David Goltzman, Michael Mannstadt, Claudio Marcocci
{"title":"Physiology of the Calcium-Parathyroid Hormone-Vitamin D Axis.","authors":"David Goltzman, Michael Mannstadt, Claudio Marcocci","doi":"10.1159/000486060","DOIUrl":"https://doi.org/10.1159/000486060","url":null,"abstract":"<p><p>Classic endocrine feedback loops ensure the regulation of blood calcium. Calcium in the extracellular fluid (ECF) binds and activates the calcium sensing receptor (CaSR) on the parathyroid cells, leading to an increase in intracellular calcium. This in turn leads to a reduced parathyroid hormone (PTH) release. Hypocalcemia leads to the opposite sequence of events, namely, lowered intracellular calcium and increased PTH production and secretion. PTH rapidly increases renal calcium reabsorption and, over hours to days, enhances osteoclastic bone resorption and liberates both calcium and phosphate from the skeleton. PTH also increases fibroblast growth factor 23 (FGF23) release from mature osteoblasts and osteocytes. PTH stimulates the renal conversion of 25-hydroxyvitamin D (25[OH]D) to 1,25(OH)2D, likely over several hours, which in turn will augment intestinal calcium absorption. Prolonged hypocalcemia and exposure to elevated PTH may also result in 1,25(OH)2D-mediated calcium and phosphorus release from bone. These effects restore the ECF calcium to normal and inhibit further production of PTH and 1,25(OH)2D. Additionally, FGF23 can be released from bone by 1,25(OH)2D and can in turn reduce 1,25(OH)2D concentrations. FGF23 has also been reported to decrease PTH production. When ECF calcium is in the hypercalcemic range, PTH secretion is reduced and renal 1,25(OH)2D production is decreased. In addition, the elevated calcium per se stimulates the renal CaSR, thus inducing calciuria. Therefore, suppression of PTH release and 1,25(OH)2D synthesis and stimulation of the renal CaSR lead to reduced renal calcium reabsorption, decreased skeletal calcium release, and decreased intestinal calcium absorption, resulting in the normalization of the elevated ECF calcium.</p>","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"50 ","pages":"1-13"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000486060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35960666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic Complications of Acromegaly.","authors":"Moisés Mercado, Claudia Ramírez-Rentería","doi":"10.1159/000486001","DOIUrl":"https://doi.org/10.1159/000486001","url":null,"abstract":"<p><p>Diabetes is recognized as one of the most common acromegaly co-morbidities with a prevalence ranging 20-53%, while over one-third of these patients have an altered lipid profile. In fact, as in the non-acromegalic population, carbohydrate and lipid metabolism abnormalities are closely linked. Long term exposure to an excess of growth hormone (GH) and Insulin-like growth factor-1 concentrations results in insulin resistance and an increased hepatic glucose production. The lipolytic effect of GH results in the mobilization of free fatty acids that further contributes to the decreased insulin sensitivity found in these patients. Some studies suggest that the presence of diabetes contributes to the increased mortality of acromegaly, although this remains controversial. Successful treatment of acromegaly usually results in significant, albeit incomplete improvements of the abnormal metabolic profile.</p>","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"49 ","pages":"20-28"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000486001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36215680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic Complications in Adrenal Insufficiency.","authors":"Grethe A Ueland, Eystein S Husebye","doi":"10.1159/000486004","DOIUrl":"https://doi.org/10.1159/000486004","url":null,"abstract":"<p><p>Pharmacological glucocorticoid treatment is associated with adverse metabolic consequences such as hypertension, overweight, reduced glucose tolerance, diabetes mellitus and ultimately increased mortality in cardiovascular disease. Here we review the evidence of detrimental effects of hormone replacement therapy in adrenal insufficiency (AI). Registry studies indicate increased cardiovascular mortality, hypertension, diabetes, and dyslipidemia in both primary and secondary AI, but when cohorts with carefully characterized patients are studied the picture is less clear, and recently patients with primary AI was reported to have less hypertension and lower body mass index than controls. Whether near physiological replacement therapy increase long-term cardiovascular morbidity and mortality in AI is still unclear.</p>","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"49 ","pages":"104-113"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000486004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36216480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G. Mazziotti, A. Formenti, S. Frara, M. Doga, A. Giustina
{"title":"Vitamin D and Glucocorticoid-Induced Osteoporosis","authors":"G. Mazziotti, A. Formenti, S. Frara, M. Doga, A. Giustina","doi":"10.1159/000486078","DOIUrl":"https://doi.org/10.1159/000486078","url":null,"abstract":"","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"50 1","pages":"149-160"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000486078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65282300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic Syndrome in Cushing's Syndrome Patients.","authors":"Francesco Ferraù, Márta Korbonits","doi":"10.1159/000486002","DOIUrl":"https://doi.org/10.1159/000486002","url":null,"abstract":"<p><p>Cushing's syndrome (CS), including visceral obesity, dyslipidemia, hypertension and diabetes among its many manifestations, is \"a model\" of metabolic syndrome. Glucocorticoid (GC) excess, through a combination of effects on liver, muscle, adipose tissue and pancreas, increases gluconeogenesis and impairs insulin sensitivity, leading to carbohydrate abnormalities. Dyslipidemia is a common finding in CS as a consequence of GC-related increased lipolysis, lipogenesis and adipogenesis. CS patients experience typical changes in body composition, with fat redistribution resulting in accumulation of visceral adipose tissue. Hypertension, myocardial and vascular abnormalities along with the metabolic changes and the characteristic coagulopathy increase cardiovascular morbidity and mortality. Metabolic syndrome features can persist long after normalisation of cortisol levels.</p>","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"49 ","pages":"85-103"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000486002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36216476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Practical Issues in Vitamin D Replacement.","authors":"Robert A Adler","doi":"10.1159/000486068","DOIUrl":"https://doi.org/10.1159/000486068","url":null,"abstract":"<p><p>Practical clinical guidance for vitamin D assessment and management relies on a strong evidence base, but unfortunately there are many deficiencies in our current knowledge. For the general population the Institute of Medicine recommendations are likely to provide adequate vitamin D levels without harms. Thus, most adults should ingest 600-800 IU (international units) in diet and supplements with up to 4,000 IU daily likely to be safe. In certain populations, such as those with osteoporosis or after bariatric surgery, it is important to know the levels of circulating 25-hydroxyvitamin D, but general screening has not been shown to improve health. One expert group has recommended a \"reasonable\" level of 30 ng/mL in those individuals for whom testing is required.</p>","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"50 ","pages":"66-71"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000486068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35960670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic Syndrome in Polycystic Ovary Syndrome.","authors":"Renato Pasquali","doi":"10.1159/000485995","DOIUrl":"https://doi.org/10.1159/000485995","url":null,"abstract":"<p><p>Both prevalence and incidence of the metabolic syndrome is very high in women with polycystic ovary syndrome (PCOS). Obesity and visceral fat enlargement play a dominant role in determining the final phenotype of PCOS. Androgen excess and insulin resistance may be responsible for the development of all features of the metabolic syndrome. The major factors responsible for this association seem to be related to a triumvirate including androgen excess, insulin resistance and associated hyperinsulinemia, and obesity, particularly the abdominal-visceral phenotype. With respect to obesity, it can be suggested that the association may be bidirectional, in the sense that obesity can worsen the phenotype of PCOS when present and can also be responsible for the development of a secondary form of PCOS even in susceptible subjects. In spite of the strong association among a long list of cardiovascular risk factors, there is no evidence that women with PCOS may be affected by an increased risk for cardiovascular mortality. Future research should carry out a detailed investigation into the potential role of androgen excess in determining the insulin resistant state and, specifically, the very high risk of developing type 2 diabetes.</p>","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"49 ","pages":"114-130"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000485995","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36216479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolic Syndrome in Parathyroid Diseases.","authors":"Sabrina Corbetta, G Mantovani, A Spada","doi":"10.1159/000486003","DOIUrl":"https://doi.org/10.1159/000486003","url":null,"abstract":"<p><p>Parathyroid glands are the main regulator of body mineral metabolism through parathormone (PTH) actions on bone and kidney. Experimental evidence suggests that PTH may have non-classical target organs such as adipose tissue, arterial vascular wall, cardiac muscle cells, and adrenal cortex cells, where it may play a role in controlling body energy, blood pressure, and metabolism. Cardiometabolic features have been investigated in the wide spectrum of clinical parathyroid disorders, from hyperparathyroidism to pseudohypoparathyroidism and hypoparathyroidism. Indeed, in parathyroid disorders, besides altered PTH secretion, impaired serum calcium levels and vitamin D status occur. Both calcium and vitamin D have been shown to regulate metabolism and to be associated with cardiovascular diseases. However, despite the complexity of parathyroid disorders, features of metabolic syndrome, such as obesity, insulin resistance, and glucose intolerance, arterial blood hypertension, and dyslipidemia, are frequently diagnosed in primary and secondary hyperparathyroidism as well as in pseudohyperparathyroidism. Here, we reviewed the most consistent data highlighting challenges and providing clinical remarks.</p>","PeriodicalId":50428,"journal":{"name":"Frontiers of Hormone Research","volume":"49 ","pages":"67-84"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000486003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36216662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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