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  • 8/9/2019 Jurnal Proposal 4

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    International Journal of Biomedical Research ISSN: 0976-9633 (Online)

    Journal DOI:10.7439/ijbr

    CODEN:IJBR!

    Research Article

    Glycated albumin and glycated hemoglobin- A comparison

    Brijesh Mukherjee*,Saurav Patra and Ashok Kumar Das

    Department of Biochemistry, Kalinga Institute of Medical Sciences, Bhubaneswar, India

    *Correspondence Info:

    Dr. Brijesh Mukherjee

    Department of Biochemistr!Kalin"a #nstitute of Medical Sciences! Bhu$anes%ar! #ndia.

    &'maildr$rijeshkims"mail.com

    1. Introduction

    *he pro"ressive complications of unmana"ed dia$etes include heart disease! $lindness! kidne failure! amputation

    of e+tremities due to circulation pro$lems! and nerve disorders! as %ell as other chronic conditions. ,!-!*he process ofprotein "lcation is no% understood to $e $oth a marker for the pro"ress of dia$etes complications and an underlin" cause

    of man of the most serious complications. Dia$etes monitorin" for protein "lcation! an essential element for the lon"'term

    control of the complications of dia$etes mellitus! is currentl mana"ed $ a com$ination of dail self'monitorin" of $lood

    "lucose (SMB/) measurements and phsician'assessed hemo"lo$in A,c (A,0) levels ever 12 months.3!4!2!5!6

    IJBR "#013$ 04 "0%$ &&&.''journal'.(o)

    AbstractIntroduction:*he pro"ressive complications of unmana"ed dia$etes include heart disease! $lindness! kidne failure!

    amputation of e+tremities due to circulation pro$lems! and nerve disorders! as %ell as other chronic conditions. Decades

    of research have esta$lished that prolon"ed e+posure to e+cess "lucose is the cause of dia$etes complications! and that

    lon"'term control of $lood "lucose levels is re7uired to avoid or lessen the dama"e caused $ e+cess "lucose. *he

    process of protein "lcation is no% understood to $e $oth a marker for the pro"ress of dia$etes complications and an

    underlin" cause of man of the most serious complications.

    Dia$etes monitorin" for protein "lcation! an essential element for the lon"'term control of the complications of

    dia$etes mellitus! is currentl mana"ed $ a com$ination of dail self'monitorin" of $lood "lucose (SMB/)

    measurements and phsician'assessed hemo"lo$in A,c (A,0) levels ever 12 months. Short term methods like self

    monitorin" of $lood "lucose and lon" term methods like measurement of 8$A,c have limitations. 9arious researchers

    have identified "lcated al$umin (/A) as the ideal marker for an intermediate inde+ to measure "lcation.

    Methods:4: patients %ith DM histor more than 4 ears %ere divided into - "roups! -4 %ith micral positive and -4

    %ith micral ne"ative in spot urine sample. 8$a,c and /A %ere estimated in the patients and findin"s %ere noted

    Results: Microal$uminuric patients had si"nificantl hi"her /A levels (p;:.:4) than normoal$uminuric patients.

    0orrelation $et%een 8$A,c and /A %as ver "ood (r

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    Mukherjee et al 382

    "i#ure I$ "actors in%ol%ed in patho#enesis of &iabetic 'ephropath

    1.1 (lcated )aeo#lobin

    A form of hemo"lo$in that is measured primaril to identif the avera"e plasma "lucose concentration over

    prolon"ed periods of time. #t is formed in a non'en=matic "lcation path%a $ hemo"lo$in>s e+posure to plasma "lucose.

    ?ormal levels of "lucose produce a normal amount of "lcated hemo"lo$in. As the avera"e amount of plasma "lucose

    increases! the fraction of "lcated hemo"lo$in increases in a predicta$le %a.@!,:!,,

    #n the normal ,-:'da lifespan of the red $lood cell! "lucose molecules react %ith hemo"lo$in! formin" "lcated

    hemo"lo$in. Once a hemo"lo$in molecule is "lcated! it remains that %a. *he 8$A,c

    level is proportional to avera"e $lood

    "lucose concentration over the previous four %eeks to three month.,-!,

    1.+ (lcated Albuin

    8uman serum al$umin is the most a$undant protein in human $lood plasma. #t is produced in the liver. Al$umin

    constitutes a$out half of the $lood serum protein. #t is solu$le and monomeric. *he reference ran"e for al$umin

    concentrations in $lood is .3 to 4.3 "dC.#t has a serum half'life of appro+imatel -: das. #t has a molecular mass of 25

    kDa. Appro+imatel ,: of the al$umin in normal human serum is modified $ nonen=matic "lcoslation! primaril at

    the epsilon'amino "roup of lsine residue 4-4. *he amount of "lcoslated al$umin in serum is markedl elevated in

    dia$etes and thus its determination ma help in the monitorin" of the disease.,3!,4

    "i#ure II$ -idati%e stress and A(/s

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    Mukherjee et al 383

    "i#ure III$ "oration of )bA1c and A(/s

    +. Materials

    8ospitalEs &thical 0ommittee clearance %as o$tained to carr out the stud.

    *he patients for the stud %ere selected from Medicine OPD! K#MS and %ere divided into three "roups

    -4 health patients (non dia$etic) %ere included as controls.

    -4 patients %ere included %ith dia$etic histor of more than five ears and urine micral levels less than -:F"ml.

    -4 patients %ere included %ith dia$etic histor of more than five ears and urine microal$umin levels $et%een -:'

    -::F"ml.

    #nclusion criteria for the project %as patient %ith DM G4 ears and presence of hpercholeteremia (G-4: m"dl).

    &+clusion criteria %ere patient %ith &SHD and participation in another clinical trial. 8$A,c levels and /lcatedAl$umin levels %ere measured in all the three "roups alon" %ith Iastin" /lucose levels.

    0. Methods

    Iastin" $lood "lucose levels %ere measured $ /lucose O+idase Pero+idase Method.

    Jrine Micral levels %ere measured $ #mmunotur$idimetric Method usin" late+ coated anti al$umin anti$odies.

    8$A,c levels %ere measured $ 8i"h Performance Ci7uid 0hromato"raph usin" D,: 8$A,c Anal=er.

    /lcated Al$umin %as measured $ en=matic method (Cucica /A'C "lcated al$umin assa kit) usin" al$umin

    specific protease! ketoamine o+idase and al$umin assa rea"ent. /A %as hdrol=ed to amino acids $ al$umin specific

    proteinase and then o+idi=ed $ ketoamine o+idase to produce hdro"en pero+ide! %hich %as measured 7uantitativel. *he

    /A value %as calculated as the percenta"e of /A relative to total al$umin! %hich %as measured %ith $romocresol purple

    method.

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    Mukherjee et al 384

    "i#ure I$ 2rinciple of #lcated albuin assa

    3able 1. Correlation of )bA1c and (A in different (roups

    ariables (roup 1 4n5+67 (roup + 4n5+67 (roup 0 4n5+67

    IBS (m") 63.- 6.54 ,2:.4 -: -34.: 5:.2

    8$A,c () 4.4 :. 5.4 :.6, ,:. -.:

    /lcated Al$umin () ,.5 :.@ ,@.2 -., -3., 4.

    Jrine Micral (F" ml) ?e"ative ?e"ative @,.3 3,.4

    "i#ure $ Correlation of )bA1c and (A in different (roups

    "i#ure I$ Increasin# "B8 9e%els !ith duration of &M in patient

    IJBR "#013$ 04 "0%$ &&&.''journal'.(o)

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    Mukherjee et al 385

    3able +. Correlation of &uration of &M and )pertension

    ariable (roup 1 4n5+67 (roup + 4n5+67 (roup 0 4n5+67

    DM in ears ?A 4' 5 2' ,4

    8pertension(?o. of patients)

    ?A ,:

    "i#ure II$ Correlation of &uration of &M and )pertension

    . &iscussion

    *he normal cut of value for /A %as calculated usin" the control "roup and %as found to $e around ,3. /A %as

    si"nificantl hi"her in dia$etic patients indicatin" its role in assessin" "lcemic control. Microal$uminuric patients had

    si"nificantl hi"her /A levels (?ormal Han"e' ,, to ,2) than normoal$uminuric patients (p;:.:4) indicatin" poor

    "lcemic control patients are more likel to have dia$etic complications. *he increase in /A levels correlated %ith the

    increase in 8$A,c levels (r

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    Mukherjee et al 386

    (A/&s) and heart failure Pathophsiolo" and clinical implications.#ur. ". $eart %ail.-::5! @! ,,32',,44.

    2. Olijhoeka! . K.L /raaf$! N. 9. D.L Ban"aa! . D.L Al"ra$! A.L Ha$elinka! *. .L 9isserena! I. C. . *he meta$olicsndrome is associated %ith advanced vascular dama"e in patients %ith coronar heart disease! stroke! peripheral

    arterialdisease or a$dominal aortic aneursm.#ur. $eart ".-::3! -4! 3-'36.

    5. Perne"er! *. 9.L Brancati! I. C.L helton! P. K.L Kla"! M. . &nd'sta"e renal disease attri$uta$le to dia$etes mellitus.Ann. Intern. Med.,@@3! ,-,! @,-'@,6.

    6. *urk! .L Misur! #.L *urk! ?. *emporal association $et%een lens protein "lcation and cataract development in dia$etic

    rats.Acta Diabetol.,@@5! 3! 3@'43.

    @. Bild! D. &.L Sel$! . 9.L Sinnock! P.L Bro%ner! . S.L Braveman! P.L Sho%stack! . A. Co%er'e+tremit amputation inpeople %ith dia$etes. &pidemiolo" and prevention. Dia$etes 0are. ,@6@! ,-! -3',.

    ,:. *hornalle! P. .L Can"$or"! A.L Minhas! 8. S. Iormation of "lo+al! methl"lo+al and 'deo+"lucosone in the

    "lcation of proteins $ "lucose.Biochem. ".,@@@! 33! ,:@',,2.

    ,,. /e$hardt! 0.L Hiehl! A.L Durchde%ald! M.L ?emeth! .L Iursten$er"er! /.L Muller'Decker! K.L &nk! A.L Arnold! B.

    HA/& si"nalin" sustains inflammation and promotes tumor development.". #&p. Med.-::6! -:4! -54'-64.

    ,-. Stern! D. M.L Nan! S. D.L Nan! S. I.L Schmidt! A. M. Heceptor for advanced "lcation endproducts (HA/&) and the

    complications of dia$etes.Ageing Res. Re.-::-! ,! ,',4.

    ,. Bro%nlee! M. ?e"ative conse7uences of "lcation.Metab. 'lin. #&p. -:::! 3@! @',.

    ,3. ansiraniL Anathanaranan! P. 8. A comparitive stud of lens protein "lcation in various forms of cataracht. Indian ".'lin. Biochem. -::3! ,@! ,,:',,-.

    ,4. Ce%is! B. S.L 8ardin"! . . *he effects of amino"uanidine on the "lcation (nonen=matic "lcoslation) of lens

    proteins.#&p. #ye Res. ,@@:! 4:! 32'325.

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