Etiketter

söndag 30 juni 2019

MZ-xTC scaffold , luuta parantavaa biomateriaalia kehitteillä , Magnesium-sinkki-tetrasykliini-perusteinen ehdokas

https://www.ncbi.nlm.nih.gov/pubmed/31147024

2019 Sep;102:53-65. doi: 10.1016/j.msec.2019.04.010. Epub 2019 Apr 5.

Magnesium-zinc scaffold loaded with tetracycline for tissue engineering application: In vitro cell biology and antibacterial activity assessment.

Dayaghi E1, Bakhsheshi-Rad HR2, Hamzah E3, Akhavan-Farid A4, Ismail AF5, Aziz M5, Abdolahi E1.

Abstract

Recently, porous magnesium and its alloys are receiving great consideration as biocompatible and biodegradable scaffolds for bone tissue engineering application. However, they presented poor antibacterial performance and corrosion resistance which limited their clinical applications. In this study, Mg-Zn (MZ) scaffold containing different concentrations of tetracycline (MZ-xTC, x = 1, 5 and 10%) were fabricated by space holder technique to meet the desirable antibacterial activity and corrosion resistance properties. The MZ-TC contains total porosity of 63-65% with pore sizes in the range of 600-800 μm in order to accommodate bone cells. The MZ scaffold presented higher compressive strength and corrosion resistance compared to pure Mg scaffold. However, tetracycline incorporation has less significant effect on the mechanical and corrosion properties of the scaffolds. Moreover, MZ-xTC scaffolds drug release profiles show an initial immediate release which is followed by more stable release patterns. The bioactivity test reveals that the MZ-xTC scaffolds are capable of developing the formation of HA layers in simulated body fluid (SBF). Next, Staphylococcus aureus and Escherichia coli bacteria were utilized to assess the antimicrobial activity of the MZ-xTC scaffolds. The findings indicate that those scaffolds that incorporate a high level concentration of tetracycline are tougher against bacterial organization than MZ scaffolds. However, the MTT assay demonstrates that the MZ scaffolds containing 1 to 5% tetracycline are more effective to sustain cell viability, whereas MZ-10TC shows some toxicity. The alkaline phosphatase (ALP) activity of the MZ-(1-5)TC was considerably higher than that of MZ-10TC on the 3 and 7 days, implying higher osteoblastic differentiation. All the findings suggest that the MZ-xTC scaffolds containing 1 to 5% tetracycline is a promising candidate for bone tissue healing due to excellent antibacterial activity and biocompatibility.
Copyright © 2019. Published by Elsevier B.V.

KEYWORDS:

Antibacterial activity; Bioactivity; Biocompatibility; Drug delivery; Mg composite scaffold
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onsdag 19 juni 2019

Luuytimen glykaatiosta (haku )

Search results
Items: 1 to 20 of 134
1.
High mobility group box 1 protein regulates osteoclastogenesis through direct actions on osteocytes and osteoclasts in vitro.
Davis HM, Valdez S, Gomez L, Malicky P, White FA, Subler MA, Windle JJ, Bidwell JP, Bruzzaniti A, Plotkin LI.
J Cell Biochem. 2019 May 20. doi: 10.1002/jcb.28932. [Epub ahead of print]
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2.
Mesenchymal stromal cells for bone sarcoma treatment: Roadmap to clinical practice.
Stamatopoulos A, Stamatopoulos T, Gamie Z, Kenanidis E, Ribeiro RDC, Rankin KS, Gerrand C, Dalgarno K, Tsiridis E.
J Bone Oncol. 2019 Mar 19;16:100231. doi: 10.1016/j.jbo.2019.100231. eCollection 2019 Jun. Review.
Free PMC Article
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3.
Hyperglycemia effect on red blood cells indices.
Alamri BN, Bahabri A, Aldereihim AA, Alabduljabbar M, Alsubaie MM, Alnaqeb D, Almogbel E, Metias NS, Alotaibi OA, Al-Rubeaan K.
Eur Rev Med Pharmacol Sci. 2019 Mar;23(5):2139-2150. doi: 10.26355/eurrev_201903_17259.
Free Article
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4.
Papaverine identified as an inhibitor of high mobility group box 1/receptor for advanced glycation end-products interaction suppresses high mobility group box 1-mediated inflammatory responses.
Tamada K, Nakajima S, Ogawa N, Inada M, Shibasaki H, Sato A, Takasawa R, Yoshimori A, Suzuki Y, Watanabe N, Oyama T, Abe H, Inoue S, Abe T, Yokomizo T, Tanuma S.
Biochem Biophys Res Commun. 2019 Apr 9;511(3):665-670. doi: 10.1016/j.bbrc.2019.01.136. Epub 2019 Feb 27.
PMID:
30826057
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5.
Melatonin protects endothelial progenitor cells against AGE-induced apoptosis via autophagy flux stimulation and promotes wound healing in diabetic mice.
Jin H, Zhang Z, Wang C, Tang Q, Wang J, Bai X, Wang Q, Nisar M, Tian N, Wang Q, Mao C, Zhang X, Wang X.
Exp Mol Med. 2018 Nov 21;50(11):154. doi: 10.1038/s12276-018-0177-z.
Free PMC Article
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6.
[Role of HMGB1-RAGE/TLRs-NF-κB signaling pathway on bone mesenchymal stem cells transplantation therapy for lipopolysaccaride-induced coagulation disorder rats].
Xiu G, Xiong W, Yin Y, Chen X, Liu P, Sun J, Ling B.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2018 Sep;30(9):830-835. doi: 10.3760/cma.j.issn.2095-4352.2018.09.003. Chinese.
Free Article
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7.
Exosomes Derived From Mesenchymal Stromal Cells Pretreated With Advanced Glycation End Product-Bovine Serum Albumin Inhibit Calcification of Vascular Smooth Muscle Cells.
Wang Y, Ma WQ, Zhu Y, Han XQ, Liu N.
Front Endocrinol (Lausanne). 2018 Sep 21;9:524. doi: 10.3389/fendo.2018.00524. eCollection 2018.
Free PMC Article
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8.
Pharmacologic control of oxidative stress and inflammation determines whether diabetic glomerulosclerosis progresses or decreases: A pilot study in sclerosis-prone mice.
Grosjean F, Yubero-Serrano EM, Zheng F, Esposito V, Swamy S, Elliot SJ, Cai W, Vlassara H, Salem F, Striker GE.
PLoS One. 2018 Sep 25;13(9):e0204366. doi: 10.1371/journal.pone.0204366. eCollection 2018.
Free PMC Article
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9.
An enriched environment prevents diabetes-induced cognitive impairment in rats by enhancing exosomal miR-146a secretion from endogenous bone marrow-derived mesenchymal stem cells.
Kubota K, Nakano M, Kobayashi E, Mizue Y, Chikenji T, Otani M, Nagaishi K, Fujimiya M.
PLoS One. 2018 Sep 21;13(9):e0204252. doi: 10.1371/journal.pone.0204252. eCollection 2018.
Free PMC Article
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10.
Bone disorders associated with diabetes mellitus and its treatments.
Cortet B, Lucas S, Legroux-Gerot I, Penel G, Chauveau C, Paccou J.
Joint Bone Spine. 2019 May;86(3):315-320. doi: 10.1016/j.jbspin.2018.08.002. Epub 2018 Aug 8.
Both type 1 and type 2 diabetes mellitus are associated with bone disorders, albeit via different mechanisms. Early studies in patients with type 1 diabetes suggested a 10-fold increase in the hip fracture risk compared to non-diabetic controls. Meta-analyses published more recently indicate a somewhat smaller risk increase, with odds ratios of 6 to 7. Diminished bone mineral density is among the contributors to the increased fracture risk. Both types of diabetes are associated with decreased bone strength related to low bone turnover. The multiple and interconnected pathophysiological mechanisms underlying the bone disorders seen in type 1 diabetes include insulin deficiency, accumulation of advanced glycation end (AGE) products, bone microarchitecture alterations, changes in bone marrow fat content, low-grade inflammation, and osteocyte dysfunction. The bone alterations are less severe in type 2 diabetes. Odds ratios for hip fractures have ranged across studies from 1.2 to 1.7, and bone mineral density is higher than in non-diabetic controls. The odds ratio is about 1.2 for all bone fragility fractures combined. The pathophysiological mechanisms are complex, particularly as obesity is very common in patients with type 2 diabetes and is itself associated with an increased risk of fractures at specific sites (humerus, tibia, and ankle). The main mechanisms underlying the bone fragility are an increase in the risk of falls, sarcopenia, disorders of carbohydrate metabolism, vitamin D deficiency, and alterations in cortical bone microarchitecture and bone matrix. The medications used to treat both types of diabetes do not seem to play a major role. Nevertheless, thiazolidinediones and, to a lesser extent, sodium-glucose cotransporter inhibitors may have adverse effects on bone, whereas metformin may have beneficial effects. For the most part, the standard management of bone fragility applies to patients with diabetes. However, emphasis should be placed on preventing falls, which are particularly common in this population. Finally, there is some evidence to suggest that anti-fracture treatments are similarly effective in patients with and without diabetes.
Copyright © 2018 Société française de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.

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11.
The pathogenesis and available prevention options in patients with diabetic thrombophilia.
Kwiatkowski J, Halupczok-Żyła J, Bolanowski M, Kuliszkiewicz-Janus M.
Adv Clin Exp Med. 2018 Oct;27(10):1447-1452. doi: 10.17219/acem/71054. Review.
Diabetes mellitus (DM), a growing health problem itself, is accompanied by an increased risk of cardiovascular and thrombotic complications. The imbalance between coagulation and fibrinolysis processes observed in patients with diabetes may be defined as diabetic thrombophilia. Several mechanisms are involved in the hypercoagulability state in diabetics, including endothelial cell damage, altered platelet structure and function, increased microparticle formation, different structure of fibrin clots, disturbances in the activity of coagulation factors, fluctuations in the concentrations of fibrinolysis activators and inhibitors, and qualitative changes of proteins due to glycation and oxidation processes. These all are the reasons why DM is the most common cause of acquired thrombophilia. Moreover, diabetes changes the efficacy of certain medications. Results of various trials seem to suggest that thrombolytic drugs are less effective in patients suffering from this disease. The impact of DM on the effectiveness of treatment with acetylsalicylic acid (ASA) remains unclear. Awareness of thrombotic complications in diabetic patients may enable earlier diagnosis and proper therapy.Free Article
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12.
Glycation of the Major Milk Allergen β-Lactoglobulin Changes Its Allergenicity by Alterations in Cellular Uptake and Degradation.
Perusko M, van Roest M, Stanic-Vucinic D, Simons PJ, Pieters RHH, Cirkovic Velickovic T, Smit JJ.
Mol Nutr Food Res. 2018 Sep;62(17):e1800341. doi: 10.1002/mnfr.201800341. Epub 2018 Jul 29.
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13.
TLR4 and RAGE conversely mediate pro-inflammatory S100A8/9-mediated inhibition of proliferation-linked signaling in myeloproliferative neoplasms.
Kovačić M, Mitrović-Ajtić O, Beleslin-Čokić B, Djikić D, Subotički T, Diklić M, Leković D, Gotić M, Mossuz P, Čokić VP.
Cell Oncol (Dordr). 2018 Oct;41(5):541-553. doi: 10.1007/s13402-018-0392-6. Epub 2018 Jun 26.Abstract PURPOSE:
Previously, the family of S100A proteins has been found to be associated with inflammation and myelopoiesis and to be able to induce or support myeloproliferation during chronic inflammation. Here, we studied the inflammatory myeloid-related proteins S100A4, S100A8, S100A9 and S100A12 in myeloproliferative neoplasms (MPNs) in order to assess the involvement of chronic inflammation in the pathogenesis of MPN. METHODS: We analyzed the S100A4, S100A8, S100A9 and S100A12 mRNA and protein levels in the bone marrow and circulation of 140 patients with MPN and 15 healthy controls using Western blotting, microarray-based mRNA expression profiling and ELISA assays, respectively. In addition we performed functional studies on the proliferation-related AKT and ERK1/2 signaling pathways in MPN-derived granulocytes using Western blotting and proteomic analyses. RESULTS: We found that the S100A mRNA levels were increased in MPN patient-derived circulatory CD34+ cells, and that their protein expression levels were also augmented in their granulocytes and bone marrow stroma cells, depending on the JAK2V617F mutation allele burden. We also found that calreticulin (CALR) mutations were related to reduced S100A8 plasma levels in primary myelofibrosis (PMF). The S100A8 plasma levels were found to be increased in MPN, the S100A9 plasma levels in PMF and essential thrombocythemia (ET), and the S100A12 plasma levels in polycythemia vera (PV). These S100A plasma levels showed a positive correlation with the systemic inflammation marker IL-8, as well as with the numbers of leukocytes and thrombocytes, depending on the JAK2V617F mutation status. Additionally, we found that heterodimeric S100A8/9 can inhibit the AKT pathway in MPN-derived granulocytes mediated by the Toll-like receptor 4 (TLR4), depending on the CALR mutation status. Conversely, we found that blocking of the receptor for advanced glycation end products (RAGE) increased the S100A8/9-mediated inhibition of AKT signaling in the MPN-derived granulocytes. Moreover, we found that heterodimeric S100A8/9 generally induced TLR4-mediated ERK1/2 dephosphorylation proportionally to the JAK2V617F mutation allele burden. TLR4/RAGE blocking prevented the S100A8/9-mediated inhibition of ERK1/2 phosphorylation in PV. CONCLUSIONS:
From our data we conclude that the S100A8 and S100A9 granulocyte and plasma levels are increased in MPN patients, along with inflammation markers, depending on their JAK2V617F mutation allele burden. We also found that S100A8/9-mediated inhibition of the proliferation-related AKT and ERK1/2 signaling pathways can be decreased by CALR mutation-dependent TLR4 blocking and increased by RAGE inhibition in MPN.
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14.
Advanced Glycation End Products Enhance Murine Monocyte Proliferation in Bone Marrow and Prime Them into an Inflammatory Phenotype through MAPK Signaling.
Jin X, Liu L, Zhang Y, Xiang Y, Yin G, Lu Y, Shi L, Dong J, Shen C.
J Diabetes Res. 2018 Mar 22;2018:2527406. doi: 10.1155/2018/2527406. eCollection 2018.
Free PMC Article
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15.
It's reticulated: the liver at the heart of atherosclerosis.
Nagareddy PR, Noothi SK, Flynn MC, Murphy AJ.
J Endocrinol. 2018 Jul;238(1):R1-R11. doi: 10.1530/JOE-18-0082. Epub 2018 May 2. Review.

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16.
Advanced Glycation End-Products-, C-Type Lectin- and Cysteinyl/ Leukotriene-Receptors in Distinct Mesenchymal Stromal Cell Populations: Differential Transcriptional Profiles in Response to Inflammation.
Najar M, Fayyad-Kazan M, Raicevic G, Fayyad-Kazan H, Meuleman N, Bron D, Lagneaux L.
Cell J. 2018 Jul;20(2):250-258. doi: 10.22074/cellj.2018.5104. Epub 2018 Mar 18.
Free PMC Article
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17.
HMGB1 regulates T helper 2 and T helper17 cell differentiation both directly and indirectly in asthmatic mice.
Li R, Wang J, Zhu F, Li R, Liu B, Xu W, He G, Cao H, Wang Y, Yang J.
Mol Immunol. 2018 May;97:45-55. doi: 10.1016/j.molimm.2018.02.014. Epub 2018 Mar 19.

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18.
Methylglyoxal induced advanced glycation end products (AGE)/receptor for AGE (RAGE)-mediated angiogenic impairment in bone marrow-derived endothelial progenitor cells.
Kim JH, Kim KA, Shin YJ, Kim H, Majid A, Bae ON.
J Toxicol Environ Health A. 2018;81(9):266-277. doi: 10.1080/15287394.2018.1440185. Epub 2018 Feb 23.Abstract
Endothelial cells (ECs) maintain the structure and function of blood vessels and are readily exposed to exogenous and endogenous toxic substances in the circulatory system. Bone marrow-derived endothelial progenitor cells (EPCs) circulate in the blood and differentiate to EC, which are known to participate in angiogenesis and regeneration of injured vessels. Dysfunction in EPC contributes to cardiovascular complications in patients with diabetes, but the precise molecular mechanisms underlying diabetic EPC abnormalities are not completely understood.
 The aim of this study was to investigate the mechanisms underlying diabetic EPC dysfunction using methylglyoxal (MG), an endogenous toxic diabetic metabolite. Data demonstrated that MG decreased cell viability and protein expression of vascular endothelial growth factor receptor (VEGFR)-2 associated with functional impairment of tube formation in EPC. The generation of advanced glycation end (AGE) products was increased in EPC following exposure to MG.
Blockage of receptor for AGE (RAGE) by FPS-ZM1, a specific antagonist for RAGE, significantly reversed the decrease of VEGFR-2 protein expression and angiogenic dysfunction in MG-incubated EPC. Taken together, data demonstrated that MG induced angiogenic impairment in EPC via alterations in the AGE/RAGE-VEGFR-2 pathway which may be utilized in the development of potential therapeutic and preventive targets for diabetic vascular complications.
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19.
Identification of megakaryocytes as a target of advanced glycation end products in diabetic complications in bone marrow.
Wang B, Yu J, Wang T, Shen Y, Lin D, Xu X, Wang Y.
Acta Diabetol. 2018 May;55(5):419-427. doi: 10.1007/s00592-018-1109-z. Epub 2018 Feb 8.

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20.
[The Immunosuppressive Function of Myeloid-derived Suppressor Cells Is Regulated by the HMGB1-TLR4 Axis].
Tachibana M.
Yakugaku Zasshi. 2018;138(2):143-148. doi: 10.1248/yakushi.17-00158. Review. Japanese.
Free Article
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AGEs, kehittyneet glykaation lopputuotteet

https://fi.wikipedia.org/wiki/Kehittyneet_glykaation_lopputuotteet
Kehittynyt glykaation lopputuote (eng. advanced glycation end-product, AGE) on yleisnimitys suurelle joukolle erilaisia proteiineja tai rasvoja, jotka ovat glykatoituneet ei-entsymaattisesti altistuttuaan joillekin sokereille, eli liittyneet näihin sokereihin.[1] Glykaatiota ei tule sekoittaa entsymaattiseen glykosylaatioon.[2] AGE:ja voidaan myös kutsua glykotoksiineiksi[2] ja ne saattavat olla pahentava osatekijä ikääntymisessä ja osallistua useiden rappeuttavien sairauksien kuten Alzheimerin taudin, diabeteksen, valtimonkovettumataudin ja kroonisen munuaisten vajaatoiminnan kehittymiseen.[1] Lisäksi niiden on tutkittu osallistuvan harmaakaihin,[3] lihasheikkouden[4] ja syöpäkasvainten kehittymiseen.[5]

AGE:ja ja niiden esiasteita

Tässä osiossa on ei-tyhjentävä esimerkkilista AGE:ista.
Glukosepaani.

Sisäsyntyiset AGE:t ja AGE:jen vaikutukset

AGE:jen muodostumiskaavio: jokin sokeri (kuvassa glukoosi) ja proteiini reagoivat muun muassa Schiffin emäs- ja Amadori-yhdisteiden kautta AGE:iksi.
Osa AGE:ista on sisä- ja osa ulkosyntyisiä. Ulkosyntyisiä AGE:ja ihminen saa ravinnon kautta. Toisin kuin aiemmin on oletettu, ovat kokeet ihmisillä sekä eläimillä osoittaneet näistä ravinnon AGE:ista 10-30% imeytyvän ravinnosta ja päätyvän verenkiertoon.[2][6] Sisäsyntyisten AGE:jen muodostuminen voi olla lisääntynyttä tietyissä aineenvaihdunnallisissa sairauksissa kuten diabeteksessä ja hyperlipidemiassa, sillä nämä lisäävät kehon kokemaa oksidatiivista stressiä.[6]

AGE:t vaikuttavat lähes jokaiseen solutyyppiin ja molekyyliin kehossa.[1] Haitallisia AGE:ista tekee erityisesti niiden kyky reagoida verkkoutumisreaktioiden kautta muun muassa kehon rakenneproteiinien kuten kollageenin ja elastiinin kanssa.[2][7] AGE:t siis polymeroivat näitä proteiineja yhteen suuriksi ryppäiksi estäen siten niiden normaalia toimintaa. AGE:t voivat olla osatekijänä valtimonkovettumataudissa, sillä ne ryppäyttävät verisuonten pintojen kollageeniä, jonka seurauksena suonet kovettuvat. Kovettuminen helpottaa veren haitallisen LDL-kolesterolin kertymistä suonten sisäpintaan. AGE:t voivat lisäksi tehostaa LDL:n hapettumista ja hapettunutta LDL-kolesterolia pidetään yhtenä ateroskeleroosiin johtavien valtimoiden rasvoittumien muodostumisen päätekijöistä.[8]

AGE:t lisäävät kehon tulehdusta aktivoimalla syöjäsoluja (makrofageja) RAGE/NF-κB-signalointireitin kautta. AGE:t kykenevät sitoutumaan monista soluista löytyviin AGE reseptoreihin (eli RAGE:ihin), joiden kautta ne lisäävät oksidatiivista stressiä ja aiheuttavat makrofagivälitteisiä tulehdusreaktioita. Tämä johtaa tuman transkriptiotekijä kappa B:n (NFκB) aktivoitumiseen, joka puolestaan ohjaa monia tulehdusreaktioihin liittyviä geenejä.[2][9] Tulehduksilla on terveyden kannalta merkitystä sillä tulehdusreaktiot liittyvät useisiin sairauksiin: esimerkiksi valtimonkovettumatauti alkaa makrofageja houkuttevilla tulehdusreaktioilla. Osa makrofageista voi muuntua tulehduskohdassa siihen jääviksi vaahtosoluiksi niellessään hapettunutta LDL-kolesterolia. Solut toimivat alustana suoneen kasvavalle plakille ja plakin kasvaessa voi suoneen lopulta muodostua vaikkapa veritulppa.

AGE:t pystyvät myös Auringon UV-säteilyn ja tupakoinnin ohella aiheuttamaan vanhenemiseen liittyviä ulkoisia muutoksia: esimerkiksi ihon rypistymistä ja joustavuuden vähenemistä. Vanhentavat ja rappeuttavat vaikutukset ihossa myös vähentävät sen kykyä tuottaa D-vitamiinia ja heikentävät haavojen parantumista.[2] Nämä ilmiöt liittyvät todennäköisesti useiden soluja rappeuttavien vaikutusten yhteisvaikutukseen, jossa AGE:t osaltaan muun muassa heikentävät solujen DNA:n korjausta ja synteesiä, mitokondrioiden toimintaa, solukalvojen lipidien biosynteesiä, hormonien tuotantoa jne.[5]

Terveysvaikutusten yhteenveto

AGE:jen on tutkittu
  • lisäävän verisuoniston läpäisevyyttä[10]
  • lisäävän verisuoniston kovettumista[1]
  • estävän verisuoniston laajentumista häiritsemällä typpioksidin toimintaa[11]
  • hapettavan LDL-kolesterolia[8]
  • lisäävän tulehdusreaktioita muun muassa makrofagien ja sytokiinien erittymisen kautta[9]
  • lisäävän oksidatiivista stressiä[6]
  • lisäävän kasvainten muodostumista suosivia vaikutuksia[5]
  • rappeuttavan kokonaisvaltaisesti kehon sisäisiä toimintoja ja lisäävän ulkoisia vanhenemisen merkkejä[5]
Ulkosyntyiset AGE:t

Pitoisuudet elintarvikkeissa

AGE:ja esiintyy erityisesti eläinperäisissä rasvaisissa, paistetuissa ja grillatuissa ruuissa. Sitä vastoin niitä on yleensä suhteessa vähemmän esimerkiksi höyrytetyissä tai raaoissa vähärasvaisissa ruuissa kuten kasviksissa, maidossa, hedelmissä ja viljoissa.[2] Osasyinä pitoisuuksien eroon on muun muassa se, että korkeat valmistuslämpötilat suosivat ruokamolekyylien keskinäisiä reaktioita ja kasviperäisissä ruuissa on luonnostaan enemmän AGE:jen muodostumista estäviä hapettumisenastoaineita.[1]
AGE:jen muodostumista yleisesti vähentävät ruuan matala valmistuslämpötila, lyhyt kuumennusaika, suuri kosteus valmistuksen aikana, vähäinen rasvan käyttö ja happamat valmistusolot (kuten sitruunamehun tai etikan lisääminen ruokaan ennen sen valmistusta).[6]
Muun muassa rasvojen härskiintymisen lisäksi Maillard-reaktiossa ja karamellisaatiossa muodostuvista maku- ja väriaineista osa on AGE:ja. Muodostuvista aineista osa myös suosii AGE:jen ja niiden esiasteiden muodostumista.[12] Lisäksi matalissa lämpötiloissa valmistetuissa eläinperäisissä ruuissa, kuten vanhoissa juustoissa, on pastöroinnin ja/tai pitkäaikaisen kypsennyksen seurauksena runsaasti AGE:ja. Lihan, myös vähärasvaisen, on arveltu vaikuttavan ihmisten päivittäiseen AGE:jen saantiin määrällisesti muunlaisia ruokia enemmän. Syynä on lihan luonne pääruokana ja siten suurempi päiväsaanti. Lisäksi lihassa on lähekkäin hyvin reaktiivisia amino-lipidejä ja pelkistäviä sokereita (kuten fruktoosia ja glukoosi-6-fosfaattia), jotka keskenään kuumennettaessa reagoivat herkästi AGE:iksi.[6]
Alla on lueteltu taulukossa (linkki koko taulukkoon) eri elintarvikkeiden tilannekohtaisesti vaihtelevia (kuten valmistustavasta riippuvia), mutta yleisesti kuvaavia ja suuntaa antavia AGE-pitoisuuksia

Alla on lueteltu taulukossa (linkki koko taulukkoon) eri elintarvikkeiden tilannekohtaisesti vaihtelevia (kuten valmistustavasta riippuvia), mutta yleisesti kuvaavia ja suuntaa antavia AGE-pitoisuuksia:[6]
Taulukko eri ruokien AGE-pitoisuuksista[6]
Elintarvike AGE pitoisuus kU/100g* Elintarvike AGE pitoisuus kU/100g*
Rasvaiset ruoat ja juustot Liha ja lihankorvikkeet
Voi 26480 Omassa rasvassa 5 min käristetty pekoni 91577
Kasvimargariini (60% rasvaa) 17520 Esipaahdettu kanankoipi iholla, sitten grillattu 18520
Raastettu parmesaani 16900 Paahdettu kanankoipi iholla 11149
Pehmeä kermajuustolevite 10883 Oliiviöljyssä paistettu naudanlihapihvi 10058
Paahdetut cashewpähkinät 9807 Paistinpannulla ruskistettu naudan jauheliha (20% rasvaa) 4928
Majoneesi 9400 Pariloitu tofu 4107
Maapähkinävoi 7517 Vedessä keitetty kana (1 tunti) 1123
Kuivapaahdetut maapähkinät 6447 Raaka naudanliha pihvi 800
Kevytmajoneesi 2200 Raaka tofu 788
Kypsä oliivi 1670 Ihoton raaka kananrinta 769
Avokado 1577 Raaka lohi 528
Raejuusto (1% rasvaa) 1453 Oliiviöljyssä matalalla lämmöllä 12 min valmistettu munakas 337
Ruokaöljyt Hiilihydraattipitoiset ruoat
Seesamiöljy 21680 Big Mac-hampurilainen 7801
Oliiviöljy 11900 Pizza ohuella pohjalla 6825
Ekstraneitsytoliiviöljy 10040 Perunalastut 2883
Rypsiöljy 9020 Rice Krispies-riisimurot 2000
Auringonkukkaöljy 3940 12 min keitetty pasta 242
Hedelmät ja kasvikset Kidneypavut (tölkki) 191
Kuivattu viikuna 2663 25 min keitetyt perunat 17
Kuivatut luumut 120 Keitetyt pikakaurahiutaleet 14
Kurkku 31 10 min keitetty riisi 9
Banaani 9 Valkoinen sokeri 0
*pitoisuudet osoittavat vain tietyn AGE:n (karboksimetyylilysiinin, CML) pitoisuuden. Yksiköt ovat entsyymiyksiköitä kilokertaluokassa (1 U=1/60 µkat).

Ulkoisen saannin vaikutukset

Eniten ravinnon tulleiden AGE:jen vähentämisestä hyötyvät mahdollisesti muun muassa diabeteksen kaltaisia aineenvaihdunnallisia sairauksia potevat henkilöt, mutta merkittävistä vaikutusten olemassaolosta on vain koeputki- (in vitro) ja eläinkokeisiin pohjautuvaa näyttöä. Vahvoja kliinisiä todisteita näistä vaikutuksista ihmisillä ei ole. Eläimillä AGE:jen välttämisen on tutkittu parantavan diabeteksessä muun muassa insuliiniherkkyyttä ja haavojen parantumista. AGE:jen merkittävän vähentämisen on osoitettu myös pidentävän elinikää hiirillä ja tämän on arveltu olevan osatekijänä kalorirajoitteisen ruokavalion koe-eläinten elinikää pidentävässä vaikutuksessa. AGE:jen saannin rajoittamisen on myös osoitettu eläimillä estävän valtimonkovettumatautia, munuaisten vajaatoimintaa sekä aikuistyypin diabeteksen kehittymistä. Vastaavasti suuria AGE-pitoisuuksia sisältävät ruokavaliot ovat lisänneet edellä mainittujen sairauksien kehittymisen todennäköisyyksiä eläimillä.[6] Koska tutkimukset ovat osoittaneet AGE:jen olevan haitallisia koe-eläimillä ja esimerkiksi diabeettisillä ihmisillä, on ulkoisesti saatujen AGE:jen arveltu olevan tilastollisesti merkittävällä tavalla haitallisia myös sairailla sekä terveillä ihmisillä. Kliiniset todisteet ihmisillä huomattavista vaikutuksista ovat kuitenkin heikot ja esimerkiksi eräässä tutkimuksessa dialyysipotilailla veren AGE-pitoisuuden ja kuolleisuuden väliltä ei löydetty yhteyttä. Yhteys ravinnon AGE-pitoisuuden ja ihmisten terveyden välillä on edelleen tuntematon.[13]
Ihon autofluoresenssin mittauslaite.
AGE:jen pitoisuuksia on arvioitu aikuistyypin diabeetikoilla ihon autofluoresenssimittausten avulla ja AGE:jen suuren ihopitoisuuden ja kuolleisuuden välillä on todistettu olevan merkittävämpi tilastollinen yhteys kuin esimerkiksi terveydenhuollon mittauksissa käytetyn glykatoituneen hemoglobiinin (A1c) kohdalla. On kuitenkin hyvä ottaa huomioon että diabetes itsessään suosii AGE:jen muodostumista ja niiden suuri esiintyvyys voi olla pikemminkin todiste taudin huonosta hallinnasta kuin itsessään kuolleisuutta lisäävä syy.[2]

Poistuminen kehosta

Keho pystyy tuhoamaan AGE:ja rajoitetusti. Se pilkkoo suurimpia AGE-molekyylejä entsyymien suorittaman proteolyysin kautta lyhyiksi glykatoiduiksi peptideiksi ja aminohapoiksi, jotka siirtyvät veriplasmaan ja sieltä virtsaan.[14]
Solunulkoisen tilan (matriisin) AGE:t ovat kuitenkin proteolyysille vastustuskykyisiä. Tätä ominaisuutta lisää matriisin proteiinien AGE:ja suojaava verkkoutuminen, joten solunulkoisessa tilassa esiintyvät AGE:t poistuvat huonommin kuin muilta solualueilta ja ovat siksi hyvin pysyviä.[15][16] Tärkeitä AGE:jen pilkkomista suorittavia proteiineja ovat muun muassa matriisin metalloproteinaasit (MMP).[2]
Suurimmat AGE:t eivät kokonsa vuoksi pysty poistumaan verestä munuaiskeräsen kalvon kautta virtsaan ennen pilkkoutumistaan. Solutasolla pilkkomiseen osallistuvat todennäköisesti erityisesti periferaaliset makrofagit,[14] sinusoidiset endoteelisolut ja maksan Kupfferin syöjäsolut,[17] joista jälkimmäisten osallisuus pilkkomiseen on kuitenkin kyseenalaistettu.[18]
Vaikka pilkotut AGE:t ovat ainoita AGE:ja joita keho kykenee erittämään, ovat ne myös reaktiivisempia kuin suuret AGE:t. Tämän vuoksi pienet AGE:t voivat noidankehämäisesti pahentaa esimerkiksi diabeetikon AGE:ista johtuvia ongelmia myös senkin jälkeen kun korkea verensokeri on saatu kuriin.[14]

Hoitomuodot

AGE:jen mahdollisesti aiheuttamiin ongelmiin kolmentyyppisiä ratkaisuja: AGE:jen muodostumisen estäminen, verkkosidosten rikkominen niiden muodostumisen jälkeen ja jo ilmenneiden AGE:jen haittavaikutusten hoito.

AGE:jen muodostumisen ehkäisy

Ihmisillä C-vitamiinin on havaittu vähentävän merkittävästi veriseerumin proteiinien glykaatiota,[2] vaikka ei olekaan vahvoja todisteita tämän merkityksestä parempaa terveyttä edistävänä tekijänä.[13]
AGE:jen muodostumista on onnistuttu estämään koeputkikokeissa muun muassa C-, B2- ja B3-vitamiinilla, pyridoksaalilla (B6), sinkillä, mangaanilla,[2] metformiinilla[19] ja aspiriinilla.[20]
 Rotilla alfalipoiinihapon on osoitettu vähentävän rakenneproteiinien verkkoutumista. Hiirillä vastaavanlaisia vaikutuksia on havaittu kun niille on annettu vihreää teetä, vihreässä teessä luontaisesti esiintyvää EGCG:tä, C- ja E-vitamiinia tai N-asetyylikysteiiniä. Kanelin, inkiväärin ja monien muiden mausteiden kohdalla on havaittu positiivisia vaikutuksia seebrakaloilla.[2]
Osa edellä mainituista aineista on hapettumisenestoaineita (C-vitamiini), kelatoivia aineita (pyridoksaali),[2] tulehduskipulääkkeitä (aspiriini) ja glukoosin muodostumista vähentäviä diabeteslääkkeitä (metformiini).
Pyridoksaalilla vaikutukset ovat kuitenkin moninaiset ja se pystyy muun muassa toimimaan antioksidanttina.[21]
Kelatoivat aineet sitovat metalli-ioneita (kuten Fe2+), jotka katalyyttisesti muodostavat hyvin reaktiivisia ja yleisesti haitallisia vapaita radikaaleja. Radikaalit puolestaan pystyvät muuttamaan kehon molekyylejä AGE:iksi tai niiden esiasteiksi ainakin koeputkikokeissa. Metalli-ionit pystyvät myös suoraan katalysoimaan AGE:jen ja esiasteiden muodostusta.[21] Hapettumisenestoaineet puolestaan tuhoavat muodostuneita radikaaleja.[2] Metformiini paitsi alentaa maksan glukoosin tuottoa ja vapautumista, siten vaikuttaen glykatoivan verensokerin määrään, se myös hillitsee tulehdusta vaimentamalla makrofageja aktivoivan RAGE/NF-κB-signalointireitin toimintaa. Tätä reittiä AGE:t puolestaan aktivoivat.[22]

Verkkosidosten rikkominen

AGE:jen muodostamia verkkosidoksia proteiinien välillä kykenevät in vitro rikkomaan muun muassa alagebriumi,[23] N-fenasyyli tioatsolium bromidi[24] ja rosmariinihappo,[25] joista jälkimmäisen on eräässä in vitro tutkimuksessa todettu olevan alagebriumia hieman tehokkaampi verkkosidosten rikkoja.[26] Alagebriumia on tutkittu vanhoilla ihmisillä ja sen on havaittu alentavan korkeaa verenpainetta ja vähentävän verisuonten jäykistymistä. Nämä vaikutukset todennäköisesti johtuvat alagebriumin kyvystä rikkoa AGE:jen muodostamia verkkosidoksia.[23][27]
Ei kuitenkaan tunneta mitään yhdistettä joka kykenee pilkkomaan yleisimmän AGE:n, glukosepaanin, muodostamia sidoksia. Se on iästä riippuen 10-10000 kertaa yleisempi ihmiskudoksissa kuin mikään muu verkkosidoksia muodostava AGE.[28][29]

Katso myös

Lähteet

 

 



Upplagd av kl. Inga kommentarer:

Pentosidine

https://www.ncbi.nlm.nih.gov/pubmed/?term=pentosidine

 
 

Haku:   Pentosidine 

 
Upplagd av kl. Inga kommentarer:
Etiketter:

Hyperhomocysteinemia (HHCy) ja luustovaikutukset

 (1)
https://www.ncbi.nlm.nih.gov/pubmed/30116976
2018 Oct;16(5):554-560. doi: 10.1007/s11914-018-0469-1.

The Effects of Homocysteine on the Skeleton.

Saito M1, Marumo K2. Abstract  PURPOSE OF REVIEW:
Homocystinuria is a congenital metabolic disorder in which cystathionine β-synthase (CBS) deficiency results in a prominent increase in homocysteine (Hcy)  (serum levels > 100 μM), causing mental retardation, atherosclerotic cerebral infarction, and osteoporosis accompanied by fragility fractures. Encountering a case with excessive homocysteinemia such as that seen in hereditary homocystinuria is unlikely during usual medical examinations. However, in individuals who have vitamin B or folate deficiency, serum homocysteine concentrations are known to increase. These individuals may also have a polymorphism in methylenetetrahydrofolate reductase, MTHFR (C677T: TT type), which regulates homocysteine metabolism. These changes in homocysteine levels may elicit symptoms resembling those of homocystinuria (e.g., Alzheimer's disease, atherosclerosis, osteoporosis).
RECENT FINDINGS:
High serum homocysteine has been shown to have detrimental effects on neural cells, vascular endothelial cells, osteoblasts, and osteoclasts. Homocysteine is also known to increase oxidative stress, disrupt cross-linking of collagen molecules, and increase levels of advanced glycation end products, which results in reduced bone strength through a mechanism that goes beyond low bone density and increased bone resorption. Therefore, high serum homocysteine may be regarded as a factor that can reduce both bone mass and impair bone quality. In this review, we outline the epidemiology and pathophysiology of osteoporosis associated with hyperhomocysteinemia.
KEYWORDS:
Advanced glycation end products; Bone quality; Collagen; Cross-links; Fracture risk; Homocysteine; Pentosidine
PMID:
30116976
DOI:
10.1007/s11914-018-0469-1
(2)
https://www.ncbi.nlm.nih.gov/pubmed/19860214
2009 Sep;57(9):876-83.
[Bone quality markers: pentosidine, homocysteine, and MTHFR polymorphism].
[Article in Japanese]
Saito M1. Abstract
Bone quality is thought to encompass the structural and material properties of bone that are affected by the turnover rate. Evidence has accumulated that collagen cross-links play important roles in bone strength. We have demonstrated that the quantitative and qualitative deterioration of lysyl oxidase control and non enzymatic cross-links (advanced glycation end products, AGEs, pentosidine) of collagen in patients with osteoporotic femoral neck fracture might be affected by hyperhomocysteinemia, oxidative stress, and vitamin B6 insufficiency.

 Recently, Shiraki et al. demonstrated that a functional polymorphism in methylenetetrahydrofolate reductase (MTHFR) polymorphism, T allele (C677T), may be a risk factor for future fracture in addition to the traditional risk factors.

 Further, we reported that a higher urinary pentosidine level was an independent risk factor for vertebral fracture in a 5-year prospective study involving Japanese women.

If confirmed in large, prospective trials, measurements of serum homocysteine and serum or urine levels of pentosidine might be characterized as markers reflecting bone collagen deterioration.


Upplagd av kl. Inga kommentarer:
Etiketter:

Ravinnon menakinonit vaikuttavat luustoon

Best matches for natto,menaquinones:

Search results  Items: 1 to 20 of 29

1.
Determination of vitamin K composition of fermented food.
Tarvainen M, Fabritius M, Yang B.
Food Chem. 2019 Mar 1;275:515-522. doi: 10.1016/j.foodchem.2018.09.136. Epub 2018 Sep 24.
A rapid ultra-high performance liquid chromatography-atmospheric pressure chemical ionization tandem mass spectrometric (UHPLC-APCI-MS/MS) method was developed for the analysis of vitamin K compounds: phylloquinone (PK) and menaquinones (MK-n). Non-chlorinated mobile phase composition was optimized for separation of eight vitamin K compounds on a reversed phase column in 10 min. Sample treatment with liquid and solid phase extractions and by the use of MK-4 as an internal standard enabled the quantitation of microgram level of vitamin K compounds in food. The method was used to screen and quantitate vitamin K from 17 fermented food products. The highest amount of PK was detected in kimchi (42 µg/100 g), whereas the highest MK-7 content was detected in natto (902 µg/100 g). Some MK-9 was present in kefir (5 µg/100 g). Two Chinese fermented soybean pastes contained significant amount of MK-6 (5-36 µg/100 g), MK-7 (12-86 µg/100 g), and MK-8 (22-44 µg/100 g).
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2.
Enhanced Vitamin K (Menaquinone-7) Production by Bacillus subtilis natto in Biofilm Reactors by Optimization of Glucose-based Medium.
Mahdinia E, Demirci A, Berenjian A.
Curr Pharm Biotechnol. 2018;19(11):917-924. doi: 10.2174/1389201020666181126120401.Benefits of vitamin K have been reported by many studies recently, due to its ability to reduce the risk of cardiovascular diseases and its potential benefits against osteoporosis. Specifically, menaquinone-7 (MK-7), being the most potent form of vitamin K, has definitely received most of the attention. Currently, solid or static liquid fermentation strategies are utilized for industrial production of MK-7 by Bacillus strains. However, these strategies face fundamental operational and scale-up issues as well as intense pellicle and biofilm formations which is problematic in static liquid fermentation, due to heat and mass transfer inefficiencies they create.
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3.
Implementation of fed-batch strategies for vitamin K (menaquinone-7) production by Bacillus subtilis natto in biofilm reactors.
Mahdinia E, Demirci A, Berenjian A.
Appl Microbiol Biotechnol. 2018 Nov;102(21):9147-9157. doi: 10.1007/s00253-018-9340-7. Epub 2018 Sep 14.

7.
Magnetic immobilization of Bacillus subtilis natto cells for menaquinone-7 fermentation.
Ebrahiminezhad A, Varma V, Yang S, Berenjian A.
Appl Microbiol Biotechnol. 2016 Jan;100(1):173-80. doi: 10.1007/s00253-015-6977-3. Epub 2015 Sep 24.
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8.
Effects of gamma-glutamyl carboxylase gene polymorphism (R325Q) on the association between dietary vitamin K intake and gamma-carboxylation of osteocalcin in young adults.
Haraikawa M, Tsugawa N, Sogabe N, Tanabe R, Kawamura Y, Okano T, Hosoi T, Goseki-Sone M.
Asia Pac J Clin Nutr. 2013;22(4):646-54. doi: 10.6133/apjcn.2013.22.4.01.
It has been demonstrated that single nucleotide polymorphism (SNP) (R325Q, 974G>A) in the gamma-glutamyl carboxylase (GGCX) gene is associated with the bone mineral density (BMD). In the present study, we investigated the effect of GGCX polymorphism (974G>A) on the correlations among the vitamin K in-take, level of serum vitamin K, and ratio of undercarboxylated osteocalcin (ucOC) to intact osteocalcin (OC) in healthy young Japanese subjects.
Healthy young adult subjects (n=189) were genotyped for the poly-morphism, and we measured the levels of serum vitamin K, intact OC, ucOC, and dietary nutrient intakes.
Dietary vitamin K intake from vegetables was significantly correlated with the level of serum phylloquinone (PK), and vitamin K intake from fermented beans, natto, was also significantly correlated with the level of serum menaquinone-7 (MK-7). Moreover, the total dietary vitamin K intake showed a significant negative correlation with the ratio of ucOC to intact OC. Interestingly, on grouping by the GGCX genotype, there was a significant interaction between the ratio of ucOC to intact OC with vitamin K intake in homozygotes (GG-type) and heterozygotes (GA-type) (p<0.001). These results suggest that an adequate nutritional strategy is necessary for people with high-risk genotypes (GG- or GA-type).
We demonstrated the effects of SNP (974G>A) in the GGCX gene on the correlation between dietary vitamin K intake and gamma-carboxylation of serum OC. Our data may be useful for planning strategies to prevent osteoporosis.
Free Article
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9.
Designing of an intensification process for biosynthesis and recovery of menaquinone-7.
Berenjian A, Mahanama R, Talbot A, Regtop H, Kavanagh J, Dehghani F.
Appl Biochem Biotechnol. 2014 Feb;172(3):1347-57. doi: 10.1007/s12010-013-0602-7. Epub 2013 Oct 31.
A nutritional food rich in menaquinone-7 has a potential in preventing osteoporosis and cardiovascular diseases. The static fermentation of Bacillus subtilis natto is widely regarded as an optimum process for menaquinone-7 production. The major issues for the bulk production of menaquinone-7 are the low fermentation yield, biofilm formation and the use of organic solvents for the vitamin extraction. In this study, we demonstrate that the dynamic fermentation involving high stirring and aeration rates enhances the yield of fermentation process significantly compared to static system. The menaquinone-7 concentration of 226 mg/L was produced at 1,000 rpm, 5 vvm, 40 °C after 5 days of fermentation. This concentration is 70-fold higher than commercially available food products such as natto. Additionally, it was found that more than 80% of menaquinone-7 was recovered in situ in the vegetable oil that was gradually added to the system as an anti-foaming agent. The intensification process developed in this study has a capacity to produce an oil rich in menaquinone-7 in one step and eliminate the use of organic solvents for recovery of this compound. This oil can, therefore, be used for the preparation of broad range of supplementary and dietary food products rich in menaquinone-7 to reduce the risk of osteoporotic fractures and cardiovascular diseases.
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10.
Effect of biofilm formation by Bacillus subtilis natto on menaquinone-7 biosynthesis.
Berenjian A, Chan NL, Mahanama R, Talbot A, Regtop H, Kavanagh J, Dehghani F.
Mol Biotechnol. 2013 Jun;54(2):371-8. doi: 10.1007/s12033-012-9576-x.

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12.
Vitamin K2 supplementation does not influence bone loss in early menopausal women: a randomised double-blind placebo-controlled trial.
Emaus N, Gjesdal CG, Almås B, Christensen M, Grimsgaard AS, Berntsen GK, Salomonsen L, Fønnebø V.
Osteoporos Int. 2010 Oct;21(10):1731-40. doi: 10.1007/s00198-009-1126-4. Epub 2009 Nov 25.
Vitamin K2 may preserve bone strength and reduce fracture risk. In this randomised double-blind placebo-controlled trial among healthy postmenopausal Norwegian women, 1 year supplementation of vitamin K2 in the form of Natto capsules had no effect on bone loss rates.
Japanese studies indicate that vitamin K2 (menaquinone-7 (MK-7)) intake may preserve bone strength, but this has not been documented in Europeans. The aim of this study was to assess the effect of MK-7 on bone mineral density (BMD) changes in postmenopausal Norwegian women.
Three hundred thirty-four healthy women between 50 and 60 years, 1-5 years after menopause, were recruited to a randomised double-blind placebo-controlled trial. The participants were randomly assigned into two groups, one receiving 360 microg MK-7 in the form of Natto capsules and the other the same amount of identical-looking placebo capsules containing olive oil. BMD was measured at total hip, femoral neck, lumbar spine and total body at baseline and 12 months together with serum levels of bone-specific alkaline phosphatase, Crosslaps, total osteocalcin (N-mid OC), carboxylated (cOC) and under-carboxylated osteocalcin (ucOC).
After 12 months, there were no statistical differences in bone loss rates between the groups at the total hip or any other measurement site. Serum levels of cOC increased and ucOC decreased in the treatment versus the placebo group (p < 0.001).
MK-7 taken as Natto over 1 year reduced serum levels of ucOC but did not influence bone loss rates in early menopausal women.
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13.
[Foods rich in fat-soluble vitamins and bone health].
Kuwabara A.
Clin Calcium. 2009 Sep;19(9):1362-9. doi: CliCa090913621369. Review. Japanese.
Intervention studies and meta-analyses have shown that vitamin D(3) at 700-800 IU/day decreases the fracture incidence. Higher phylloquinone (vitamin K(1)) intake or "natto" intake was associated with lower fracture incidence. In contrast, current intake of vitamin D and K in Japanese is likely to be unsatisfactory for preventing fracture. The intake of fish, abundant in vitamin D(3) is encouraged. Regarding vitamin K, "natto" intake is strongly recommended, since it contains extraordinary amount of menaquinone-7. Phylloquinone in green vegetables would be efficiently absorbed when cooked with oil. Thus Japanese traditional foods seem to be appropriate for bone health.
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14.
Vitamin K content of foods and dietary vitamin K intake in Japanese young women.
Kamao M, Suhara Y, Tsugawa N, Uwano M, Yamaguchi N, Uenishi K, Ishida H, Sasaki S, Okano T.
J Nutr Sci Vitaminol (Tokyo). 2007 Dec;53(6):464-70.
Several reports indicate an important role for vitamin K in bone health as well as blood coagulation. However, the current Adequate Intakes (AI) might not be sufficient for the maintenance of bone health. To obtain a closer estimate of dietary intake of phylloquinone (PK) and menaquinones (MKs), PK, MK-4 and MK-7 contents in food samples (58 food items) were determined by an improved high-performance liquid chromatography method. Next, we assessed dietary vitamin K intake in young women living in eastern Japan using vitamin K contents measured here and the Standard Tables of Food Composition in Japan. PK was widely distributed in green vegetables and algae, and high amounts were found in spinach and broccoli (raw, 498 and 307 microg/100 g wet weight, respectively). Although MK-4 was widely distributed in animal products, overall MK-4 content was lower than PK. MK-7 was observed characteristically in fermented soybean products such as natto (939 microg/100 g). The mean total vitamin K intake of all subjects (using data from this study and Japanese food composition tables) was about 230 microg/d and 94% of participants met the AI of vitamin K for women aged 18-29 y in Japan, 60 microg/d. The contributions of PK, MK-4 and MK-7 to total vitamin K intake were 67.7, 7.3 and 24.9%, respectively. PK from vegetables and algae and MK-7 from pulses (including fermented soybean foods) were the major contributors to the total vitamin K intake of young women living in eastern Japan.Free Article
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15.
Treatment of natto, a fermented soybean preparation, to prevent excessive plasma vitamin K concentrations in patients taking warfarin.
Homma K, Wakana N, Suzuki Y, Nukui M, Daimatsu T, Tanaka E, Tanaka K, Koga Y, Nakajima Y, Nakazawa H.
J Nutr Sci Vitaminol (Tokyo). 2006 Oct;52(5):297-301.
The purpose of this study is to find a method of cooking natto that prevents the appearance of high-plasma vitamin K concentrations after the consumption of natto, so that patients taking warfarin can benefit from eating natto. Five cooking methods were examined to determine which could most effectively decrease the count of the living Bacillus subtilis in natto. Volunteers ate natto or treated natto, and their plasma vitamin K level was measured at 5, 8, 24 and 48 h thereafter. One gram of natto contained 9.7+/-0.1 Log cfu/mL of Bacillus subtilis. Boiling significantly reduced the Bacillus subtilis count to 5.1+/-0.3 Log cfu/mL, and concomitantly reduced the content of menaquinone-7 (MK-7), which is a form of vitamin K synthesized by Bacillus subtilis, from 660.40+/-65.32 ng/mL to 78.50+/- 11.12 ng/mL. Untreated natto increased the MK-7 concentration in blood from 1.86+/-1.51 ng/mL to 14.54+/-4.12 ng/mL at 5 h after intake, and the MK-7 concentration remained elevated at 8, 24 and 48 h (7.29+/-2.20, 6.97+/-2.60, and 5.37+/-1.94 ng/mL, respectively). In contrast, boiled natto increased plasma MK-7 only mildly (from 1.61+/-1.11 to 4.02+/-0.82 ng/ mL at 5 h) and the concentration remained relatively stable up to 48 h (3.46+/-0.83, 4.22+/-1.51 and 2.77+/-0.75 ng/mL at 8, 24 and 48 h, respectively). In conclusion, boiled natto did not cause a marked increase in the plasma concentration of vitamin K in subjects who consumed it. Thus, patients on warfarin may be able to eat boiled natto without ill effects.Free Article
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16.
Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7.
Schurgers LJ, Teunissen KJ, Hamulyák K, Knapen MH, Vik H, Vermeer C.
Blood. 2007 Apr 15;109(8):3279-83. Epub 2006 Dec 7.
Vitamin K is a cofactor in the production of blood coagulation factors (in the liver), osteocalcin (in bone), and matrix Gla protein (cartilage and vessel wall). Accumulating evidence suggests that for optimal bone and vascular health, relatively high intakes of vitamin K are required. The synthetic short-chain vitamin K(1) is commonly used in food supplements, but recently the natural long-chain menaquinone-7 (MK-7) has also become available as an over-the-counter (OTC) supplement. The purpose of this paper was to compare in healthy volunteers the absorption and efficacy of K(1) and MK-7. Serum vitamin K species were used as a marker for absorption and osteocalcin carboxylation as a marker for activity. Both K(1) and MK-7 were absorbed well, with peak serum concentrations at 4 hours after intake. A major difference between the 2 vitamin K species is the very long half-life time of MK-7, resulting in much more stable serum levels, and accumulation of MK-7 to higher levels (7- to 8-fold) during prolonged intake. MK-7 induced more complete carboxylation of osteocalcin, and hematologists should be aware that preparations supplying 50 mug/d or more of MK-7 may interfere with oral anticoagulant treatment in a clinically relevant way.Free Article
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17.
[Prevention of osteoporosis by foods and dietary supplements. "Kinnotsubu honegenki": a fermented soybean (natto) with reinforced vitamin K2 (menaquinone-7)].
Takemura H.
Clin Calcium. 2006 Oct;16(10):1715-22. Review. Japanese.
In recent years, it has been proven that vitamin K(2) has important roles not only in blood coagulation but also in bone metabolism. We developed a Bacillus subtilis (natto) strain with high productivity of vitamin K(2) (Menaquinone-7), and commercialized a natto with reinforced vitamin K(2) by use of the strain. The natto, named "Kinnotsubu honegenki", was granted a health claim based on our clinical studies which demonstrated that intake of the natto stimulated gamma-carboxylation of osteocalcin.
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18.
[Protective effects of vitamin K against osteoporosis and its pleiotropic actions].
Kaneki M.
Clin Calcium. 2006 Sep;16(9):1526-34. Review. Japanese.
Vitamin K is a nutrient originally identified as an essential factor for blood coagulation. Recently, vitamin K has emerged as a potential protector against osteoporosis and hepatocarcinoma. Accumulated evidence indicates that subclinical non-hemostatic vitamin K deficiency in extrahepatic tissues, particularly in bone, exists widely in the otherwise healthy adult population. Both vitamin K(1) and K(2) have been shown to exert protective effects against osteoporosis. Moreover, therapeutic potential of vitamin K(2) as an anti-hepatoma drug has been recently highlighted. Most of the new biological functions of vitamin K in bone and hepatoma cells are considered to be attributable to promotion of gamma-carboxylation of glutamic acid residues in vitamin K-dependent proteins, which is shared by both vitamins K(1) and K(2). In contrast, vitamin K(2)-specific, gamma-carboxylation-unrelated functions have also been demonstrated. These functions include stimulation of steroid and xenobiotic receptor (SXR)-mediated transcription and anti-oxidant property. Thus, biological differences between vitamins K(1) and K(2), and a potential involvement of gamma-carboxylation-independent actions in the new roles of vitamin K remain open issues. Molecular bases of coagulation-unrelated pleiotropic actions of vitamin K and its implications in human health deserve further investigations.
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19.
Menaquinone-7 regulates the expressions of osteocalcin, OPG, RANKL and RANK in osteoblastic MC3T3E1 cells.
Katsuyama H, Otsuki T, Tomita M, Fukunaga M, Fukunaga T, Suzuki N, Saijoh K, Fushimi S, Sunami S.
Int J Mol Med. 2005 Feb;15(2):231-6.
Epidemiological studies show that dietary intake of natto, which contains significant amount of vitamin K(2), reduces the risk of bone formation loss. However, many confounding factors, such as calcium and isoflavone, are found in natto, because it is made from soybeans. In this study, the direct effects of MK-7, a vitamin K(2) analogue, were assessed in osteoblasts. Osteoblastic MC3T3E1 cells were cultured with or without MK-7 for 10 days and the number of cells was calculated. The cell count was not different between MK-7 treated cells and control cells for 1, 2, and 4 days. However, it was significantly suppressed in MK-7 treated cells at 10 days, suggesting that MK-7 suppressed cell proliferation. Real-time PCR analysis showed that mRNAs of osteocalcin (OC), osteoprotegerin (OPG), and the receptor activator of the NFkappaB ligand (RANKL) were induced after MK-7 administration to the culture medium. RANK mRNA expression was also enhanced by MK-7 administration. Immunocytochemical analysis showed that MK-7 increased the protein levels of OC and RANKL. RANK protein was also enhanced, but this induction was suppressed by anti-RANK antibody administration. This suppression was recovered when anti-RANK antibody and MK-7 were administered. These observations suggest that MK-7 may directly affect MC3T3E1 cells and stimulate osteoblastic differentiation, not proliferation.
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20.
Studies on action of menaquinone-7 in regulation of bone metabolism and its preventive role of osteoporosis.
Tsukamoto Y.
Biofactors. 2004;22(1-4):5-19.
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