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Vitamins and Hormones

Gerald Litwack
No abstract text is available yet for this article.
2019: Vitamins and Hormones
Laura Silvestri, Antonella Nai, Alessandro Dulja, Alessia Pagani
Hepcidin, the main regulator of iron metabolism, is synthesized and released by hepatocytes in response to increased body iron concentration and inflammation. Deregulation of hepcidin expression is a common feature of genetic and acquired iron disorders: in Hereditary Hemochromatosis (HH) and iron-loading anemias low hepcidin causes iron overload, while in Iron Refractory Iron Deficiency Anemia (IRIDA) and anemia of inflammation (AI), high hepcidin levels induce iron-restricted erythropoiesis. Hepcidin expression in the liver is mainly controlled by the BMP-SMAD pathway, activated in a paracrine manner by BMP2 and BMP6 produced by liver sinusoidal endothelial cells...
2019: Vitamins and Hormones
Gautam Rishi, V Nathan Subramaniam
Since its discovery in 2001, there have been a number of important discoveries and findings that have increased our knowledge about the functioning of hepcidin. Hepcidin, the master iron regulator has been shown to be regulated by a number of physiological stimuli and their associated signaling pathways. This chapter will summarize our current understanding of how these physiological stimuli and downstream signaling molecules are involved in hepcidin modulation and ultimately contribute to the regulation of systemic or local iron homeostasis...
2019: Vitamins and Hormones
Alice Santos-Silva, Sandra Ribeiro, Flávio Reis, Luís Belo
Chronic kidney disease (CKD) is associated with several complications that worsen with progression of disease; anemia, disturbances in iron metabolism and inflammation are common features. Inflammatory response starts early, releasing pro-inflammatory cytokines, acute phase reactants and hepcidin. Hepcidin production is modulated by several factors, as hypoxia/anemia, erythropoietin and erythropoiesis products, transferrin saturation (TSAT) and liver iron levels, which are altered in CKD. Treatment of CKD anemia is based on pharmaceutical intervention, with erythropoietic stimulating agents and/or iron supplementation; however, in spite of the erythropoietic benefits, this therapy, on a regular basis, involves risks, namely iron overload...
2019: Vitamins and Hormones
James C Barton, Ronald T Acton
Hepcidin, an oligopeptide, has two major functions in mammals. Hepcidin regulates iron homeostasis by controlling iron export from absorptive enterocytes, hepatocytes, and macrophages into the circulation via ferroportin inactivation. Hepcidin is also an innate antimicrobial agent that is induced by invasive bacteria, limits bacterial proliferation by reducing iron in plasma and extracellular fluids, and kills bacteria. Herein, we review hepcidin and hepcidin genes, iron acquisition by bacteria, hepcidin actions in mice infected with selected extracellular and intracellular bacteria, and reports of corresponding serious human infections...
2019: Vitamins and Hormones
Martha-Spyridoula Katsarou, Maria Papasavva, Rozana Latsi, Nikolaos Drakoulis
Hereditary Hemochromatosis (HH) is an autosomal recessive genetic disease, characterized by an excessively increased absorption of dietary iron. Excess iron can be accumulated because of the lack of an effective excretory mechanism leading to toxic effects. HH is one of the most common genetic disorders in individuals of European descent. Genetic polymorphisms of the HFE gene (rs1800562, rs1799945 and rs1800730) also affect the normal activity of another protein, hepcidin, a negative regulator of iron homeostasis...
2019: Vitamins and Hormones
S Lakhal-Littleton
Cellular iron is required for the utilization of oxygen in the cell. Iron in iron-sulfur and heme groups is required for electron transfer and oxygen activation in oxidative phosphorylation, while labile free iron is required for oxygen activation by dioxygenases, and as a catalyst for redox signaling. At the same time, this reactivity with oxygen underpins the production of cell-damaging free radicals in the presence of excess iron. Because the cardiac cell is a major site of oxygen flux, it requires tight control of intracellular iron levels...
2019: Vitamins and Hormones
Yelena Z Ginzburg
Hepcidin is central to regulation of iron metabolism. Its effect on a cellular level involves binding ferroportin, the main iron export protein, resulting in its internalization and degradation and leading to iron sequestration within ferroportin-expressing cells. Aberrantly increased hepcidin leads to systemic iron deficiency and/or iron restricted erythropoiesis. Furthermore, insufficiently elevated hepcidin occurs in multiple diseases associated with iron overload. Abnormal iron metabolism as a consequence of hepcidin dysregulation is an underlying factor resulting in pathophysiology of multiple diseases and several agents aimed at manipulating this pathway have been designed, with some already in clinical trials...
2019: Vitamins and Hormones
Michela Asperti, Andrea Denardo, Magdalena Gryzik, Paolo Arosio, Maura Poli
Hepcidin is considered the major regulator of systemic iron homeostasis in human and mice, and its expression in the liver is mainly regulated at a transcriptional level. Central to its regulation are the bone morphogenetic proteins, particularly BMP6, that are heparin binding proteins. Heparin was found to inhibit hepcidin expression and BMP6 activity in hepatic cell lines and in mice, suggesting that endogenous heparan sulfates are involved in the pathway of hepcidin expression. This was confirmed by the study of cells and mice overexpressing heparanase, the enzyme that hydrolyzes heparan sulfates, and by cellular models with altered heparan sulfates...
2019: Vitamins and Hormones
Yohei Kanamori, Masaru Murakami, Makoto Sugiyama, Osamu Hashimoto, Tohru Matsui, Masayuki Funaba
Hepcidin expression is determined through transcriptional regulation by systemic iron status. However, acute or chronic inflammation also increases the expression of hepcidin, which is associated with the dysregulation of iron metabolism in pathological conditions. Interleukin (IL)-6 has been suggested to be a principal molecule to confer inflammation-related hepcidin transcription, which is mediated via signal transducer and activator of transcription (STAT)-binding site on the hepcidin promoter. Recently, it has been uncovered that another pro-inflammatory cytokine IL-1β stimulates hepcidin expression through the distinct mechanism underlying IL-6-mediated hepcidin transcription...
2019: Vitamins and Hormones
Katsunori Sasaki, Yutaka Kohgo, Takaaki Ohtake
Hepcidin is a main regulator of iron metabolism, of which abnormal expression affects intestinal absorption and reticuloendothelial sequestration of iron by interacting with ferroportin. It is also noted that abnormal iron accumulation is one of the key factors to facilitate promotion and progression of cancer including hepatoma. In this study, we firstly revealed that a new alternative HAMP transcript was found in hepatoma-derived cell line HLF, which was identical to the wild-type preprohepcidin sequence except lacking of an internal 60 bases...
2019: Vitamins and Hormones
Marie-Paule Roth, Delphine Meynard, Hélène Coppin
Iron, an essential nutrient, is required for many biological processes but is also toxic in excess. The lack of a mechanism to excrete excess iron makes it crucial for the body to regulate the amount of iron absorbed from the diet. This regulation is mediated by the hepatic hormone hepcidin. Hepcidin also controls iron release from macrophages that recycle iron and from hepatocytes that store iron. Hepcidin binds to the only known iron export protein, ferroportin, inducing its internalization and degradation and thus limiting the amount of iron released into the plasma...
2019: Vitamins and Hormones
Mohamed Boumaiza, Sondes Abidi
Hepcidin, belonging to the β-defensin family, was isolated for the first time from plasma and human urine. It is a cationic peptide, rich in cysteine bound with four disulfide bridges, which plays a major role in innate immunity and iron homeostasis. Some vertebrate species have multiple hepcidin homolog genes and each contains only one copy that functions as an iron regulator except hepcidin sequences in the pigeon (Columba livia). The aim of this chapter is to investigate the molecular evolution of several hepcidin gene from searches of the literature and public genomic databases from 17 different species, all among the vertebrates...
2019: Vitamins and Hormones
Gerald Litwack
No abstract text is available yet for this article.
2019: Vitamins and Hormones
Michael B Butterworth, Diego Alvarez de la Rosa
The mineralocorticoid hormone aldosterone is released by the adrenal glands in a homeostatic mechanism to regulate blood volume. Several cues elicit aldosterone release, and the long-term action of the hormone is to restore blood pressure and/or increase the retrieval of sodium from filtered plasma in the kidney. While the signaling cascade that results in aldosterone release is well studied, the impact of this hormone on tissues and cells in various organ systems is pleotropic. Emerging evidence indicates aldosterone may alter non-coding RNAs (ncRNAs) to integrate the hormonal response, and these ncRNAs may contribute to the heterogeneity of signaling outcomes in aldosterone target tissues...
2019: Vitamins and Hormones
Per Hellman, Peyman Björklund, Tobias Åkerström
Aldosterone-producing adenomas (APA) are more common than initially anticipated. APA cause primary aldosteronism (PA), which affect 3-10% of the hypertensive population. Research during recent years has led to an increased knowledge of the background dysregulation of the increased aldosterone release, where mutation in the gene encoding the potassium channel GIRK4-KCNJ5-is the most common. Moreover, the discovery of aldosterone-producing cell clusters in apparently normal adenomas has also led to increased understanding of the development of PA, and presumably also APA...
2019: Vitamins and Hormones
Alessandro Cannavo, Andrea Elia, Daniela Liccardo, Giuseppe Rengo, Walter J Koch
Aldosterone (Aldo) has been intensively studied for years since its isolation by Simpson and Tait in the 1950s. Interestingly, although most early research around Aldo's actions focused primarily on its interaction with the kidney, it was soon evident that this hormone is able to exert unexplained extra-renal effects, on various target organs including the heart. Importantly, over the course of the last decade a number of studies in pre-clinical models (in vitro and in vivo) and in humans have clearly demonstrated that Aldo, following the interaction with its receptor, the mineralocorticoid receptor (MR), is able to activate specific intracellular genomic and non-genomic pathways thus, regulating the homeostasis of the entire cardiovascular system...
2019: Vitamins and Hormones
Peter J Fuller, Jun Yang, Morag J Young
The cellular response to aldosterone is mediated by the mineralocorticoid receptor (MR). This response is best characterized in the renal epithelia with control of sodium and water homeostasis. However, the MR binds more than one ligand and has wide tissue distribution with multiple roles in cardiovascular function, immune cell signaling, neuronal fate and adipocyte differentiation. This chapter will provide a review of MR structure and function, and an analysis of the critical interactions involved in MR-mediated signal transduction, which contribute to ligand- and tissue-specificity...
2019: Vitamins and Hormones
Morag J Young, Gail K Adler
The mineralocorticoid receptor (MR) and aldosterone play a critical role in the regulation of plasma volume homeostasis and are critical for the control of normal physiological regulation blood pressure (BP) and organ perfusion and as a potent mediator of hypertension. Aldosterone and the MR also play a key role in regulating tissue volume expansion in many tissues, via the regulation of hypertrophy and/or hyperplasia of cardiac or vascular smooth muscle cells and through regulation of the extra cellular matrix (ECM) and tissue fibrosis...
2019: Vitamins and Hormones
Sofia Kanatsou, Marian Joels, Harm Krugers
Exposure to stressful experiences triggers the release of-among others-glucocorticoids from the adrenal glands. These hormones, cortisol and corticosterone in humans and rodents respectively, activate mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) that regulate neuronal activity and behavioral adaptation to stressful experiences. This review discusses molecular properties of MRs, the role of MRs in regulating neuronal function and behavior and, ultimately, evidence that enhanced MR function may confer resilience to stressful experiences...
2019: Vitamins and Hormones
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