鐵吸收的生物化學

basic knowledge

There are two types of absorbable dietary iron: heme and non-heme iron.

  • Heme iron from hemoglobin and myoglobin from animal food sources (meat, seafood, poultry) is the most easily absorbed form (15% to 35%) and accounts for 10% or more of our total absorbed iron.
  • Non-heme iron comes from plants and iron-fortified foods and is poorly absorbed.

Despite its relative abundance in the environment and relatively low human daily iron requirements, iron is often a growth-limiting nutrient in the human diet. Low iron intake is responsible for most anemia in developed countries and nearly half of anemia in non-industrialized countries. One reason for insufficient iron absorption is that upon exposure to oxygen, iron forms highly insoluble oxides that cannot be absorbed in the human gastrointestinal tract. Human intestinal epithelial cells contain apical membrane-bound enzymes whose activity can be regulated and which reduce insoluble iron (Fe3+) to absorbable ferrous iron (Fe2+) ions.

While iron deficiency is a relatively common problem, it's not the only extreme on the iron balance spectrum that must be avoided. Iron overload is particularly harmful to the heart, liver, and endocrine organs. Excess ferrous iron forms free radicals through the Fenton reaction, causing damage to tissues through oxidative reactions with lipids, proteins and nucleic acids. Therefore, where possible, dietary iron absorption and factors affecting bioavailability in the body are tightly controlled.

cellular level

Most dietary iron absorption occurs in the duodenum and proximal jejunum and depends largely on the physical state of the iron atoms. At physiological pH, iron exists in the oxidized ferric (Fe3+) state. To be absorbed, iron must be in the ferrous (Fe2+) state or bound by proteins such as heme. The low pH of gastric acid in the proximal duodenum allows the ferric reductase duodenal cytochrome B (Dcytb) to convert insoluble iron (Fe3+) into absorbable ferrous (Fe2+) ions at the brush border of enterocytes. . Gastric acid production plays a key role in plasma iron homeostasis. Iron absorption is greatly reduced when proton pump inhibitors such as omeprazole are used. Once ferric iron is reduced to ferrous iron in the intestinal lumen, a protein on the apical membrane of the enterocyte called divalent metal cation transporter 1 (DMT1) transports the iron across the apical membrane into the cell. Hypoxia-inducible factor 2 (HIF-2α) upregulates DMT1 and Dcytb levels in the hypoxic environment of the intestinal mucosa.

Certain dietary compounds inhibit or enhance the duodenal pH-dependent iron absorption process.

  • Inhibitors of iron absorption include phytate, a compound found in plant-based diets that exhibits dose-dependent effects on iron absorption. Polyphenols are found in black and herbal teas, coffee, wine, legumes, grains, fruits and vegetables, and have been shown to inhibit iron absorption. Unlike other inhibitors, such as polyphenols and phytates, which only block non-heme iron absorption, calcium inhibits both heme and non-heme iron when initially absorbed by enterocytes. Animal proteins such as casein, whey, egg whites, and plant proteins have been shown to inhibit the body's absorption of iron. Oxalic acid, found in spinach, beets, legumes and nuts, binds and inhibits iron absorption.
  • The enhancer of iron absorption is primarily the effect of vitamin C, which can overcome the effects of all dietary inhibitors when included in a diet high in non-heme iron (usually a diet high in vegetables). Ascorbic acid forms a chelate with ferric iron (Fe3+) in the low pH of the stomach, which persists and remains soluble in the alkaline environment of the duodenum.

molecular level

Once inside enterocytes, iron can be stored as ferritin or transported across the basolateral membrane into the circulation bound to ferroportin.

Ferritin is a hollow, globular protein composed of 24 subunits that enhances the storage and regulation of iron levels in the body. Iron is stored in the interior of the ferritin globules in the Fe3+ state by incorporation into a solid crystalline mineral called ferrihydrite [FeO(OH)]8[FeO(H2PO4)].

The monomer of the ferritin molecule has ferroxidase activity (Fe3+ ↔ Fe2+), which causes the Fe2+ ions to migrate out of the ferrihydrite lattice structure, allowing them to subsequently flow out of the intestinal epithelial cells through ferroportin and cross the basolateral membrane of the intestinal epithelial cells. Enter the loop. The transmembrane protein ferroportin is the only efflux pathway for cellular iron and is almost entirely regulated by hepcidin levels. High levels of iron, inflammatory cytokines, and oxygen lead to increased levels of the peptide hormone hepcidin. Hepcidin binds to ferroportin, causing its internalization and degradation, and effectively shunts cellular iron into ferritin stores and prevents its absorption into the blood. thereby,

If hepcidin levels are low and ferroportin is not downregulated, ferrous iron (Fe2+) can be released from the enterocyte, where it is again oxidized to ferric iron (Fe3+) to bind to transferrin, which is present in Carrier proteins in plasma. Two copper-containing enzymes, ceruloplasmin in plasma and hephaestin on the basolateral membrane of enterocytes, catalyze the oxidation of ferrous iron and subsequently bind to transferrin in plasma. The main function of transferrin is to chelate iron to make it soluble, prevent the formation of reactive oxygen species, and facilitate its transport into the cell.

clinical significance

Enterocyte DMT1 and Dcytb levels are upregulated in the setting of iron deficiency anemia, and mutations in DMT1 have been shown to cause microcytic anemia and hepatic iron overload.

Conditions that degrade the duodenal mucosa that reduce iron absorption include:

  • Celiac disease
  • tropical sprue
  • Crohn's disease
  • duodenal cancer
  • duodenal ulcer
  • familial adenomatous polyposis

Anemia of chronic disease is a normocytic, normocytic anemia characterized by elevated ferritin stores but reduced systemic iron levels. Inflammatory states increase cytokine release (IL-6), which stimulates hepcidin expression in the liver. Hepcidin degradation through ferroportin leads to reduced iron absorption and reduced iron release from macrophages. The iron accumulated in the cells of anemia of chronic disease is stored in the form of ferritin.

Iron deficiency anemia is a hypochromic microcytic anemia caused by bleeding, reduced dietary iron, or reduced iron absorption. Menstruating women of childbearing age need twice the amount of iron as men of the same age. Pregnancy and breastfeeding also significantly increase a woman's iron requirements, helping to make iron deficiency the most common dietary deficiency in the world.

Review

All comments are moderated before being published

HealthyPIG Magazine

View all
牛骨湯食譜大全|Instant Pot 壓力煲 & 傳統老火湯版本

牛骨湯食譜大全|Instant Pot 壓力煲 & 傳統老火湯版本

牛骨湯食譜係香港家庭常見嘅煲湯之一,牛骨湯香濃滋補,配合中藥材更具養生功效。本文介紹肉骨類選擇、牛骨湯建議配搭、常見中藥材分類,以及Instant Pot壓力煲與傳統老火湯版本食譜,並引用科學研究支持。
澳洲飲用水發現「食腦變形蟲」:全球風險與地區對策(含各國/各州實用指南)

澳洲飲用水發現「食腦變形蟲」:全球風險與地區對策(含各國/各州實用指南)

澳洲飲用水發現「食腦變形蟲」:全球風險與地區對策(含各國/各州實用指南) 澳洲飲用水發現「食腦變形蟲」:全球風險與地區對策(含各國/各州實用指南) 重點:事件本身不代表飲水會感染;主要風險來自水經鼻腔進入。 目錄 ...
如何判斷雞翅是否變壞?

如何判斷雞翅是否變壞?

重點摘要 雞翅會變質嗎? 如何判斷雞翅是否變壞? 過期雞翅還能食嗎? 雞翅可存放多久? 如何儲存雞翅? 雞翅可以冷凍嗎? 結論 雞翅會變質嗎? 會。皮脂較多、表面不潔或溫度過高時,細菌繁殖更快。 如何判斷雞翅是否變壞? 外觀:皮色發黃、出黑斑或血水。 觸感:表面黏滑、軟爛。 氣...
如何判斷雞蛋是否變壞?

如何判斷雞蛋是否變壞?

重點摘要 雞蛋會變質嗎? 如何判斷雞蛋是否變壞? 過期雞蛋還能食嗎? 雞蛋可存放多久? 如何儲存雞蛋? 雞蛋可以冷凍嗎? 結論 雞蛋會變質嗎? 會。殼面有微孔,溫差及濕度變化會令細菌入侵。 如何判斷雞蛋是否變壞? 水測:沉底=較新鮮;浮起=多半變壞。 打開觀察:蛋白渾濁水樣、蛋黃...
如何判斷羊肉是否變壞?

如何判斷羊肉是否變壞?

重點摘要 羊肉會變質嗎? 如何判斷羊肉是否變壞? 過期羊肉還能食嗎? 羊肉可存放多久? 如何儲存羊肉? 羊肉可以冷凍嗎? 結論 羊肉會變質嗎? 會。脂肪多而易氧化,處理或存放唔好就會變壞。 如何判斷羊肉是否變壞? 顏色:紅轉黑,或出現綠斑。 脂肪:由白轉黃兼有酸味。 氣味:由輕...
如何判斷豬肉是否變壞?

如何判斷豬肉是否變壞?

重點摘要 豬肉會變質嗎? 如何判斷豬肉是否變壞? 過期豬肉還能食嗎? 豬肉可存放多久? 如何儲存豬肉? 豬肉可以冷凍嗎? 結論 豬肉會變質嗎? 會。豬肉表面水活度高,加上處理不潔或溫度過高,容易腐敗。 如何判斷豬肉是否變壞? 顏色:粉紅轉灰、發綠或出斑。 氣味:酸臭、腥臭味濃 ...
如何判斷牛肉是否變壞?

如何判斷牛肉是否變壞?

重點摘要 牛肉會變質嗎? 如何判斷牛肉是否變壞? 過期牛肉還能食嗎? 牛肉可存放多久? 如何儲存牛肉? 牛肉可以冷凍嗎? 結論 牛肉會變質嗎? 會。牛肉含高蛋白同水分,若溫度控制或衛生不當,細菌會快速繁殖,導致變壞。 如何判斷牛肉是否變壞? 顏色:鮮紅轉深褐甚至發黑;脂肪變黃。 ...
成年後懷疑自己有注意力不足過動症(ADHD),應該接受診斷嗎?

成年後懷疑自己有注意力不足過動症(ADHD),應該接受診斷嗎?

在過去,注意力不足過動症(Attention-Deficit/Hyperactivity Disorder, ADHD)多被視為「小孩的病」,很多成年人小時候從未被評估或診斷。直到近年社會對心理健康重視度提升,許多成人才開始懷疑,自己長期以來的專注困難、健忘、衝動或時間管理不良,可能與 ADHD 有關。這種「晚發現」的情況相當普遍,也引發了問題:成年後是否值得接受 ADHD 診斷?

哪些職業對健康影響最大?科學與現實的分析

哪些職業對健康影響最大?科學與現實的分析

在現代社會中,工作佔據了人們生命中相當大的一部分。然而,不同職業對健康的風險並不相同。一些工作性質或環境,會顯著增加慢性病、心理壓力、甚至縮短壽命的風險。以下從科學研究與醫學角度,探討幾類對健康損害較大的職業,並附上相關統計數據。