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":"New insights on diagnosis and treatment of AVP deficiency","authors":"Julie Refardt, Cihan Atila, Mirjam Christ-Crain","doi":"10.1007/s11154-023-09862-w","DOIUrl":"https://doi.org/10.1007/s11154-023-09862-w","url":null,"abstract":"<p>Arginine vasopressin deficiency (AVP-D) is one of the main entities of the polyuria-polydipsia syndrome. Its correct diagnosis and differentiation from the other two causes - AVP resistance and primary polydipsia – is crucial as this determines the further management of these patients.</p><p>Over the last years, several new diagnostic tests using copeptin, the stable surrogate marker of AVP, have been introduced. Among them, hypertonic saline stimulated copeptin was confirmed to reliably and safely improve the diagnostic accuracy to diagnose AVP-D. Due to its simplicity, arginine stimulated copeptin was put forward as alternative test procedure. Glucagon-stimulated copeptin also showed promising results, while the oral growth hormone secretagogue Macimorelin failed to provide a sufficient stimulus. Interestingly, an approach using machine learning techniques also showed promising results concerning diagnostic accuracy.</p><p>Once AVP-D is diagnosed, further workup is needed to evaluate its etiology. This will partly define the further treatment and management. In general, treatment of AVP-D focuses on desmopressin substitution, with oral formulations currently showing the best tolerance and safety profile. However, in addition to desmopressin substitution, recent data also showed that psychopathological factors play an important role in managing AVP-D patients.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138627817","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}
Stephanie Chacar, Abdulhamid Abdi, Khalifa Almansoori, Jawaher Alshamsi, Cynthia Al Hageh, Pierre Zalloua, Ali A. Khraibi, Stephen G. Holt, Moni Nader
{"title":"Role of CaMKII in diabetes induced vascular injury and its interaction with anti-diabetes therapy","authors":"Stephanie Chacar, Abdulhamid Abdi, Khalifa Almansoori, Jawaher Alshamsi, Cynthia Al Hageh, Pierre Zalloua, Ali A. Khraibi, Stephen G. Holt, Moni Nader","doi":"10.1007/s11154-023-09855-9","DOIUrl":"https://doi.org/10.1007/s11154-023-09855-9","url":null,"abstract":"<p>Diabetes mellitus is a metabolic disorder denoted by chronic hyperglycemia that drives maladaptive structural changes and functional damage to the vasculature. Attenuation of this pathological remodeling of blood vessels remains an unmet target owing to paucity of information on the metabolic signatures of this process. Ca<sup>2+</sup>/calmodulin-dependent kinase II (CaMKII) is expressed in the vasculature and is implicated in the control of blood vessels homeostasis. Recently, CaMKII has attracted a special attention in view of its chronic upregulated activity in diabetic tissues, yet its role in the diabetic vasculature remains under investigation.</p><p>This review highlights the physiological and pathological actions of CaMKII in the diabetic vasculature, with focus on the control of the dialogue between endothelial (EC) and vascular smooth muscle cells (VSMC). Activation of CaMKII enhances EC and VSMC proliferation and migration, and increases the production of extracellular matrix which leads to maladaptive remodeling of vessels. This is manifested by activation of genes/proteins implicated in the control of the cell cycle, cytoskeleton organization, proliferation, migration, and inflammation. Endothelial dysfunction is paralleled by impaired nitric oxide signaling, which is also influenced by CaMKII signaling (activation/oxidation). The efficiency of CaMKII inhibitors is currently being tested in animal models, with a focus on the genetic pathways involved in the regulation of CaMKII expression (microRNAs and single nucleotide polymorphisms). Interestingly, studies highlight an interaction between the anti-diabetic drugs and CaMKII expression/activity which requires further investigation. Together, the studies reviewed herein may guide pharmacological approaches to improve health-related outcomes in patients with diabetes.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"64 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138556854","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}
Andrea Giustina, Luigi di Filippo, Antonio Facciorusso, Robert A. Adler, Neil Binkley, Jens Bollerslev, Roger Bouillon, Felipe F. Casanueva, Giulia Martina Cavestro, Marlene Chakhtoura, Caterina Conte, Lorenzo M. Donini, Peter R. Ebeling, Angelo Fassio, Stefano Frara, Claudia Gagnon, Giovanni Latella, Claudio Marcocci, Jeffrey I. Mechanick, Salvatore Minisola, René Rizzoli, Ferruccio Santini, Joseph L. Shaker, Christopher Sempos, Fabio Massimo Ulivieri, Jyrki K. Virtanen, Nicola Napoli, Anne L. Schafer, John P. Bilezikian
{"title":"Correction: Vitamin D status and supplementation before and after Bariatric Surgery: Recommendations based on a systematic review and meta‑analysis","authors":"Andrea Giustina, Luigi di Filippo, Antonio Facciorusso, Robert A. Adler, Neil Binkley, Jens Bollerslev, Roger Bouillon, Felipe F. Casanueva, Giulia Martina Cavestro, Marlene Chakhtoura, Caterina Conte, Lorenzo M. Donini, Peter R. Ebeling, Angelo Fassio, Stefano Frara, Claudia Gagnon, Giovanni Latella, Claudio Marcocci, Jeffrey I. Mechanick, Salvatore Minisola, René Rizzoli, Ferruccio Santini, Joseph L. Shaker, Christopher Sempos, Fabio Massimo Ulivieri, Jyrki K. Virtanen, Nicola Napoli, Anne L. Schafer, John P. Bilezikian","doi":"10.1007/s11154-023-09837-x","DOIUrl":"https://doi.org/10.1007/s11154-023-09837-x","url":null,"abstract":"","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"58 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135770478","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":"Interactions between nuclear receptors glucocorticoid receptor α and peroxisome proliferator-activated receptor α form a negative feedback loop.","authors":"Hongjiao Gao, Yujue Li, Xiang Chen","doi":"10.1007/s11154-022-09725-w","DOIUrl":"10.1007/s11154-022-09725-w","url":null,"abstract":"<p><p>Both nuclear receptors glucocorticoid receptor α (GRα) and peroxisome proliferator-activated receptor α (PPARα) are involved in energy and lipid metabolism, and possess anti-inflammation effects. Previous studies indicate that a regulatory loop may exist between them. In vivo and in vitro studies showed that glucocorticoids stimulate hepatic PPARα expression via GRα at the transcriptional level. This stimulation of PPARα by GRα has physiological relevance and PPARα is involved in many glucocorticoid-induced pathophysiological processes, including gluconeogenesis and ketogenesis during fasting, insulin resistance, hypertension and anti-inflammatory effects. PPARα also synergizes with GRα to promote erythroid progenitor self-renewal. As the feedback, PPARα inhibits glucocorticoid actions at pre-receptor and receptor levels. PPARα decreases glucocorticoid production through inhibiting the expression and activity of type-1 11β-hydroxysteroid dehydrogenase, which converts inactive glucocorticoids to active glucocorticoids at local tissues, and also down-regulates hepatic GRα expression, thus forming a complete and negative feedback loop. This negative feedback loop sheds light on prospective multi-drug therapeutic treatments in inflammatory diseases through a combination of glucocorticoids and PPARα agonists. This combination may potentially enhance the anti-inflammatory effects while alleviating side effects on glucose and lipid metabolism due to GRα activation. More investigations are needed to clarify the underlying mechanism and the relevant physiological or pathological significance of this regulatory loop.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"44 1","pages":"893-903"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82341908","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}
Omar Al-Massadi, Paolo Parini, Johan Fernø, Serge Luquet, Mar Quiñones
{"title":"Metabolic actions of the growth hormone-insulin growth factor-1 axis and its interaction with the central nervous system.","authors":"Omar Al-Massadi, Paolo Parini, Johan Fernø, Serge Luquet, Mar Quiñones","doi":"10.1007/s11154-022-09732-x","DOIUrl":"10.1007/s11154-022-09732-x","url":null,"abstract":"<p><p>The growth hormone/insulin growth factor-1 axis is a key endocrine system that exerts profound effects on metabolism by its actions on different peripheral tissues but also in the brain. Growth hormone together with insulin growth factor-1 perform metabolic adjustments, including regulation of food intake, energy expenditure, and glycemia. The dysregulation of this hepatic axis leads to different metabolic disorders including obesity, type 2 diabetes or liver disease. In this review, we discuss how the growth hormone/insulin growth factor-1 axis regulates metabolism and its interactions with the central nervous system. Finally, we state our vision for possible therapeutic uses of compounds based in the components of this hepatic axis.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"19 1","pages":"919-930"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74155604","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":"Diagnostic accuracy of bilateral inferior petrosal sinus sampling using desmopressin or corticotropic- releasing hormone in ACTH-dependent Cushing's syndrome: A systematic review and meta-analysis.","authors":"Majid Valizadeh, Amirhossein Ramezani Ahmadi, Amir Ebadinejad, Fatemeh Rahmani, Behnaz Abiri","doi":"10.1007/s11154-022-09723-y","DOIUrl":"10.1007/s11154-022-09723-y","url":null,"abstract":"<p><p>The current gold standard diagnostic method for Cushing disease (CD) is bilateral inferior petrosal sinus sampling (BIPSS) after corticotropin-releasing hormone (CRH) stimulation. Due to shortages of CRH, BIPSS has been performed with desmopressin (DDAVP) instead. The objective of this systematic review and meta-analysis was to estimate the diagnostic accuracy of BIPSS using DDAVP or CRH for the differential diagnosis of Cushing's syndrome (CS). A literature review was done in PubMed, Scopus, EMBASE, and google scholar databases to derive summary estimates of the overall diagnostic sensitivity and accuracy of BIPSS using DDAVP or CRH in Cushing's syndrome. Pooled sensitivity, specificity, diagnostic odds ratio and summary receiver operating characteristic curves (SROC) for differential diagnosis of Cushing's syndrome in the random-effects models, were computed. Overall, 11 different studies with a total of 612 participants, were eligible for the analysis. Five articles with data on BIPSS using DDAVP, 5 papers on BIPSS using CRH, and another one evaluated the results of stimulation using DDAVP, with or without CRH, for differential diagnosis of Cushing's syndrome. The pooled (95% CI) sensitivity and specificity of BIPSS using DDAVP, were 96% (91-98%) and 1.00 (0.00-1.00), respectively. The area under the SROC curve was 0.95. The pooled (95% CI) sensitivity and specificity of BIPSS using CRH, were 98% (92-99%) and 1.00 (0.00-1.00), respectively, and the area under the SROC curve was 0.98. The I<sup>2</sup> index (95% CI) was 0% (0-100%) for both BIPSS using DDAVP and using CRH. As a result, DDAVP stimulation is a safe, effective, less expensive, valuable and available alternative to CRH in the setting of BIPSS for all age groups of patients with CS. Registration code in PROSPERO: CRD42021292531.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"239 1","pages":"881-892"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89122802","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":"Ser/Thr phosphatases: One of the key regulators of insulin signaling.","authors":"Yamini Yadav, Chinmoy Sankar Dey","doi":"10.1007/s11154-022-09727-8","DOIUrl":"10.1007/s11154-022-09727-8","url":null,"abstract":"<p><p>Protein phosphorylation is an important post-translational modification that regulates several cellular processes including insulin signaling. The evidences so far have already portrayed the importance of balanced actions of kinases and phosphatases in regulating the insulin signaling cascade. Therefore, elucidating the role of both kinases and phosphatases are equally important. Unfortunately, the role of phosphatases is less studied as compared to kinases. Since brain responds to insulin and insulin signaling is reported to be crucial for many neuronal processes, it is important to understand the role of neuronal insulin signaling regulators. Ser/Thr phosphatases seem to play significant roles in regulating neuronal insulin signaling. Therefore, in this review, we discussed the involvement of Ser/Thr phosphatases in regulating insulin signaling and insulin resistance in neuronal system at the backdrop of the same phosphatases in peripheral insulin sensitive tissues.</p>","PeriodicalId":21105,"journal":{"name":"Reviews in Endocrine and Metabolic Disorders","volume":"33 1","pages":"905-917"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87489737","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}