Magnesium hauv Kev Laus, Kev Noj Qab Haus Huv thiab Kab Mob
Jun 21, 2022
Thov hu rauoscar.xiao@wecistanche.comyog xav paub ntxiv
Abstract:Ntau qhov kev hloov pauv hauv magnesium (Mg) metabolism tau tshaj tawm nrog kev laus, suav nrog txo qis Mg kom tsawg, ua rau lub plab hnyuv Mg tsis txaus, thiab lub raum Mg nkim. Mg qhov tsis txaus yog feem ntau asymptomatic thiab cov tsos mob tshwm sim feem ntau tsis yog tshwj xeeb lossis tsis tuaj. Asthenia, pw tsis tsaug zog, hyperemotionality, thiab kev paub tsis meej yog tshwm sim nyob rau hauv cov neeg laus uas tsis muaj Mg me me thiab tej zaum yuav tsis meej pem nrog cov tsos mob ntawm hnub nyoog. Chronic Mg tsis txaus ua rau muaj kev tsim tawm ntawm cov dawb radicals uas tau cuam tshuam rau kev txhim kho ntau yam mob uas muaj hnub nyoog. Ntau tus tib neeg cov kab mob tau cuam tshuam nrog Mg qhov tsis txaus, suav nrog cov kab mob plawv, ntshav siab thiab mob stroke, cardio-metabolic syndrome thiab hom 2 mob ntshav qab zib mellitus, cov hlab ntsws constrictive syndromes thiab hawb pob, kev nyuaj siab, kev ntxhov siab thiab kev puas siab puas ntsws, Alzheimer's disease (AD) thiab Lwm cov kab mob dementia, cov kab mob ntawm cov leeg (cov leeg mob, mob nkees, thiab fibromyalgia), pob txha fragility, thiab mob qog noj ntshav. Kev noj haus Mg thiab/lossis Mg noj hauv cov dej haus (feem ntau bioavailable dua Mg muaj nyob rau hauv cov zaub mov) los yog lwm yam tshuaj Mg yuav tsum tau muab coj los xav rau hauv kev kho Mg deficits.cistanche noov lojKev tswj kom zoo Mg sib npaug thoob plaws hauv lub neej tuaj yeem pab tiv thaiv oxidative kev nyuaj siab thiab mob ntev uas cuam tshuam nrog kev laus. Qhov no yuav tsum tau ua kom pom los ntawm kev tshawb fawb yav tom ntej.
Ntsiab lus:magnesium; oxidative kev nyuaj siab; kab mob; dementia; ntshav qab zib; osteoporosis; kev laus; ntshav siab; noj qab haus huv; kev nyob ntev
Thov nias ntawm no kom paub ntxiv
1. Taw qhia
Magnesium ion (Mg) yog divalent intracellular cation feem ntau tam sim no nyob rau hauv tib neeg lub cell thiab lub thib ob cation tom qab poov tshuaj (K). Mg lub atomic hnyav yog 24.305 g / mol, thiab nws tus lej atomic yog 12 (Table 1). Mg muaj lub luag haujlwm tseem ceeb hauv ntau cov txheej txheem lom neeg, suav nrog oxidative phosphorylation, lub zog tsim tawm, glycolysis, protein, thiab nucleic acid synthesis [1]. Mg ua lub luag haujlwm hauv mitochondrial synthesis ntawm adenosine triphosphate (ATP) los ua MgATP[2]. Cell signaling xav tau MgATP rau cov protein phosphorylation thiab ua kom cov cyclic adenosine monophosphate (cAMP), uas koom nrog ntau cov txheej txheem biochemical [3]. Mg ions koom nrog hauv kev thauj mus los ntawm lwm cov ions los ntawm cov cell membranes, hauv cov leeg nqaij, thiab tswj cov neuron excitability.cistanche hmoovCellular Mg homeostasis yog txuas nrog cov cellular metabolism ntawm lwm cov ions, piv txwv li, K, sodium (Na), calcium (Ca), ntawm Na plus / K ntxiv / ATPase, Ca ntxiv ntxiv rau K channels, thiab lwm yam txheej txheem [4].
Mg muaj lub luag haujlwm tseem ceeb hauv cellular homeostasis thiab lub cev ua haujlwm. Yog li, Mg muaj lub luag haujlwm ntawm lub cev hauv kev tswj hwm ntau yam kev ua haujlwm ntawm tes thiab cov txheej txheem metabolic, suav nrog enzyme-substrate, thiab cov qauv thiab cov txheej txheem ua haujlwm [2,5]. Mg yog ib cofactor nyob rau hauv ntau tshaj 600 enzymatic cov tshuaj tiv thaiv thiab yuav tsum tau rau cov kev ua ntawm cov protein kinases, glycolytic enzymes, tag nrho cov txheej txheem phosphorylation, thiab tag nrho cov kev cuam tshuam uas cuam tshuam ATP [25]. Mg ion muaj ib qho me me Ca antagonist kev ua thiab koom nrog ntau yam kev ua haujlwm (ntau-enzyme complexes, piv txwv li, G-proteins, proteins thiab nucleic acids synthesis, N-methyl-D-aspartic acid (NMDA) receptors, mitochondria, polyribosomes, thiab lwm yam). Hauv kaum xyoo dhau los, cov kab mob pathophysiological thiab kev kho mob tseem ceeb ntawm Mg tau lees paub, nrog rau qhov ua tau ntawm Mg tsis txaus rau ntau tus neeg mob.
2. Mg Metabolism thiab Yuav Tsum Tau
Cov ntsiab lus Mg nyob rau hauv tib neeg lub cev yog nyob ib ncig ntawm 24-29 g ntawm Mg, ntawm uas ze li ntawm 2/3 yog tso rau hauv pob txha thiab 1/3 nyob rau hauv lub hlwb. Tsuas yog<1% of="" the="" total="" mg="" is="" extracellular.="" mg="" levels="" in="" the="" serum="" range="" between="" 0.75="" and="" 0.95="" mmol/l.="" serum="" mg="" levels="" in="" healthy="" subjects="" are="" very="" constant="" and="" tightly="" preserved="" within="" this="" narrow="" range="" by="" a="" dynamic="" balance="" among="" mg="" intake,="" intestinal="" absorption,="" kidney="" excretion,="" bone="" storage,="" and="" the="" mg="" requirement="" of="" different="" tissues.="" mg="" absorption="" is="" increased="" under="" conditions="" of="" mg="" limited="" assumption.="" if="" mg="" deprivation="" persists,="" bone="" storage="" would="" help="" to="" preserve="" serum="" mg="" levels="" by="" replacing="" part="" of="" its="" content="" in="" the="" extracellular="" compartment="" [6]="" (figure="" 1).="" serum="" mg="" levels="" are="" considered="" low="" if="" inferior="" to="" 0.75="" mmol/l,="" while="" frank="" hypomagnesemia="" is="" generally="" considered="" a="" serum="" mg="" level="" lower="" than="" 0.7="" mmol/l="" [1,2,7].="" total="" serum="" mg="" levels="" (mgt)="" are="" not="" a="" sufficiently="" precise="" measurement="" of="" the="" body's="" mg="" status;="" mgt="" levels="" are="" more="" useful="" in="" epidemiological="" studies="" but="" are="" not="" enough="" accurate="" to="" detect="" subclinical="" mg="" deficits="" in="" a="" single="" subject="" [8].="" this="" is="" because="" serum="" total="" mg="" levels="" do="" not="" accurately="" mirror="" intracellular="" concentrations,="" and="" low="" intracellular="" mg="" levels="" generally="" precede="" alterations="" of="" serum="" mg.="" it="" is="" thus="" possible="" to="" have="" intracellular="" and="" storage="" mg="" depletion="" with="" still="" normal="" total="" serum="" mg="" values="">
Daim duab 1. Mg tshuav nyiaj li cas (cov xub qhia feem ntau qhov chaw ntawm Mg depletion nrog kev laus), suav nrog Mg noj txhua hnub thiab kev tso tawm. Tag nrho tib neeg lub cev cov ntsiab lus ntawm Mg yog 24 txog 29 g. Txhawm rau tswj hwm Mg tshuav nyiaj li cas, tus neeg noj qab haus huv yuav tsum tau noj ib ncig ntawm 5-7 mg/kg/hnub. Kev nqus ntawm cov hnyuv txhua hnub txawv ntawm 25 mus rau 60 feem pua ntawm Mg kom tsawg. Hauv lub raum, 80 feem pua ntawm kev ncig Mg yog lim thiab kwv yees li 60 feem pua yog reabsorbed raws lub raum tubule. Qhov no ua rau muaj kev tso tawm tawm ntawm kwv yees li 5 mmol / hnub. Fecal excretion yog hais txog 7.5 mmol / hnub.cistanche salsa extractIntracellular compartment muab cov khw muag khoom Mg tseem ceeb tshaj plaws.
Cistanche tuaj yeem tiv thaiv kev laus
Qhov kev xav tau Mg zoo tshaj plaws nrog zaub mov yog suav tias yog 320 mg / hnub rau cov poj niam thiab 420 mg / hnub rau cov txiv neej, raws li 2015-2020 Cov Lus Qhia Txog Kev Noj Qab Haus Huv rau Neeg Asmeskas[9], tab sis cov kev xav tau siab dua tuaj yeem xav tau hauv qee qhov kev mob physiologic. xws li cev xeeb tub, laus, los yog thaum lub sij hawm cev xeeb tub thiab nyob rau hauv ib co pathological mob (xws li, kab mob, hom 2 mob ntshav qab zib mellitus (T2DM), thiab lwm yam).
Ntau yam yuav hloov Mg tshuav nyiaj li cas: cov ntsiab lus siab hauv kev noj zaub mov ntawm Na, Ca, protein, cawv, lossis caffeine, lossis siv qee yam tshuaj (diuretics, piv txwv li, furosemide; proton-pump inhibitors, xws li omeprazole, thiab lwm yam). Mg nqus feem ntau tshwm sim hauv cov hnyuv [10]. Yuav kom tswj tau qhov sib npaug, tus neeg noj qab haus huv yuav tsum tau noj ib ncig ntawm 5-7 mg/kg/hnub (Table2). Mg tso rau hauv cov pob txha tsis yooj yim pauv thiab ib qho kev xav tau ntawm Mg sai yog muab los ntawm Mg tam sim no nyob rau hauv lub hauv nruab nrog cev. Lub raum pab tswj thiab hloov kho Mg tshuav nyiaj li cas; Txhua hnub ib ncig ntawm 120 mg ntawm Mg raug tshem tawm mus rau hauv cov zis [1]. Kev tswj lub raum Mg nruj me ntsis nyob ntawm Mg xwm txheej, txij li Mg depletion txhawb nqa Mg reabsorption thoob plaws nephron, thaum Mg tso zis txo qis hauv cov xwm txheej ntawm lub cev Mg depletion [11].cistanche qiaDiuretics hloov lub raum Mg tuav nce Mg nkim [12]. Tsis muaj cov tshuaj hormones paub tias yog Mg regulator. Txawm li cas los xij, ntau yam hormonal muaj feem cuam tshuam rau Mg homeostasis (piv txwv li, insulin, parathyroid hormone (PTH), calcitonin, thiab catecholamines) [6,13].
3. Mg Deficiencies txuam nrog txo Mg kom tsawg
Ntau qhov kev tshawb fawb tau pom tsis tu ncua hais tias nyob rau sab hnub poob lub teb chaws qhov nruab nrab kev noj haus Mg feem ntau tsis txaus [14] thiab qis dua qhov pom zoo noj txhua hnub ntawm Mg [15]. King et al. xyoo 2005 tau tshaj tawm tias yuav luag 2/3 ntawm cov neeg Amelikas muaj kev noj Mg qis dua qhov kev pom zoo txhua hnub (RDA). Hauv plaub caug-tsib feem pua ntawm cov ntsiab lus, kev noj txhua hnub tsawg dua li xya caum-tsib feem pua ntawm RDA, thiab hauv kaum cuaj feem pua qhov kev noj txhua hnub tsawg dua tsib caug feem pua ntawm RDA [16]. Hauv Tebchaws Europe, qhov xwm txheej zoo sib xws [15]. Txawm hais tias cov poj niam cev xeeb tub thiab kawm tau zoo nyob sab Europe, cov lus pom zoo ntawm kev noj haus tsis ua raws li [17]. Cov zaub mov sab hnub poob feem ntau yog nplua nuj nyob rau hauv cov khoom noj uas tsis zoo hauv Mg thaum tseem muaj cov ntsiab lus tsawg heev ntawm cov nplej thiab zaub ntsuab, uas yog cov khoom noj uas muaj Mg cov ntsiab lus. Kev ua noj thiab cov txheej txheem ua kom zoo tuaj yeem txo qis Mg cov ntsiab lus hauv cov zaub mov vim tias Mg poob ntau thaum cov txheej txheem no. Yog li, cov khoom noj uas nplua nuj nyob hauv cov zaub mov ua kom zoo los yog ua tiav cov khoom noj muaj feem yuav tsawg Mg. Tshwj xeeb, qhov kub ntawm cov zaub mov yog qhov ua rau poob ntawm Mg [18]. Qhov muaj ntau ntawm cov zaub mov ua kom zoo thiab ua tiav hauv cov khoom noj sab hnub poob tuaj yeem pab piav qhia feem pua ntawm cov tib neeg uas muaj qhov tsis txaus Mg [19].
Pathogenic plab microbiota tuaj yeem hloov Mg nqus los ntawm kev noj haus. Nyob rau hauv ruminants, cov kab mob hloov pauv trans-aconitate rau tricarballylate, tricarboxylic acid uas chelates ntshav divalent cations, xws li Mg, thiab txo lawv qhov muaj. Tricarballylate tau raug pom zoo los ua ib qho tseem ceeb hauv kev hypomagnesemia uas ua rau cov nyom tetany [20,21].
Tsis tas li ntawd, phytic acid muaj nyob rau hauv qee cov khoom noj tuaj yeem txo Mg nqus. Glyphosate, tshuaj tua kab uas nquag siv hauv cov qoob loo, tuaj yeem chelate cov zaub mov suav nrog Mg [22], ntxiv txo cov ntsiab lus ntawm Mg hauv av thiab hauv qee cov qoob loo. Organic zaub mov, los ntawm cov av tsis muaj tshuaj tua kab, tau pom tias muaj Mg cov ntsiab lus ntau dua li cov khoom noj uas tsis muaj tshuaj tiv thaiv kab mob [23].
Mg yog dav siv nyob rau hauv ntau yam khoom noj khoom haus, nrog rau ntau yam confectionery, spices thiab ci cov khoom xyaw, thiab qhov ncauj tshuaj formulations raws li ib tug anticaking tus neeg saib xyuas, thiab tiv thaiv kom txhob muaj kab mob nyob rau hauv cov zaub mov thiab dej haus [24].
Mg noj los ntawm cov dej-nplua nuj Mg yuav raug muab coj los txiav txim raws li lwm qhov ntawm Mg [25]. Cov dej haus, tshwj xeeb tshaj yog cov dej ntxhia muaj zog, tuaj yeem muaj cov ntsev Mg; Yog li, dej tuaj yeem muab qhov tseem ceeb ntxiv rau kev noj Mg tag nrho, sawv cev rau lwm txoj hauv kev ntxiv rau qhov ncauj, txawm hais tias qhov sib piv Ca / Mg hauv dej tuaj yeem ua lub luag haujlwm. Hauv pawg SU.VI.MAX, cov neeg uas tau haus dej nplua nuj hauv Mg ua rau muaj kev noj ntau Mg ntau dua li cov neeg siv haus dej tsawg lossis dej kais dej [25].cistanche tubulosa cov txiaj ntsig thiab kev phivThe bio-availability of Mg in drinking water is generally higher when compared to Mg in food and while it is easy to add Mg to water, it is virtually impossible to add Mg to foods. The water content of Mg may be significant not only in the water used for drinking, but also in water used for cooking, since a higher concentration of Mg in the water used for boiling may reduce the leakage of Mg in food during cooking, and may reduce the loss of Mg in the boiled food. With the increasing shortage of fresh water globally, the use of desalinated seawater (DSW) is becoming very common in many areas of the world [26]. In Israel,>50 feem pua ntawm cov dej haus tam sim no tau los ntawm DSW. Desalination tshem tawm Mg, thiab hypomagnesemia tau cuam tshuam nrog kev mob plawv thiab kev tuag [27].
4. Mg Deficits Associated with Aging
Kev laus feem ntau cuam tshuam nrog tag nrho lub cev Mg tsis txaus [19]. Serum Mg qib tseem nyob tas li nrog hnub nyoog [28]. Kev hloov pauv hauv cov ntshav Mg feem ntau cuam tshuam nrog kev muaj cov kab mob thiab / lossis kev hloov pauv hauv lub raum ua haujlwm. Hauv cov neeg laus noj qab haus huv, qhov muaj hnub nyoog-raws li kev txo qis hauv cellular Mg concentration tau pom yav dhau los [29] thaum tsis muaj kev hloov pauv hauv tag nrho cov ntshav Mg. Nws tau raug lees paub tias qhov mob latent Mg tsis muaj peev xwm muaj ntau heev hauv cov neeg laus nyob rau sab hnub poob. Cov txheej txheem ua tau ntawm qhov pom tau tias Mg tsis txaus nrog kev laus yog cov ncauj lus kom ntxaws hauv Table 3. Qhov Mg tsis txaus no feem ntau cuam tshuam nrog kev noj tsawg Mg [30,31], thaum Mg cov txheej txheem rau lub cev tsis hloov nrog lub hnub nyoog [32].
Cov ntaub ntawv los ntawm National Health and Nutrition Examination (NHANES)III tau lees paub tias kev laus yog qhov muaj feem pheej hmoo ntxiv rau kev noj tsis txaus Mg thiab nce zuj zus nrog hnub nyoog [30].
Cov plab hnyuv nqus ntawm Mg nyiam poob nrog lub hnub nyoog, thiab qhov kev poob qis no yuav yog ib qho ua rau Mg tsis txaus nrog kev laus [33]. Kev hloov pauv ntawm txoj hnyuv nqus ntawm Mg thaum muaj hnub nyoog laus feem ntau ua rau lub cev tsis zoo ntawm cov vitamin D homeostasis, feem ntau hauv cov laus. Lub raum reabsorption ntawm Mg yog cov txheej txheem nquag tshwm sim nyob rau hauv lub voj ntawm Henle thiab nyob rau hauv proximal convoluted tubule. Txo lub raum ua haujlwm, feem ntau hauv cov neeg laus, yog qhov ua tau ntxiv ntawm Mg poob.
Secondary Mg deficiency nyob rau hauv cov neeg laus tej zaum yuav txuas nrog rau muaj ntau yam mob thiab muaj feem xyuam rau polypharmacotherapy [34]. Kev kho diuretic tuaj yeem ua rau Mg tso zis ntau dhau. Diuretic-induced hypomagnesemia feem ntau nrog hypokalemia. Hypomagnesemia tuaj yeem tshwm sim nyob ib ncig ntawm 40 feem pua ntawm cov neeg mob hypokalemia, thiab yuav tsum tau kho qhov Mg deficit kom ua tiav qhov kho ntawm K tsis txaus. Yog li nws raug nquahu kom ntsuas Mg qib hauv cov neeg mob hypokalemia. Lwm cov tshuaj uas nquag siv hauv cov neeg laus tuaj yeem ua rau Mg tsis txaus (xws li, tshuaj tiv thaiv kab mob, H2 blockers, proton twj tso kua mis inhibitors, tshuaj tiv thaiv kab mob, tshuaj tua kab mob, tshuaj tua kab mob, thiab tshuaj tua kab mob, thiab lwm yam).
5. Mg, Qhov mob thiab Oxidative Stress
Mg deprivation, tsawg cov ntshav Mg, thiab txo cov kev noj haus Mg tau tag nrho cov cuam tshuam rau hauv cov kev tshawb fawb hauv preclinical, epidemiological, thiab kev soj ntsuam tib neeg nrog rau kev tsim cov dawb radicals ntawm oxygen, qib qis systemic o, nce qib ntawm cov cim o thiab proinflammatory molecules ( IL-6, qog necrosis factor-alpha(TNF-alfa), IL-1-beta, vascular cell adhesion molecule (VCAM)-1, thiab plasminogen activator inhibitor (PAI){{6} }, ntxiv, alfa2-macroglobulin, fibrinogen)[16,{9}}]. King li al., siv cov ntaub ntawv NHANES, pom tias kev noj haus Mg tau txais kev cuam tshuam cuam tshuam rau cov protein C ntau ntau [16]. Similar results were found by Nkauj Hmoob et al. siv cov ntaub ntawv los ntawm Kev Tshawb Fawb Cov Poj Niam Kev Noj Qab Haus Huv hauv cov poj niam laus [42]. Mg depletion ua rau muaj kev tsim tawm ntawm oxygen-derived dawb radicals (ROS) nce oxygen peroxide ntau lawm thiab nce ntau lawm ntawm superoxide anion los ntawm inflammatory cells. Mg deficiency tsis tsuas yog ua rau oxidative kev nyuaj siab tab sis kuj txo cov antioxidant tiv thaiv muaj peev xwm [35,43]. Mg yuav tsum muaj rau kev ua haujlwm zoo ntawm gamma-glutamyl transpeptidase, uas ua lub luag haujlwm tseem ceeb hauv kev tsim cov tshuaj tiv thaiv antioxidant glutathione [44], lees paub tias Mg yuav muaj cov tshuaj tua kab mob me me [45]. Hauv tib neeg, kev sib raug zoo ntawm intracellular Mg thiab circulating txo / oxidized glutathione piv tau raug tshaj tawm [46]. Hauv lwm txoj kev tshawb fawb, kev sib raug zoo ntawm Mg qib thiab cov cim kev ntxhov siab oxidative (plasma superoxide anions thiab malondialdehyde) tau kuaj pom hauv cov pej xeem raug kev nyuaj siab ntev [47].
Kev laus yog nrog los ntawm cov qib qis qis uas tau raug hu ua "inflam-maging"[48]. Peb tau tshaj tawm yav dhau los hais tias qhov mob ntev Mg tsis txaus ua rau muaj kev mob tshwm sim no thiab qhov ua tsis taus ntawm cov xwm txheej redox tuaj yeem pab txhawb kev loj hlob ntawm cov kab mob uas muaj hnub nyoog (Daim duab 2) [19,49]. Tshwj xeeb, peb tau hais txog qhov sib txuas ntawm Mg tsis txaus thiab qhov tshwm sim ntawm cov tshuaj insulin tsis kam, T2DM, thiab cardiometabolic syndrome [2].
Daim duab 2. Mg deficit, o, oxidative stress, thiab laus. Kev sib raug zoo ntawm Mg qis yog tsim los ntawm ntau yam (piv txwv li, Mg tsis txaus thiab nqus tau, Mg thauj cov caj ces tsis xws luag, rog rog, hom 2 mob ntshav qab zib mellitus (T2DM) thiab cardio-metabolic syndrome, polypharmacotherapy, thiab haus cawv), uas tuaj yeem ua rau kev tsim cov dawb radicals (ROS), oxidative puas tsuaj, thiab ua kom cov teeb liab redox (piv txwv li, NF-KB, AP-1, thiab lwm yam kev hloov pauv). Qhov siab ntawm oxidative kev nyuaj siab tuaj yeem ua rau kev tso tawm ntawm cov neeg kho mob inflammatory ua raws li lub xeev ntawm cov mob qis qis, uas tau thov kom nrog kev laus thiab hu ua "inflammaging". TRPMZ: Transient Receptor Potential cation channel, subfamily M, tus tswv cuab 7; ROS: reactive oxygen hom; NF-KB nuclear factor kappa-light-chain-enhancer ntawm activated B hlwb; AP-1: activator protein 1; TNF-alpha: qog necrosis factor-alpha; IL: interleukin; CRP: C-reactive protein.
6. Mg thiab cov tshuaj tiv thaiv kab mob
Mg modulates ob qho tib si hauv lub cev thiab tau txais cov lus teb tiv thaiv kab mob thiab ua raws li tus neeg nruab nrab hauv txoj kev taw qhia kev tswj hwm lub cev tiv thaiv kab mob, homeostasis, thiab ua kom 35]. Mg yog ib qho tseem ceeb cofactor rau T helper-beta cell adherence, immunoglobulin synthesis, antibody-dependent cytolysis, IgM lymphocyte binding, thiab macrophage teb rau lymphokines [37,50]. Mg cuam tshuam tau txais kev tiv thaiv kab mob los ntawm kev hloov pauv kev loj hlob thiab kev loj hlob ntawm lymphocytes [51]. Transient Receptor Potential cation channel, subfamily M, tus tswv cuab 7 (TRPM7) yog qhov tseem ceeb rau Mg homeostasis hauv lub cev tiv thaiv kab mob. Ib qho kev poob hauv dawb cytosolic Mg thiab lub voj voog ntawm tes raug ntes tau pom nyob rau hauv TRPM7- cov kab B cell tsis txaus, uas tau khaws cia los ntawm kev tsim cov hlwb hauv nruab nrab uas muaj Mg siab. Kev txhim kho tsis zoo ntawm T hlwb tau pom hauv TRPM7 knockout nas [52].
Mg deficiency tuaj yeem ua rau thymus involution. Hauv thymuses los ntawm Mg-tsis muaj nas, qib siab ntawm apoptosis tau pom, piv nrog cov tswj [53]. Kev noj zaub mov tsis zoo Mg ua rau muaj kev hloov pauv ntawm polymorphonuclear cell xov tooj thiab kev ua haujlwm thiab ua kom phagocytosis [38]. Mg koom nrog hauv kev tswj hwm ntawm cell apoptosis. Fas-induced -cell apoptosis kuj xav tau Mg. Kev nce qib hauv cellular dawb Mg yog qhov tsim nyog rau kev qhia ntawm Fas molecule khi rau ntawm -cell nto kom ua rau muaj kev taw qhia txoj hauv kev uas pib cellular apoptosis thiab tuag [54]. Tsis tas li ntawd, Mg koom nrog hauv kev sib txuas, kev thauj mus los, thiab ua kom cov vitamin D, uas yog ib qho tseem ceeb immunomodulator hauv ntau yam kab mob sib kis, suav nrog tus kab mob SARS-Cov2 [37]. Mg tsis txaus kuj tseem tuaj yeem koom nrog lwm cov txheej txheem uas tau piav qhia hauv COVID-19, xws li lub cev tsis muaj zog tiv thaiv nrog kev tso tawm ntau dhau ntawm cov neeg kho mob uas ua rau muaj cua daj cua dub cytokine, endothelial dysfunction, thrombotic complications, thiab pre-exposing tej yam kev mob uas ua rau lub Kev kuaj mob ntawm KEVD-19 chav kho mob, xws li hnub nyoog laus, ntshav qab zib, thiab ntshav siab (saib hauv qab).
7. Cov tsos mob ntawm kev kho mob cuam tshuam nrog Mg Deficits
Cov tsos mob thiab cov tsos mob feem ntau yog tsis tuaj los yog tsis yog qhov tshwj xeeb ntawm Mg tsis txaus thiab cov neeg mob hypomagnesemia me ntsis feem ntau asymptomatic. Cov tsos mob tsis tshwj xeeb yuav suav nrog kev ntxhov siab, insomnia, qaug zog, hyperemotionality, cov tsos mob ntawm kev nyuaj siab, mob taub hau, lub teeb taub hau, thiab kiv taub hau. Feem ntau ntawm cov tsos mob no tsis yog tshwj xeeb thiab muaj nyob rau hauv cov neeg mob laus thiab tej zaum yuav yuam kev rau ib txwm muaj hnub nyoog tshwm sim. Lwm cov tsos mob tuaj yeem cuam tshuam, xws li myalgias, acroparesthesias, thiab cramps. Lwm yam kev tsis txaus siab ntawm kev ua haujlwm tsis zoo yuav suav nrog mob hauv siab, sine khoom dyspnea, precordialgia, palpitations, extrasystoles, lwm yam arrhythmias, thiab lwm yam. [55].
Ntau cov cim qhia thiab cov tsos mob tau txuas nrog Mg qhov tsis txaus xws li qaug zog, tshee tshee, nqaij fasciculation, dysphagia, muaj Chvostek's kos npe (lub ntsej muag twitching raws li cov tshuaj tiv thaiv rau tapping ntawm lub ntsej muag paj), los yog Trousseau's kos npe (spasm ntawm cov leeg ntawm lub ntsej muag). tes thiab forearm tom qab daim ntawv thov ntawm lub siab cuff, mus rau transiently occlude lub brachial hlab ntsha), orthostatic hypotension thiab / los yog ciam teb kub siab [55].
Elin tau hais qhia lub npe ntawm cov neeg mob uas tsis yog cov tsos mob tshwj xeeb cuam tshuam nrog kev mob ntev, tsis zoo Mg tshuav nyiaj li cas ntawm "Chronic Latent Mg Deficiency" (CLMD) [8]. Cov ntsiab lus cuam tshuam los ntawm CLMD feem ntau tam sim no qis dua tsis yog-mal tag nrho cov ntshav qab zib Mg qib (latent) thiab feem ntau tsis kuaj pom, tsis muaj hypomagnesemia, tab sis yuav tau txais txiaj ntsig los ntawm Mg supplementation.
8. Kev xav txog lub luag haujlwm ua tau ntawm Mg nyob rau hauv cov txheej txheem kev laus thiab lub neej ntev
Mg yog qhov tseem ceeb rau kev khaws cia genomic stability nyob rau hauv cellular systems, vim hais tias ntawm nws stabilizing teebmeem ntawm DNA thiab chromatin lug. Yog li, Mg ion yog xav tau nyob rau hauv nucleotide excision kho, kho lub hauv paus excision, thiab kho qhov tsis sib haum, thiab yog qhov tseem ceeb rau kev tshem tawm DNA puas los ntawm cov txheej txheem endogenous, ib puag ncig mutagens, thiab DNA replication [56]. Mg deficiency ua rau lub cev tsis muaj zog rau oxidation thiab tuaj yeem cuam tshuam rau kev ua haujlwm ntawm lub cev; Qhov tsis muaj Mg yuav hloov qhov kev ncaj ncees ntawm daim nyias nyias thiab kev ua haujlwm thiab tuaj yeem pab txhawb kev hloov pauv ntawm mitochondrial (tsawg tus lej, hloov kho morphology, nce apoptosis, nce DNA hloov pauv, txo qis biogenesis, de-creased autophagy) [19]. Mg muaj lub luag haujlwm tseem ceeb hauv kev hloov pauv ntawm cov protein synthesis thiab kho daim nyias nyias [56,57]. DNA yog hloov tsis tu ncua los ntawm cov txheej txheem endogenous thiab ib puag ncig mutagens. Kev nce hauv cellular Mg tau pom nyob rau hauv cov theem pib ntawm apoptosis, tejzaum nws txuas mus rau kev mobilization ntawm Mg los ntawm mitochondria; Mg tuaj yeem ua "tus xa xov thib ob" rau cov xwm txheej hauv qab hauv apoptosis [54]. Mg deprivation tsub kom lub susceptibility rau oxidative kev puas tsuaj uas yooj yim alterations ntawm daim nyias nyias kev ncaj ncees thiab muaj nuj nqi.
Qee qhov kev hloov pauv hauv cell physiology tshwm sim hauv senescence hauv ntau hom cell [58] zoo ib yam li cov uas tshwm sim los ntawm Mg deficit. Mg-depletion-related-related alterations muaj xws li txo kev tiv thaiv los ntawm oxidative kev nyuaj siab puas tsuaj, txo cell voj voog, txo kab lis kev cai loj hlob, thiab txo cellular viability raws li zoo raws li ua rau cov kev qhia ntawm proto-oncogene thiab transcription yam [59]. Culturing thawj fibroblasts hauv Mg-tsis muaj xov xwm yuav txo qis lub peev xwm rov ua dua thiab ua kom ceev cov kev qhia ntawm biomarkers txuam nrog senescence thiab telomere attrition. Kev txo qis ntawm kev ua neej nyob tau raug pom vs. fibroblast cultured nyob rau hauv ib txwm Mg media mob [60].
Vim yog lub luag haujlwm tseem ceeb ntawm Mg hauv kev ruaj ntseg ntawm DNA, tiv thaiv lub cell kom puas ROS, thiab txhawb DNA replication thiab transcription, thiab Mg deficit yuav pab txhawb genomic instability, hloov DNA kho, thiab txo mitochondria functionality, yog li yooj yim. accelerated cellular senescence thiab laus [56,61]. Mg muaj lub luag haujlwm tiv thaiv tiv thaiv cov teebmeem no thiab sib txawv ntawm qhov luv ntawm telomeres (uas cuam tshuam nrog kev laus thiab txo lub neej expectancy), uas tau pom nyob rau hauv qis Mg. Nws tau raug pom tias vim qhov kev ua no los tiv thaiv telomere shortening, kho Mg tsis txaus yuav ua rau lub neej ntev [62].
9. Mg hauv ntshav siab thiab kab mob plawv
Hauv kaum xyoo dhau los, Mg tsis txaus tau txuas nrog ntau yam mob plawv [2,63]. Kobayashi thawj zaug sau tseg hauv xyoo 1957 tias cov ntxhia hauv cov dej haus tau cuam tshuam nrog kev tuag ntawm cov hlab plawv; Qhov xwm txheej mob stroke qis dua hauv cov cheeb tsam uas muaj dej tawv (tsuas yog txuas nrog Mg thiab Ca cov ntsiab lus)[64]. Schroeder tau lees paub cov ntaub ntawv no tsuas yog ob peb xyoos tom qab, tshuaj xyuas kev sib raug zoo ntawm cov dej tawv thiab cov neeg tuag. Nws pom tias kev tuag ntawm cov hlab plawv tau qis dua hauv cov xeev uas muaj dej tawv piv rau cov xeev uas muaj dej mos [65].
Mg koom nrog hauv ntshav siab homeostasis. Txawm hais tias Mg tsis tau muaj lub luag haujlwm ncaj qha hauv cov txheej txheem biochemical ntawm kev cog lus, cov kev tshawb fawb classic los ntawm Altura li al. tau ua pov thawj tias Mg tswj lub vascular tone thiab contractility los ntawm altering Ca qib thiab cov kev hloov hauv Mg concentration modulate Ca-triggered vascular smooth nqaij contraction [66-68]. Mg nws tus kheej ua haujlwm raws li qhov tsis muaj zog physiologic Ca channel blocker [69] modulating Ca-channel kev ua hauv lub plawv hlwb [70]. Mg deficit stimulates angiotensin II-mediated aldosterone synthesis, nrog rau thromboxane thiab vasoconstrictor prostaglandins ntau lawm [71]. Mg muaj cov txiaj ntsig zoo ntawm vascular endothelium modulating tso tawm nitric oxide, prostacyclin, thiab endothelin-1 [72. Hauv tib neeg, qhov ncauj Mg supplementation tau pom los txhim kho endothelial muaj nuj nqi hauv T2DM cov neeg laus [73].
Mg ion, vim hais tias ntawm cov kev ua ntawm vascular du leeg lub suab, plays ib tug modulatory txiav txim ntawm cov ntshav siab homeostasis, thaum Mg deficits yuav muaj feem xyuam rau lub physiopathology ntawm hypertensive disorders. Altura tau qhia tias qhov txo qis ntawm Mg yuav ua rau cov hlab ntsha hyper-reactivity thiab nce ntshav siab [74. Cov ntshav tag nrho Mg feem ntau yog ib txwm nyob hauv cov neeg mob ntshav siab. Txawm li cas los xij, ntau qhov teeb meem ntawm Mg homeostasis tau raug sau tseg hauv kev kub siab. Cov kev tshawb fawb yav dhau los tau pom tias muaj kev sib cuam tshuam ntawm Mg kev noj haus thiab ntshav siab 75]. Hauv cov neeg laus, cov hnub nyoog ntsig txog kev nce ntshav siab tau ua ke nrog kev sib koom ua ke ntawm intracellular free Mg [29,76], qhia txog lub luag haujlwm ua rau Mg tsis txaus hauv lub hnub nyoog ntsig txog ntshav siab. Intracellular-free Mg concentrations tau pom tias qis dua hauv cov neeg mob ntshav siab vs. normotensive controls [77]. Mg urinary excretion kuj pom tau tias hloov pauv hauv cov qauv kev sim ntawm cov nas hypertensive [78]. Kev noj zaub mov muaj ntsev siab tau tshaj tawm kom nce ntshav siab hauv cov ntsiab lus ntsev-sensitive, reciprocally suppressing intracellular dawb Mg qib [79].
Blackfan thiab Hamilton, thaum ntxov li 1925, tau pom zoo Mg txoj kev kho kom txo cov ntshav siab hauv cov neeg mob ntshav siab [80]. Intravenous(iv) Mg tau nquag siv nrog cov txiaj ntsig zoo sib xws hauv preeclampsia thiab eclampsia [81], thiab hauv malignant hypertension [82]. Txawm li cas los xij, cov lus teb rau Mg qhov ncauj ntxiv hauv qhov tseem ceeb kub siab tsis meej [63,83-86]. Hauv kev sim ntshav siab, kev noj zaub mov siab lossis qis Mg uas, raws li, tsa lossis txo qis cellular dawb Mg, nyob rau tib lub sijhawm txo qis thiab nce ntshav siab. Hauv tib neeg, hauv qee qhov kev tshawb fawb, Mg supplementation tau pom tias muaj cov teebmeem hypotensive, thaum lwm tus tsis muaj kev cuam tshuam rau ntshav siab lossis tej zaum yuav ua rau nws hnyav dua [83,86]Txawm li cas los xij, thaum kev tshawb fawb zoo tau txheeb xyuas ua ke hauv meta - Kev tshuaj xyuas thiab kev tshuaj xyuas cov ntaub ntawv pov thawj tau lees paub, lees paub lub luag haujlwm tseem ceeb ntawm Mg hauv kev kub siab thiab kev sib raug zoo ntawm kev noj haus Mg kom tsawg nrog qhov muaj feem ntau thiab qhov tshwm sim ntawm kev kub siab [63]. Txawm li cas los xij, qhov ua tau tsis txaus ntseeg ntawm cov pov thawj tau los ntawm kev soj ntsuam kev tshawb fawb yog tias cov khoom noj uas muaj Mg kom tsawg kuj feem ntau tsawg hauv Na thiab nplua nuj nyob rau hauv K thiab lwm cov ntsiab lus nrog cov txiaj ntsig kev noj qab haus huv yog li kev noj Mg siab yuav yog, tsawg kawg hauv ib feem, tus cim. Kev noj qab haus huv ntawm lub cev [63]
Yog li, ib qho kev rov ua dua tshiab thiab tsis tu ncua ntawm qhov ncauj Mg tshuaj ntawm cov ntshav siab tseem tsis tau lees paub hauv cov kev sim mus ntev ntev hauv qhov tseem ceeb ntawm cov ntshav siab thiab cov ntaub ntawv ntxiv yog tsim nyog los qhia txog Mg supplementation raws li lub tswv yim tsis yog tshuaj rau kev tiv thaiv ntshav siab thiab / los yog kho lub hom phiaj. Muaj ntau qhov kev piav qhia txog qhov tsis paub tseeb no. Ntawm lawv: (a) qhov tsis muaj virtual tshwj xeeb ntawm kev npaj kho mob yav tom ntej ntawm kev kho Mg hauv kev kub siab; (b) ntau npaum li cas thiab cov sij hawm kho mob siv nyob rau hauv ib tug xov tooj ntawm cov ntaub ntawv kho mob me me; thiab (c) ua tsis tiav los xyuas qhov heterogeneity ntawm lub hauv paus mechanisms ua rau kom nce ntshav siab. Yog li no, kev sim tshuaj kho mob ntev ntev ntawm qhov ncauj Mg tshuaj hauv qhov tseem ceeb kub siab yog xav tau.
Mg deficit tau txuas nrog kev txhim kho atherosclerosis. Tsawg Mg xwm txheej tuaj yeem ua rau vascular calcification, hloov lipid metabolism thiab pab txhawb lipid tsub zuj zuj hauv vascular plaques [87]. Serum Mg tau pom tias muaj qhov zoo [88] lossis tsis zoo [89] cuam tshuam nrog cov ntshav lipid. Mg supplementation tau pom zoo los txhim kho lipid profiles, tiv thaiv atherosclerotic plaque tsim thiab ua raws li qhov tsis muaj zog inhibitor ntawm hydroxyl-3-methylglutaryl-coenzyme A reductase, thiab lwm yam enzymes ntawm lipid metabolism [90].
Mg koom nrog hauv lub plawv hluav taws xob conduction thiab hypomagnesemia, hypokalemia, thiab lwm yam kev cuam tshuam ntawm electrolyte tuaj yeem ua rau lub plawv arrhythmias. Mg thiab K depletion kuj ua rau muaj kev cuam tshuam rau arrhythmogenic cuam tshuam ntawm lub plawv glycosides. Mg cov teebmeem ntawm kev coj ua suav nrog kev ncua ntev ntawm atrial thiab atrioventricular nodal refractory lub sijhawm, uas tuaj yeem pab tswj tus nqi thiab kev sib dhos hauv atrial fibrillation (AF) [91. Cov tshuaj Mg tuaj yeem siv los ua kev txhawb nqa tsis yog tshuaj kho mob rau atrial thiab / lossis ventricular arrhythmias [92]. AF tuaj yeem cuam tshuam nrog hypomagnesemia [93] thiab txo cov ntshav Mg concentration tuaj yeem pab txhawb kev loj hlob ntawm AF [94].
Hauv cov poj niam postmenopausal, kev noj haus Mg tsis txaus tau cuam tshuam nrog lub plawv dhia tsis zoo, suav nrog AF thiab flutter uas tuaj yeem teb rau Mg supplementation [95]. Ib qho kev tshuaj ntsuam xyuas meta tau qhia tias iv Mg kev tswj hwm yuav muaj lub luag haujlwm hauv kev tswj xyuas mob hnyav ntawm AF [96]. Vim nws txoj kev siv sai, ua tau zoo, thiab yooj yim, iv Mg kev tswj hwm tau qhia nyob rau hauv kev kho mob ntawm torsade de cov ntsiab lus [97,98]. Antiar-rhythmic kev ua ntawm siab Mg kev noj haus tau pom zoo los kho qhov txo qis ntawm kev tuag sai ntawm cov poj niam hauv qhov siab tshaj plaws quartile ntawm Mg kom tsawg [99].
Cov tshuaj noj Oral Mg tau pom zoo los pab txhim kho cov tsos mob thiab cov txiaj ntsig ntawm kev ciaj sia vs.
Kev tshuaj xyuas thiab kev tshuaj xyuas meta-tshaj tawm ntawm cov kev tshawb fawb yav tom ntej uas suav nrog ntau dua 300,000 cov tib neeg pom tias nce qib Mg cov ntshav sib piv rau qhov txo qis ntawm cov kab mob plawv; Kev noj zaub mov kom siab Mg tau pom tias muaj kev cuam tshuam nrog cov kab mob plawv ischemic [101]. Lwm qhov kev tshuaj ntsuam meta ntawm cov kev sim yav tom ntej suav nrog tag nrho ntawm 241,378 cov ntsiab lus tau tshaj tawm txog kev sib cuam tshuam ntawm Mg noj thiab kev pheej hmoo ntawm mob stroke [102]. Kev tshuaj xyuas lub kaus tsis ntev los no uas ntsuas cov txiaj ntsig kev noj qab haus huv txuas nrog Mg kom tsawg thiab ntxiv tau lees paub qhov sib txuas ntawm Mg kom ntau dua thiab txo qis kev pheej hmoo mob stroke [86]. Mg sulfate tau pom tias muaj kev tiv thaiv ob qho tib si hauv cov qauv ua ntej ntawm kev mob stroke thiab hauv tib neeg. Mg tau raug qhia kom muaj qee qhov kev ua tau zoo, thiab kev nyab xeeb zoo yog tias xa iv ntxov tom qab mob stroke pib [103].
10. Mg hauv ntshav qab zib hom 2
Ib qho piv txwv lub cev ntawm cov pov thawj tau txuas Mg tsis txaus rau kev hloov pauv hauv insulin rhiab heev thiab T2DM. Tseeb tiag, T2DM tau cuam tshuam nrog ntau yam ntxiv-thiab hauv-cellular Mg txawv txav [2,104-106]. Tsawg cellular thiab / lossis ionized plasma Mg concentrations tau pom nyob rau hauv cov neeg mob T2DM txawm tias tseem tsis tshua muaj cov ntshav qab zib Mg qib [107,108]. Cov txheej txheem muaj peev xwm nyiam Mg depletion hauv T2DM suav nrog kev noj zaub mov tsawg Mg thiab nce Mg tso zis, thaum qhov nqus thiab khaws cia ntawm kev noj haus Mg zoo li tsis hloov pauv [109]. Nws tau raug tshaj tawm txog kev sib raug zoo ntawm Mg kom tsawg thiab qhov xwm txheej tshiab ntawm T2DM. Ob leeg hyperglycemia thiab hyperinsulinemia tau cuam tshuam rau kev ua rau Mg depletion [110]. Ob leeg hyperglycemia thiab hyperinsulinemia pom zoo rau kev tso zis ntau dhau Mg, thaum insulin tsis kam tuaj yeem hloov Mg thauj [111]. Hloov Mg metabolism tuaj yeem ua rau muaj kev txhim kho ntawm T2DM thiab ua rau muaj kev cuam tshuam ntawm insulin-mediated glucose uptake [2]. Vim tias cov ntaub ntawv pov thawj no, Mg supplementation tau pom tias yog qhov ua tau tsis yog tshuaj kho mob, kev lag luam thiab kev nyab xeeb kev kho mob rau kev tiv thaiv thiab kev tswj cov metabolic ntawm T2DM. Txawm li cas los xij, cov kev sim yav tom ntej hais txog qhov cuam tshuam ntawm Mg supplementation hauv cov neeg uas muaj lossis muaj kev pheej hmoo ntawm T2DM raug txwv [112,113]. Ib qho txiaj ntsig me me ntawm Mg tshuaj ntawm glycemic profile tau pom nyob rau hauv ntau, tab sis tsis yog tag nrho, kev tshawb fawb. Kev tshuaj xyuas thiab kev tshuaj xyuas meta-analysis suav nrog 18 qhov muag ob qhov muag tsis pom kev randomized tswj kev sim (12 hauv cov neeg mob ntshav qab zib thiab rau rau tus neeg mob uas muaj kev pheej hmoo siab T2DM) tau tshaj tawm tias Mg supplementation yuav muaj qee qhov txiaj ntsig zoo hauv kev txhim kho cov piam thaj hauv cov neeg muaj T2DM thiab txhim kho. Cov tshuaj insulin-rhiab heev rau cov neeg mob uas muaj kev pheej hmoo siab ntawm T2DM[114]. Siv lub kaus tshuaj xyuas rau daim ntawv qhia thiab qib kev noj qab haus huv tau txuas nrog Mg noj thiab ntxiv, peb pab pawg tsis ntev los no tau lees paub tias qhov nce Mg kom tsawg yog cuam tshuam nrog txo qis ntawm T2DM [86].
11. Mg hauv Cardiometabolic Syndrome
Kuj tseem muaj cov pov thawj ntseeg tau ntawm qhov sib txuas ntawm Mg tsis txaus nrog cov mob metabolic [2,6,115]. Hauv kev tshawb fawb txog kev kis kab mob, kev noj zaub mov tsis zoo Mg tau txuas nrog kev pheej hmoo siab ntawm cov piam thaj tsis kam, metabolic syndrome, thiab T2DM[115-117]. Intracellular Mg tsis txaus, ua rau muaj kev ua haujlwm tsis zoo ntawm tag nrho cov Mg-dependent kinases koom nrog hauv kev qhia cov tshuaj insulin, thiab nce oxidative kev nyuaj siab yuav ua rau cov tshuaj insulin tsis kam thiab ua rau cov mob metabolic, suav nrog cov piam thaj tsis haum, metabolic syndrome, thiab T2DM. Mg-deprivation nyob rau hauv yaj ua rau muaj kev puas tsuaj ntawm insulin-mediated qabzib uptake [118], thaum Mg supplementation ncua kev loj hlob ntawm tus kab mob nyob rau hauv ib tug nas qauv ntawm ntshav qab zib [119]. Cov tshuaj insulin qis dua tau pom nyob rau hauv cov poj niam noj qab haus huv uas tsis muaj ntshav qab zib nrog kev noj ntau dua Mg [120]. Tag nrho cov kev noj haus Mg tau cuam tshuam nrog cov lus teb ntawm insulin rau qhov kev ntsuas qhov ncauj qhov ncauj [121].
12. Mg thiab mob hawb pob thiab ua pa tsis txaus
Ua ntej, Haury hauv xyoo 1940 tau npaj lub luag haujlwm rau Mg hauv kev mob hawb pob uas qhia txog cov lus teb tau zoo tom qab iv Mg sulfate kev tswj hwm hauv ob lub tsev kho mob cov neeg mob uas muaj mob hawb pob mob hawb pob [122]. Hauv kaum xyoo tom ntej no, lwm cov ntawv tshaj tawm tau lees paub qhov txiaj ntsig zoo ntawm Mg iv kev kho mob hauv cov hlab ntsws mob hnyav, qhia txog qhov ua tau zoo ntawm Mg hauv cov txheej txheem ntawm bronchial dilation [123,124], txawm tias lwm cov ntawv ceeb toom tsis tau lees paub cov txiaj ntsig kho [125,126]. Kev tswj hwm ntawm ivMg zoo li nce ntxiv, hauv kev sib ntxiv, cov nyhuv bronchial dilating ntawm terbutaline [127] thiab salbutamol [128] hauv kev txhim kho kev ua haujlwm pulmonary.
Mg modulates lub contractile lub xeev ntawm bronchial du leeg hlwb; Mg depletion ua rau bronchial contraction thiab spasm, thaum Mg restoration ua rau bronchial so. Ob peb lub tswv yim tau raug tso tawm rau qhov zoo Mg qhov kev ua kom zoo rau cov leeg nqaij bronchial, xws li Ca channel thaiv qhov kev txiav txim ntawm Mg [69], qhov txo qis rau qhov kev txiav txim depolarizing ntawm acetylcholine [92], stabilization ntawm mast hlwb thiab T-lymphocytes [129], thiab stimulation ntawm nitric oxide [130] thiab prostacyclin [131].Nyob rau hauv cov pej xeem, tseem ceeb ywj siab koom haum ntawm kev noj haus Mg noj nrog lub ntsws muaj nuj nqi thiab inverse koom haum nrog rau txoj kev ua pa reactivity, nqus tau methacholine, thiab cov tsos mob ua pa. (hheezing) tau tshaj tawm, qhia tias kev noj tsawg Mg yuav cuam tshuam rau hauv etiology ntawm hawb pob [132].
Txawm li cas los xij, tag nrho cov tshuaj Mg hauv cov ntshav tsis muaj txiaj ntsig zoo, vim tias tsis muaj qhov sib txawv hauv cov ntshav Mg hauv cov neeg mob hawb pob thaum lub sijhawm mob hnyav dua piv rau cov neeg tsis muaj mob hawb pob, thiab cov ntshav tag nrho Mg tsis tau kwv yees qhov hnyav ntawm kev mob ntsws asthmatic, lossis ntawm bronchial dilating teb rau Mg infusion [133]. Conversely, cellular Mg (ntau dua ntsig txog lub cev Mg) tau pom tias yuav txo qis hauv cov neeg mob hawb pob thaum piv rau cov tswj tsis muaj mob hawb pob [134]. Tsis tas li ntawd, peb pab pawg tau pom muaj kev sib raug zoo, hauv cov neeg mob hawb pob, nruab nrab ntawm cov qib Mg cellular thiab cov tshuaj methacholine bronchial reactivity lees paub tias muaj kev hloov pauv ntawm Mg intracellular hauv kev mob ntsws asthma, thiab tau thov lub luag haujlwm ntxiv rau cov tshuaj tsis yog tshuaj kho mob Mg ntxiv rau cov neeg mob hawb pob [ 135] ib.
Ua ke, cov ntaub ntawv muaj qhia txog lub luag haujlwm rau cellular thiab lub cev Mg tsis txaus raws li kev hloov pauv ntawm cov leeg nqaij bronchial reactivity thiab contractility, pab txhawb bronchoconstriction hauv cov neeg mob hawb pob, thiab muaj peev xwm tiv thaiv thiab / lossis kho lub luag haujlwm rau kev siv ntxiv ntawm Mg kev tswj hwm hauv cov neeg no. [136].
13. Mg thiab Psychiatric Disorders
Ntau yam kev puas siab puas ntsws nrog rau kev ntxhov siab, kev nyuaj siab, kev chim siab, insomnia, hypochondriasis, ceeb tawm tsam, hyperexcitability, mob taub hau, kiv taub hau, tshee, thiab kev puas siab puas ntsws tus cwj pwm tau txuam nrog Mg deficiency. Cov tsos mob ntawm Neuromuscular tej zaum yuav txuam nrog, xws li asthenia, cov leeg tsis muaj zog, thiab myalgias (xws li, mob nkees nkees thiab fibromyalgia) [137].
Ntau cov enzymes thiab cov tshuaj tiv thaiv cellular koom nrog hauv cov lus teb kev ntxhov siab yog Mg-dependent [15]. Serum Mg qib tau raug npaj kom txo qis hauv cov neeg uas muaj kev nyuaj siab [138]. Kev kawm tsis ntev los no los ntawm Noah et al. qhia tau tias ze li ntawm ib nrab (plaub caug-plaub feem pua) ntawm cov neeg mob soj ntsuam kev ntxhov siab muaj qhov tsis txaus Mg latent [139].
Mg deficit tuaj yeem tsim cov pov thawj electrophysiological ntawm hyperexcitability nyob rau hauv lub hauv paus paj hlwb (CNS). Hauv cov nas uas tsis muaj Mg, kev hloov kho electroencephalogram (EEG) tau saib xyuas thaum lub sijhawm hnov mob. Ntau qhov kev hloov pauv nrog kev ua haujlwm siab dav tau pom nyob rau hauv EEG, qhia tias kev hnov mob-txhim kho kev coj cwj pwm hloov hauv Mg-tsis muaj nas, tuaj yeem txuas rau Mg-muaj feem cuam tshuam-nce excitability ntawm CNS [140].
Hauv tib neeg, Mg insufficiency tau txuas nrog neuro-muscular hyperexcitability [141]. Ntau yam kev ua tau zoo tuaj yeem txuas Mg deficiency rau lub paj hlwb hyperexcitability, xws li yav dhau los tau piav qhia Mg modulatory kev ua ntawm cellular Ca, nce per-oxidation, hyper-activated ntawm qee qhov excitatory neurotransmitters, (ie, acetylcholine, catecholamines, NMDA thiab non-NMDA. receptors ntawm excitatory amino acids), thiab txo qis kev ua ntawm inhibitory neurotransmitters (piv txwv li, gamma-aminobutyric acid (GABA), taurine, glutaurine, adenosine), ntxiv rau kev tsim cov neuropeptides, inflammatory cytokines, prostanoids, thiab txo qis kev ua haujlwm ntawm Kev tiv thaiv antioxidant [137]
Nyob rau hauv kev sib raug zoo rau cov kev sib txuas nrog cov kev hloov pauv thiab kev lom neeg muaj feem cuam tshuam rau kev nyuaj siab, thiab vim yog lub luag haujlwm ntawm Mg ntawm cov ion channel ntawm NMDA-receptor complex [142], Mg cov tshuaj tau raug npaj los pab rau kev kho kev nyuaj siab. [143, 144]. Qee cov tshuaj tiv thaiv kev ntxhov siab xws li sertraline thiab amitriptyline tau pom zoo kom nce qib Mg hauv lub cev [145]. Kev tshuaj xyuas zoo qhia tau tias kev noj ntau dua Mg cuam tshuam nrog txo cov tsos mob ntawm kev nyuaj siab [144]. Cov tshuaj Oral Mg tuaj yeem muab qhov zoo dua rau kev tiv thaiv cov tsos mob ntawm kev nyuaj siab thiab tuaj yeem txhawb nqa raws li kev kho mob ntxiv. Cov nyhuv ntawm Mg supplementation ntawm kev ntxhov siab thiab kev ntxhov siab tsis tshua muaj ntaub ntawv. Txawm li cas los xij, yuav tsum muaj kev cuam tshuam ntau ntxiv thiab cov kev tshawb fawb yav tom ntej txhawm rau txhawm rau tsim lub luag haujlwm meej rau Mg supplementation raws li kev saib xyuas ntxiv hauv kev kho kev nyuaj siab thiab lwm yam kev puas siab puas ntsws.
Mg kuj tau pom zoo tias yog kev kho mob ntxiv rau hauv kev kho mob ntawm insomnia. Mg, ntxiv rau kev ua ib tug natural NMDA antagonist thiab GABA agonist, kuj muaj ib tug so kom txaus, thiab tej zaum yuav ua rau kom melatonin ntau ntau, yog li pab kom tsaug zog [146].
14. Mg thiab kev paub tsis meej
Ib qho kev tiv thaiv kev tiv thaiv ntawm Mg hauv kev paub tsis meej thiab AD twb tau hais tawm hauv xyoo 1990 [147]. Mg ion yog ib qho tseem ceeb rau kev loj hlob ntawm lub paj hlwb thiab muaj nyob rau hauv cov kua cerebrospinal (CSF) hauv CNS [148]. Mg hla cov ntshav-hlwb teeb meem thiab nquag thauj los ntawm choroidal epithelial hlwb mus rau CSF [148].
Kev hloov pauv ntawm Mg metabolism yog tam sim no nyob rau hauv cov neeg mob uas muaj dementia: tag nrho thiab ionized serum Mg qib, thiab ntau cov ntaub so ntswg 'Mg cov ntsiab lus tau pom zoo txo qis hauv cov neeg mob AD [149-152].
Mg concentrations nyob rau hauv lub hlwb cuam tshuam rau ntau yam biochemical txheej txheem koom nrog hauv kev txawj ntse, suav nrog cell membrane stability thiab kev ncaj ncees, NMDA-receptor teb rau excitatory stimuli, thiab Ca-antagonist ua [19]. Nws tau raug pom tias cov nyhuv neurotoxic ntawm qee cov hlau, xws li txhuas, tuaj yeem cuam tshuam nrog kev hloov pauv ntawm kev koom ua ke ntawm Mg rau hauv lub hlwb neurons, yog li ua rau Mg tiv thaiv cov teebmeem ntawm lub hlwb] 147]. Mg tau raug tshaj tawm los txhawm rau txhawm rau txhawm rau tshem tawm cov co toxins, txo cov kab mob neuroinflammation, inhibit cov txheej txheem pathologic ntawm amyloid protein precursor, inhibit qhov txawv txav tau protein phosphorylation, thiab thim rov qab deregulation ntawm NMDA receptors. Txawm li cas los xij, cov txheej txheem ntawm cov teebmeem no tsis meej meej [153]. Mg-L-threonate kev tswj hwm tau raug tshaj tawm los txo qis neuroinflamation thiab txo qis beta-amyloid deposition hauv kev sim qauv ntawm AD [154,155], thiab txhim kho kev kawm muaj peev xwm, kev ua haujlwm thiab kev nco luv luv thiab ntev hauv nas [156]. Cov kev tshawb fawb tsiaj tau cog lus tseg thiab tej zaum yuav qhia tau tias Mg supplementation yog pib thaum ntxov ntawm kev txawj ntse tsis txaus yuav txo qis qhov kev nco poob thiab kev txawj ntse poob [157].
Hauv tib neeg, tsuas yog ob peb qhov kev sim tshuaj tau kawm txog lub luag haujlwm ntawm Mg hauv kev paub txog kev noj qab haus huv. Epidemiologically, nws tau raug pom tias cov neeg noj cov zaub mov uas nplua nuj nyob rau hauv Mg yuav muaj kev pheej hmoo ntawm kev txawj ntse poob. Hauv 1400 cov txiv neej noj qab haus huv tau ua raws li yim xyoo, kev noj zaub mov kom siab Mg tau cuam tshuam nrog kev txo qis ntawm kev loj hlob ntawm kev xav tsis zoo [158]. Hauv lwm txoj kev tshawb fawb suav nrog ntau dua 1000 tus neeg nyob hauv zej zog Nyij Pooj cov neeg koom nrog hnub nyoog tshaj 60 xyoo thiab ua raws li 17 xyoo, nws tau pom tias cov neeg uas xav tias ntau dua 200 mg / hnub ntawm Mg muaj peb caug-xya feem pua tsawg dua los tsim txhua yam. ntawm dementia thiab xya caum-plaub feem pua tsawg dua qhov muaj feem cuam tshuam rau vascular dementia [159]. Lub sij hawm luv luv (12 lub lis piam) randomized tswj kev sim qhia tias Mg tuaj yeem pab txhim kho kev txawj ntse hauv cov neeg laus nrog kev tsis txaus siab ntawm kev nco [160]. Kev sim mus sij hawm ntev randomized soj ntsuam nrog Mg supplementation yog xav tau kom paub meej tias Mg-nplua nuj noj zaub mov yuav pab tiv thaiv dementia thiab / los yog kev txawj ntse tsis zoo.
15. Mg thiab Osteoporosis
Dietary Mg deficit tau pom tias yog qhov muaj feem cuam tshuam rau cov kab mob osteoporotic thiab pob txha poob. Kev tshawb fawb txog kab mob kis tau pom tias kev noj zaub mov kom siab ntawm Mg tau zoo thiab muaj feem cuam tshuam rau pob txha pob txha pob txha pob txha (BMD). Ntawm qhov tsis sib xws, kev noj zaub mov tsis txaus Mg tau txuas rau qhov nce ntawm cov pob txha poob hauv cov poj niam postmenopausal osteoporotic [161,162]. Hauv Kev Tshawb Fawb Txog Kev Noj Qab Haus Huv, Kev Laus, thiab Lub Cev Muaj Zog, nws tau pom tias kev noj ntau dua Mg tau cuam tshuam nrog BMD ntau dua hauv cov neeg koom nrog noj qab haus huv, hnub nyoog 70 txog 79 xyoo ntawm lub hauv paus [163]. Tom qab xaiv Mg deprivation, Mg-depleted nas nrog frank hypomagnesemia tsim osteoporosis, nce pob txha fragility txuam nrog nce pob txha resorption, txo cov pob txha tsim, thiab cov pob txha loj hlob [164,165]. Kev nce siab ntawm cov kab mob cytokines tuaj yeem ua lub luag haujlwm hauv kev piav qhia cov pob txha hloov pauv, txawm hais tias qhov sib txuas ntawm pathophysiologic tseem tsis tau txhais. Rude thiab Gruber pom tias cov pob txha osteoclastic resorption muaj feem xyuam nrog nce qib ntawm cov tshuaj inflammatory P thiab TNF-alfa hauv cov pob txha los ntawm Mg-tsis muaj nas [166].
Tsis tas li ntawd, Mg yog tsim nyog rau vitamin D synthesis, thauj, thiab ua kom muaj zog; Vim li no, Mg qhov tsis txaus yuav ua rau tsis zoo rau kev tsim cov tshuaj vitamin D, 1, 25-OH2 D3, thiab ua rau muaj kev tiv thaiv PTH thiab vitamin D ua haujlwm [167]. Cov teebmeem ntawm Mg tsis txaus ntxiv ua ke nrog kev hloov pauv PTH kev ua haujlwm thiab qis 1,25-OH2 D3 synthesis yuav ua rau cov pob txha tsim thiab cov txheej txheem mineralization thiab yuav txo qis qhov zoo, thiab lub zog ntawm cov pob txha nrog rau BMD. Nws tau raug pom zoo tias Mg supplementation hauv koob tshuaj txaus los kho cov pob txha qub tuaj yeem txo cov pob txha poob thiab tiv thaiv kev pheej hmoo ntawm pob txha [168,169].
Hauv cov neeg koom nrog hauv pawg "Osteoarthritis Initiative" ua raws li 8 xyoo, nws tau pom tias cov poj niam uas muaj kev noj haus ntau dua Mg tau txais nees nkaum xya feem pua txo kev pheej hmoo rau cov pob txha yav tom ntej, lees paub lub luag haujlwm zoo ntawm kev tswj hwm Mg tshuav nyiaj li cas ntawm kev pheej hmoo. osteoporosis thiab fragility pob txha tawg [170]
16. Mg thiab cov leeg nqaij noj qab haus huv
Lub cheeb tsam muaj lub luag haujlwm tseem ceeb hauv tag nrho cov enzymes siv los yog synthesizing nqaij ATP, thiab yog li nyob rau hauv zus tau tej cov nqaij zog, thiab indirectly nyob rau hauv lub contraction thiab so cov txheej txheem. Mg deficit tau cuam tshuam rau cov leeg nqaij tsis zoo.
Kev mob hnyav Mg tau pom tias ua rau tsis muaj zog, mob leeg, thiab mob hmo ntuj. Nws tau raug pom zoo tias Mg qhov tsis txaus yuav ua rau muaj kev txhim kho ntawm fibromyalgia [171]. Cov ntaub ntawv hais txog qhov cuam tshuam ntawm Mg tshuaj ntawm cov tsos mob fibromyalgia yog qhov tsawg, txawm hais tias nws tau pom tias cov tshuaj Mg yuav raug siv los txo qis kev sib tw, mob, thiab cov tsos mob hnyav hauv cov ntsiab lus fibromyalgia [172]. Kev noj zaub mov Mg tsis txaus hauv cov nas boosts kev tsim cov dawb radicals hauv cov leeg pob txha thiab tuaj yeem ua rau ntau qhov kev hloov pauv hauv cov leeg nqaij cell metabolism ua ke nrog cov txheej txheem tsis zoo cuam tshuam rau kev tsim cov nqaij leeg uas xav tau rau cov leeg nqaij thiab so [173].
Hauv tib neeg, Dominguez et al. pom muaj kev sib raug zoo thiab kev ywj pheej ntawm cov ntshav Mg qib nrog cov leeg nqaij ua haujlwm thiab ntau cov leeg nqaij [174]. Hauv cov tub ntxhais hluas tuaj yeem pab dawb, Brilla et al. qhia tau tias Mg tshuaj (txog 8 mg / kg ib hnub twg) tuaj yeem txhim kho cov leeg lub zog thiab kev ua haujlwm siab thiab txo qis kev siv oxygen [175]. Hauv cov neeg laus, Veronese et al.pom qhia tias qhov ncauj Mg supplementation (peb puas mg / hnub) tuaj yeem txhim kho lub cev kev ua haujlwm, tshwj xeeb tshaj yog nyob rau hauv cov kev kawm uas muaj lub hauv paus qis Mg noj cov zaub mov, tawm tswv yim tias Mg supplementation yuav pab tiv thaiv lossis ncua qhov poob ntawm lub cev ua haujlwm nrog hnub nyoog [176].
17. Mg thiab Cancer
Hais txog kev mob qog noj ntshav, kev noj Mg tau txuas nrog qhov tshwm sim ntawm qee cov qog nqaij hlav. Txawm li cas los xij, kev sib raug zoo ntawm Mg thiab mob qog noj ntshav yog qhov nyuaj, thiab niaj hnub no muaj cov lus nug ntau dua li cov lus teb [177]. Hauv cov qauv tsiaj, Mg tuaj yeem tawm tsam ob qho tib si los tiv thaiv qog nqaij hlav xws li inhibition ntawm cov qog loj hlob ntawm nws qhov chaw tseem ceeb thiab kev yooj yim ntawm kev cog cov qog ntawm nws qhov chaw metastatic. Hauv cov nas uas tsis muaj Mg, Mg tsawg yuav txwv tsis pub thiab txhawb nqa cov qog nqaij hlav, vim tias inhibition ntawm cov qog loj hlob ntawm nws qhov chaw tseem ceeb tau pom nyob rau hauv lub ntsej muag ntawm kev nce metastatic colonization [177].
Oxidative kev nyuaj siab thiab kab kawm tau cuam tshuam rau kev txhim kho mob qog noj ntshav. Txawm li cas los xij, yuav ua li cas lawv cuam tshuam rau cov kab mob pathogenesis tseem tsis meej [178]. Cov ntshav qab zib qis Mg hauv cov poj niam uas mob qog noj ntshav mis tuaj yeem cuam tshuam cov tshuaj tiv thaiv antioxidant uas koom nrog hauv cov txheej txheem carcinogenesis. Ib txoj kev tshawb fawb soj ntsuam Mg metabolism, kev ua haujlwm ntawm superoxide dismutase, thiab nws txoj kev sib raug zoo nrog oxidation kev nyuaj siab hauv cov poj niam uas mob qog noj ntshav. Cov kws sau ntawv tau tshaj tawm tias cov neeg mob qog noj ntshav hauv lub mis qhia txog kev hloov pauv ntawm Mg homeostasis, tus cwj pwm los ntawm kev noj zaub mov tsawg Mg, txo cov ntshav plasma, thiab qib erythrocytes Mg, thiab nce Mg excretion hauv cov zis [179].
Mg supplementation tej zaum yuav muaj kev tiv thaiv ntawm kev sim ntxias fibrosarcoma hauv nas[180] thiab yuav inhibit nickel-induced carcinogenesis hauv nas raum [181].
Mg tau pom zoo kom muaj cov teebmeem tiv thaiv qog nqaij hlav hauv plab hnyuv los ntawm inhibiting c-myc qhia thiab ornithine decarboxylase kev ua haujlwm hauv mucosal epithelium ntawm txoj hnyuv [182]. Hauv kev tshawb fawb tib neeg, kev noj zaub mov ntau Mg tau pom zoo los tiv thaiv kev pheej hmoo ntawm kev mob qog noj ntshav hauv plab [183].Nyob rau hauv cov poj niam postmenopausal, nws tau pom zoo tias qhov sib piv ntau dua ntawm cov ntshav Ca rau Mg yuav ua rau muaj kev pheej hmoo rau mob qog noj ntshav [ 184] ib. Ca, Mg, lossis Ca: Mg noj piv yuav cuam tshuam nrog polymorphisms hauv SLC7A2 noob hauv cov koom haum nrog mob qog noj ntshav [185]. Kev noj ntau dua Mg tau cuam tshuam nrog kev pheej hmoo tsawg ntawm daim siab mob qog noj ntshav, raws li kev soj ntsuam ntawm National Institute of Health-American Association of Retired Persons (NIH-AARP) Kev Noj Qab Haus Huv thiab Kev Tshawb Fawb Txog Kev Noj Qab Haus Huv [186]. Ib qho laj thawj ntawm kev sib raug zoo ntawm Mg kev noj haus thiab kev tiv thaiv kab mob qog noj ntshav tsis yooj yim los txhais tau yog vim kev noj zaub mov Mg cov ntsiab lus sib npaug ntawm cov ntsiab lus fiber ntau thiab feem ntau tau los ntawm cov nplooj ntsuab ntsuab thiab tag nrho cov cereals, nplua nuj ntawm fiber ntau, uas yog lawv tus kheej tiv thaiv kab mob cancer. .
18. Cov lus xaus
Kev tsis txaus Mg ntev yog feem ntau tshwm sim hauv cov neeg laus. Tsawg-qib mob o (mob) feem ntau tshwm sim nyob rau hauv ntau yam mob uas muaj hnub nyoog, thiab nyob rau hauv txoj kev laus nws tus kheej. Txij li thaum lub sijhawm Mg tsis txaus tuaj yeem ua rau muaj kev nthuav dav ntawm cov neeg kho kom haum xeeb thiab ROS, thiab nws tuaj yeem ua rau muaj kev mob tshwm sim, peb pab pawg tau pom yav dhau los tias qhov mob Mg tsis txaus yuav yog ib qho ntawm cov neeg kho mob pab piav qhia txog kev sib txuas ntawm kev mob thiab kev laus- Cov kab mob ntsig txog [19,49](Daim duab 2). Nws muaj peev xwm los xav txog tias kev khaws cia qhov zoo Mg tshuav nyiaj li cas thaum lub sij hawm lub neej tuaj yeem pab tiv thaiv kev mob thiab cov xwm txheej cuam tshuam nrog Mg tsis txaus thiab yog li yuav pab ua kom lub neej noj qab nyob zoo.
Txawm li cas los xij, thaum nws raug nquahu kom tswj hwm qhov Mg txaus siab nrog kev noj zaub mov kom txaus ntawm Mg, lub luag haujlwm ntawm Mg tshuaj tseem tsis paub meej.
Ntau qhov kev tshawb fawb ntev ntev ntawm qhov muag tsis pom ntawm qhov cuam tshuam ntawm Mg supplementation tau ua. Qhov muaj peev xwm ua kom muaj kev txaus siab Mg qhov sib npaug thoob plaws hauv lub neej tuaj yeem dhau los ua kev lag luam thiab kev noj qab haus huv zoo hauv cov neeg laus zuj zus yog qhov kev xav pom zoo uas yuav tsum tau ua pov thawj los ntawm cov kev tshawb fawb yav tom ntej.
Kab lus no yog muab rho tawm los ntawm Nutrients 2021, 13, 463. https://doi.org/10.3390/nu13020463 https://www.mdpi.com/journal/nutrients
