scholarly journals Role of Dietary Flavonoids in Iron Homeostasis

2019 ◽  
Vol 12 (3) ◽  
pp. 119 ◽  
Author(s):  
Marija Lesjak ◽  
Surjit K. S. Srai
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Iron Absorption ◽  
Therapeutic Potential ◽  
State Of The Art ◽  
Iron Status ◽  
Dietary Factors ◽  
The Body ◽  
Dietary Flavonoids

Balancing systemic iron levels within narrow limits is critical for human health, as both iron deficiency and overload lead to serious disorders. There are no known physiologically controlled pathways to eliminate iron from the body and therefore iron homeostasis is maintained by modifying dietary iron absorption. Several dietary factors, such as flavonoids, are known to greatly affect iron absorption. Recent evidence suggests that flavonoids can affect iron status by regulating expression and activity of proteins involved the systemic regulation of iron metabolism and iron absorption. We provide an overview of the links between different dietary flavonoids and iron homeostasis together with the mechanism of flavonoids effect on iron metabolism. In addition, we also discuss the clinical relevance of state-of-the-art knowledge regarding therapeutic potential that flavonoids may have for conditions that are low in iron such as anaemia or iron overload diseases.

Intestinal Iron Absorption: Regulation by Dietary & Systemic Factors

2010 ◽  
Vol 80 (45) ◽  
pp. 231-242 ◽  
Author(s):  
Paul A. Sharp
Keyword(s):  
Iron Homeostasis ◽  
Iron Absorption ◽  
Iron Status ◽  
Heme Iron ◽  
Dietary Factors ◽  
The Body ◽  
Excess Iron ◽  
Non Heme Iron ◽  
Systemic Factors ◽  
And Function

Iron is an essential trace metal in human metabolism. However, imbalances in iron homeostasis are prevalent worldwide and have detrimental effects on human health. Humans do not have the ability to remove excess iron and therefore iron homeostasis is maintained by regulating the amount of iron entering the body from the diet. Iron is present in the human diet in number of different forms, including heme (from meat) and a variety of non-heme iron compounds. While heme is absorbed intact, the bioavailability of non-heme iron varies greatly depending on dietary composition. A number of dietary components are capable of interacting with iron to regulate its solubility and oxidation state. Interestingly, there is an emerging body of evidence suggesting that some nutrients also have direct effects on the expression and function of enterocyte iron transporters. In addition to dietary factors, body iron status is a major determinant of iron absorption. The roles of these important dietary and systemic factors in regulating iron absorption will be discussed in this review.

scholarly journals Hepcidin: A Critical Regulator of Iron Metabolism during Hypoxia

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Korry J. Hintze ◽  
James P. McClung
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Molecular Mechanisms ◽  
Iron Absorption ◽  
Iron Acquisition ◽  
Iron Status ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Response Element ◽  
Hypoxia Response ◽  
Hepcidin Expression

Iron status affects cognitive and physical performance in humans. Recent evidence indicates that iron balance is a tightly regulated process affected by a series of factors other than diet, to include hypoxia. Hypoxia has profound effects on iron absorption and results in increased iron acquisition and erythropoiesis when humans move from sea level to altitude. The effects of hypoxia on iron balance have been attributed to hepcidin, a central regulator of iron homeostasis. This paper will focus on the molecular mechanisms by which hypoxia affects hepcidin expression, to include a review of the hypoxia inducible factor (HIF)/hypoxia response element (HRE) system, as well as recent evidence indicating that localized adipose hypoxia due to obesity may affect hepcidin signaling and organismal iron metabolism.

Iron Imports. VI. HFE and regulation of intestinal iron absorption

2006 ◽  
Vol 290 (4) ◽  
pp. G590-G594 ◽  
Author(s):  
Robert E. Fleming ◽  
Robert S. Britton
Keyword(s):  
Iron Homeostasis ◽  
Iron Absorption ◽  
Iron Status ◽  
Hfe Gene ◽  
Primary Role ◽  
Intestinal Iron Absorption ◽  
Downstream Effects ◽  
Cell Type Specific ◽  
Intestinal Enterocytes

The majority of clinical cases of iron overload is caused by mutations in the HFE gene. However, the role that HFE plays in the physiology of intestinal iron absorption remains enigmatic. Two major models have been proposed: 1) HFE exerts its effects on iron homeostasis indirectly, by modulating the expression of hepcidin; and 2) HFE exerts its effects directly, by changing the iron status (and therefore the iron absorptive activity) of intestinal enterocytes. The first model places the primary role of HFE in the liver (hepatocytes and/or Kupffer cells). The second model places the primary role in the duodenum (crypt cells or villus enterocytes). These models are not mutually exclusive, and it is possible that HFE influences the iron status in each of these cell populations, leading to cell type-specific downstream effects on intestinal iron absorption and body iron distribution.

scholarly journals Erythrocytes: Central Actors in Multiple Scenes of Atherosclerosis

2021 ◽  
Vol 22 (11) ◽  
pp. 5843
Author(s):  
Chloé Turpin ◽  
Aurélie Catan ◽  
Olivier Meilhac ◽  
Emmanuel Bourdon ◽  
François Canonne-Hergaux ◽  
...  
Keyword(s):  
Iron Homeostasis ◽  
The Body ◽  
Diabetic Patients ◽  
Special Focus ◽  
Plaque Progression ◽  
Cell Dysfunction ◽  
Circulating Cells ◽  
The Impact ◽  
Progression Of Atherosclerosis

The development and progression of atherosclerosis (ATH) involves lipid accumulation, oxidative stress and both vascular and blood cell dysfunction. Erythrocytes, the main circulating cells in the body, exert determinant roles in the gas transport between tissues. Erythrocytes have long been considered as simple bystanders in cardiovascular diseases, including ATH. This review highlights recent knowledge concerning the role of erythrocytes being more than just passive gas carriers, as potent contributors to atherosclerotic plaque progression. Erythrocyte physiology and ATH pathology is first described. Then, a specific chapter delineates the numerous links between erythrocytes and atherogenesis. In particular, we discuss the impact of extravasated erythrocytes in plaque iron homeostasis with potential pathological consequences. Hyperglycaemia is recognised as a significant aggravating contributor to the development of ATH. Then, a special focus is made on glycoxidative modifications of erythrocytes and their role in ATH. This chapter includes recent data proposing glycoxidised erythrocytes as putative contributors to enhanced atherothrombosis in diabetic patients.

Wearable Technologies for Helping Human Thermophysiological Comfort

2018 ◽  
pp. 203-231
Author(s):  
Radostina A. Angelova
Keyword(s):  
State Of The Art ◽  
Wearable Devices ◽  
The State ◽  
The Body ◽  
Cold Environment ◽  
Human Comfort ◽  
Wearable Technologies ◽  
Thermoregulatory System ◽  
Intelligent Clothing

The thermophysiological comfort is one of the aspects of the human comfort. It is related to the thermoregulatory system of the body and its reactions to the temperature of the surrounding air, activity and clothing. The aim of the chapter is to present the state of the art in the wearable technologies for helping the human thermophysiological comfort. The basic processes of body's thermoregulatory system, the role of the hypothalamus, the reactions of the body in hot and cold environment, together with the related injuries, are described. In the second part of the chapter smart and intelligent clothing, textiles and accessories are presented together with wearable devices for body's heating/cooling.

scholarly journals Iron and Zinc Homeostasis and Interactions: Does Enteric Zinc Excretion Cross-Talk with Intestinal Iron Absorption?

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1885 ◽  
Author(s):  
Palsa Kondaiah ◽  
Puneeta Singh Yaduvanshi ◽  
Paul A Sharp ◽  
Raghu Pullakhandam
Keyword(s):  
Iron Absorption ◽  
Iron Status ◽  
The Body ◽  
Zinc Homeostasis ◽  
Iron Accumulation ◽  
Intestinal Cell ◽  
Deficiency Anemia ◽  
Intestinal Iron Absorption ◽  
Tissue Iron ◽  
Iron And Zinc

Iron and zinc are essential micronutrients required for growth and health. Deficiencies of these nutrients are highly prevalent among populations, but can be alleviated by supplementation and food fortification. Cross-sectional studies in humans showed positive association of serum zinc levels with hemoglobin and markers of iron status. Dietary restriction of zinc or intestinal specific conditional knock out of ZIP4 (SLC39A4), an intestinal zinc transporter, in experimental animals demonstrated iron deficiency anemia and tissue iron accumulation. Similarly, increased iron accumulation has been observed in cultured cells exposed to zinc deficient media. These results together suggest a potential role of zinc in modulating intestinal iron absorption and mobilization from tissues. Studies in intestinal cell culture models demonstrate that zinc induces iron uptake and transcellular transport via induction of divalent metal iron transporter-1 (DMT1) and ferroportin (FPN1) expression, respectively. It is interesting to note that intestinal cells are exposed to very high levels of zinc through pancreatic secretions, which is a major route of zinc excretion from the body. Therefore, zinc appears to be modulating the iron metabolism possibly via regulating the DMT1 and FPN1 levels. Herein we critically reviewed the available evidence to hypothesize novel mechanism of Zinc-DMT1/FPN1 axis in regulating intestinal iron absorption and tissue iron accumulation to facilitate future research aimed at understanding the yet elusive mechanisms of iron and zinc interactions.

scholarly journals IRON METABOLISM

Blood ◽  
1950 ◽  
Vol 5 (11) ◽  
pp. 983-1008 ◽  
Author(s):  
CLEMENT A. FINCH ◽  
MARK HEGSTED ◽  
THOMAS D. KINNEY ◽  
E. D. THOMAS ◽  
CHARLES E. RATH ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Serum Iron ◽  
Iron Absorption ◽  
Binding Protein ◽  
The Body ◽  
Iron Binding ◽  
Body Iron ◽  
Iron Administration ◽  
Parenteral Iron ◽  
Iron Binding Protein

Abstract On the basis of experimental and clinical observations and a review of the literature, a concept of the behavior of storage iron in relation to body iron metabolism has been formulated. Storage iron is defined as tissue iron which is available for hemoglobin synthesis when the need arises. This iron is stored intracellularly in protein complex as ferritin and hemosiderin. It would appear that wherever the cell is functionally intact, such iron is available for general body needs. Iron is transported by a globulin of the serum to and from the various tissues of the body to satisfy their metabolism. Surplus iron carried by this iron-binding protein is deposited chiefly in the liver. Storage iron may be increased in two ways. The first mechanism results from the inability of the body to excrete significant amounts of iron. Because of this, any decrease in circulating red cell iron (any anemia other than blood loss or iron deficiency anemia) is accompanied by a shift of iron to the tissue compartment. The total amount of body iron remains constant and is merely redistributed. This is to be contrasted with the absolute increase in body iron and enlarged iron stores which follow excessive iron absorption or parenteral iron administration. Enlarged iron stores in either instance may be evaluated by examination of sternal marrow or determination of the serum iron and saturation of the iron binding protein In states of iron excess, differences in initial distribution are observed, depending on the route of administration and type of iron compound employed. Iron absorbed from the gastro-intestinal tract and soluble iron salts injected in small amounts are transported by the iron-binding protein of the serum and stored predominantly in the liver. Colloidal iron given intravenously is taken up by the reticulo-endothelial tissue. Erythrocytes appear to localize in greatest concentration in the spleen, while greater amounts of hemoglobin iron are found in the renal parenchyma. These latter differences in distribution reflect the capacity of various body tissues to assimilate different iron compounds, which while present in the plasma are not carried by the iron-binding protein. Over a period of time an internal redistribution of iron from these various sites occurs through the serum iron compartment. The liver becomes progressively loaded with iron. When the capacity of the liver to store iron is exceeded, the serum iron increases and secondary tissue receptors begin to fill with iron. That iron in large amounts is toxic to tissues is suggested by the occurrence of fibrosis in the organs most heavily laden with iron. This sequence of events, whether following excessive iron absorption or parenteral iron administration is believed to be responsible for the clinical and pathologic picture of hemochromatosis.

scholarly journals A Short Review of Iron Metabolism and Pathophysiology of Iron Disorders

Medicines ◽  
2019 ◽  
Vol 6 (3) ◽  
pp. 85 ◽  
Author(s):  
Andronicos Yiannikourides ◽  
Gladys Latunde-Dada
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Cellular Proliferation ◽  
Peptide Hormone ◽  
Short Review ◽  
Reticuloendothelial System ◽  
Cellular Level ◽  
Feedback Mechanism ◽  
The Body ◽  
Iron Regulatory Proteins

Iron is a vital trace element for humans, as it plays a crucial role in oxygen transport, oxidative metabolism, cellular proliferation, and many catalytic reactions. To be beneficial, the amount of iron in the human body needs to be maintained within the ideal range. Iron metabolism is one of the most complex processes involving many organs and tissues, the interaction of which is critical for iron homeostasis. No active mechanism for iron excretion exists. Therefore, the amount of iron absorbed by the intestine is tightly controlled to balance the daily losses. The bone marrow is the prime iron consumer in the body, being the site for erythropoiesis, while the reticuloendothelial system is responsible for iron recycling through erythrocyte phagocytosis. The liver has important synthetic, storing, and regulatory functions in iron homeostasis. Among the numerous proteins involved in iron metabolism, hepcidin is a liver-derived peptide hormone, which is the master regulator of iron metabolism. This hormone acts in many target tissues and regulates systemic iron levels through a negative feedback mechanism. Hepcidin synthesis is controlled by several factors such as iron levels, anaemia, infection, inflammation, and erythropoietic activity. In addition to systemic control, iron balance mechanisms also exist at the cellular level and include the interaction between iron-regulatory proteins and iron-responsive elements. Genetic and acquired diseases of the tissues involved in iron metabolism cause a dysregulation of the iron cycle. Consequently, iron deficiency or excess can result, both of which have detrimental effects on the organism.

scholarly journals Role of iron metabolism-regulator hepcidin in perinatal iron homeostasis

2010 ◽  
Vol 151 (3) ◽  
pp. 83-91 ◽  
Author(s):  
Ádám Balogh ◽  
Szilvia Bősze ◽  
Kata Horváti ◽  
Gábor Mező ◽  
Sándor Kéki ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Iron Homeostasis

A hepcidin egy nemrégiben felfedezett, defenzin típusú peptid, amely központi szerepet játszik a vasháztartás szabályozásában. A hepcidin csökkenti a vastranszportban szerepet játszó molekulák expresszióját, így gátolja a vas gastrointestinalis rendszerből való felszívódását, makrofágokból való felszabadulását, csökkentve ezzel a szérum vasszintjét. A hepcidin vasháztartásban betöltött szerepének tisztázása segíthet a gyulladásos és krónikus betegségekben bekövetkező anémia pontosabb megértésében. Munkánk kezdetén a hepcidin kimutatására alkalmas, kereskedelmi forgalomban elérhető módszer nem állt rendelkezésre. Célunk volt egy, a vizelethepcidin kimutatására alkalmas módszer kidolgozása, valamint hogy ezen módszer segítségével vizsgáljuk a hepcidin jelentőségét a perinatalis vasháztartásban. Munkánk során a natív, emberi hepcidin aminosav-szekvenciájának megfelelően állítottunk elő peptidszármazékokat, amelyek közül az 1-7 peptidszármazékról igazoltuk, hogy alkalmas lehet a natív hepcidin standard helyettesítésére immunreakción alapuló módszerek fejlesztésekor. Kidolgoztunk egy, az emberi vizelethepcidin mennyiségi meghatározására alkalmas, lézerdeszorpciós tömegspektrometriás, szemikvantitatív módszert, amelyben az általunk szintetizált acetil-1-25 peptidszármazékot mint hepcidinszerű belső standardot elsőként alkalmaztuk. Kidolgoztunk a vizelet tisztítására és a vizelethepcidin koncentrálására alkalmas, szilárd fázisú extrakción alapuló módszert. Az általunk kidolgozott módszerrel elsőként mértük egészséges újszülöttek vizelethepcidin-szintjét, valamint egy kereskedelmi forgalomban elérhető módszerrel a szérumprohepcidin-szintjét. Kimutattuk, hogy az érett újszülöttek korai adaptációja során a szérumprohepcidin-szint nem változik, a vizelethepcidin viszont szignifikánsan nő. A szérumprohepcidin- és a vizelethepcidin-szintek egymással nem mutattak összefüggést. Kimutattuk, hogy az érett újszülöttek vasháztartásának korai adaptációja során a szérumprohepcidin-szintek kizárólag a vörösvérsejtek átlagos hemoglobinkoncentrációjával, míg a vizelethepcidin-szintek a szérumvasszinttel és teljes vaskötő kapacitással mutattak összefüggést. Kimutattuk, hogy az érett újszülöttek vasháztartásának korai adaptációja során a köldökzsinórvér-mintákban az alacsonyabb szérumprohepcidin-szintek esetén szabad vas jelenléte igazolható. Összefoglalva: Eredményeink alapján elmondhatjuk, hogy a hepcidinnek valószínűleg szerepe van az újszülöttek korai, a vasháztartást érintő adaptációjában, azonban további vizsgálatok szükségesek ahhoz, hogy ezt az összefüggést biztosan megállapíthassuk.

Sign in / Sign up

Export Citation Format

Share Document