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Diabetes Estimates and Projections 1994 - 2
1994 2000 2010
Type 2 Diabetes
98.9 million 157. million 215.! million
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D"#$ETE% $E&'(E% (')E * (')E"(P')T#+T #% # ,'$# P)'$E(
DE T' /
1. The Steaply Rising Prevalence
2. The Disvastating Complications3. High Number o Ris! "actors
or #ascular Dysunction
$. Di%culties in Preventing
Complications
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Patogenesis dan Evolusi DM tipe 2Patogenesis dan Evolusi DM tipe 2
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+ormal ,lcose (etabolism
,&'+E'
,E+E%"%
GLYCOGENOLYSIS
Insulin
HGP
Glucose
uptake +
,&'%E
+')(#
, &',E+
, & ' % E
%ppression
%timlation
+
LI!E" P#NC"E#S
(%&E
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Regulasi glu!osa &arahRegulasi glu!osa &arah
3PasaPasa
ebtan 6losa diperole/ebtan 6losa diperole/
prodsi 6losa ole ati 80prodsi 6losa ole ati 80
3%etela maan%etela maan
,losa dara ditean ole sel,losa dara ditean ole sel beta panreas / inslinbeta panreas / inslin
otot /menin6atan 6lcose ptaeotot /menin6atan 6lcose ptae
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Pat$op$%siolog%Pat$op$%siolog% o& '%pe 2 Dia(eteso& '%pe 2 Dia(etes
Dec)eased glucose uptakeInc)eased glucose p)oduction
H%pe)gl%ce*ia
I*pai)ed insulin action
I*pai)ed insulin sec)etion
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GGENE'ICENE'ICEEN!I"ONMEN'N!I"ONMEN'
HH YPE"GLYCEMI# YPE"GLYCEMI#
&E IINSLINNSLIN""ESIS'#NCEESIS'#NCE
GGENE'ICENE'ICOO,ESI'Y,ESI'YLLI-EI-E SS'YLE'YLE
HH YPE"INSLINEMI# YPE"INSLINEMI#
##NGIOP#'HY etcNGIOP#'HY etc
NNO"M#LO"M#L NG'NG'
DDECOMPENS#'ION ECOMPENS#'ION .. IG'DI#,E'ESIG'DI#,E'ES
DDE&'(PE+%#T"'+ -E&'(PE+%#T"'+ - 22 DI#,E'ES
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Primary defects in type 2Primary defects in type 2
diabetesdiabetes
1 Lebovitz HE. Diab Rev 1999; 7: 139-153. 2 Ward W, et al. Diab Care 198; 7: 91-5!2. 3 "#i-$arvi%e% H. E%do&ri%e Rev' 1992; 13: 15-31.
()e develo*+e%t o t*e 2diabete' i' t)e re'lt o a
&o+bi%atio% o β-&elld'%&tio% a%d i%'li%
re'i'ta%&e / L 0 C 1 2 E ( 1 3 4 C 4 (
"
ri+ar dee&t' i% t*e 2 diabete'1-3
6-&ell
d'%&tio%6-&ell
d'%&tio%
Lo'' o earl *)a'e
i%'li% relea'eLo'' o earl *)a'e
i%'li% relea'e
o't*ra%dial
l&o'e '*i#e'o't*ra%dial
l&o'e '*i#e'
4%'li% 'i%alli%
dee&t4%'li% 'i%alli%
dee&t
4%'li% re'i'ta%&e4%'li% re'i'ta%&e
4%&rea'ed ba'al
l&o'e level'4%&rea'ed ba'al
l&o'e level'
H*erl&ae+iaH*erl&ae+ia
da*ted ro+ Lebovitz, Ward a%d "#i-$rvi%e%
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Islets in Type II Diabetes:Islets in Type II Diabetes:
Loss of ß cellsLoss of ß cells
Amyloid depositsAmyloid deposits
HyalinizationHyalinization
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• DMDM defek berupa :defek berupa :
1. Desiensi insulin1. Desiensi insulin (hiperglikemia post prandial)(hiperglikemia post prandial)
2. Resistensi insulin2. Resistensi insulin (hiperglikemia puasa)(hiperglikemia puasa)
• Pemahaman patogenesisPemahaman patogenesis
memudahkan pendekatan terapi.memudahkan pendekatan terapi.
Pato6enesis D( tipe 2Pato6enesis D( tipe 2
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DM tipe 2DM tipe 2
Multifaktor Multifaktor
Sekresi insulin tergangguSekresi insulin terganggu
egagalan !el betaegagalan !el beta
Deposisi amiloidDeposisi amiloid
"bat"bat22 # hormon $ang abnormal# hormon $ang abnormalMalnutrisi in utero and earl$ %hildhoodMalnutrisi in utero and earl$ %hildhood
Mutasi glukokinaseMutasi glukokinase
Mutasi insulinMutasi insulinMutasi mitokondria D&' Mutasi mitokondria D&'
Resistensi insulinResistensi insulin
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.......... DM tipe 2DM tipe 2
Multifaktor Multifaktor Resistensi insulinResistensi insulin
Insulin signallingInsulin signalling
besitas dan dietbesitas dan diet
Penyakit !ndokrinPenyakit !ndokrin"e#amilan"e#amilan
bat$obatbat$obat
Malnutrisi in utero and earlyMalnutrisi in utero and earlyc#ild#oodc#ild#ood
Mutasi %&arang'Mutasi %&arang'
Reseptor insulinReseptor insulin
"omponen Post reseptor"omponen Post reseptor
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Dee! Se!resi 'nsulinDee! Se!resi 'nsulin
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P#ysiology of insulinP#ysiology of insulin
secretionsecretion
Islet
transcription
factors
SS
UU
RR
// ATP/ADPATP/ADP
PyruvatePyruvate
Glucose-6-PhosphateGlucose-6-Phosphate
GlucoseGlucose
GlucokinaseGlucokinase NucleusNucleusSecretorySecretory
granulesgranules
Ca Ca !!
CaCa++++
Voltage-dependentVoltage-dependent
CaCa2+2+ channelchannel
Depolari"ationDepolari"ation
ATP-sensitiveATP-sensitive
KK++ channelchannel
#itochon$ria #itochon$ria
GlucoseGlucose
G%&TG%&T
InsulinInsulin
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$ipasic "nslin )esponse to$ipasic "nslin )esponse to
&onstant ,lcose stimls&onstant ,lcose stimls
- e :
e l
o ; i n s
0 l i n
s e c r e t i o n
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(oss of !arly$ p#ase Insulin Secretion(oss of !arly$ p#ase Insulin Secretionin Type 2 Diabetesin Type 2 Diabetes
0a)d 01 et al3 Diabetes Care .45678964.:;< < >< =< 4< .2<
'i*e ?*inutes@
P l a
s * a i n s u l i n ? A
+ B * l @ .2<
.
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Resistensi Insulin
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"esistensi Insulin
De&ek uta*a pada se(agian (esa) Dia(etes Melitus tipe 2
De&inisi (
'e)ganggun%a )espon te)$adap e&ek &isiologis Insulin
te)*asuk pula *eta(olis*e glukosa le*ak p)oteindan &ungsi endotelial pe*(ulu$ da)a$
"esistensi insulin te)adi pada 9"esistensi insulin te)adi pada 9 OtotOtot
Hepa) Hepa) a)ingan adiposaa)ingan adiposa
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)#*+,S' D'-)T)S)#*+,S' D'-)T)S
+ormal
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Insulin
"esistance
'%pe 2
Dia(etes cell
D%s&unction
InsulinInsulin
"esistance"esistance
H % p e
) g l % c
a e * i a
H % p e
) g l % c
a e * i a
InsulinInsulin
Concent)ationConcent)ation
I n s u l i n # c t i o n
I n s u l i n # c t i o n
Eugl%cae*iaEugl%cae*ia
cell -ailu)ecell -ailu)e
No)*alNo)*al IG'IG' O(esit% O(esit% Diagnosis o& Diagnosis o&
t%pe 2 dia(etest%pe 2 dia(etesP)og)ession o& P)og)ession o&
t%pe 2 dia(etest%pe 2 dia(etes
D'$E DE
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Pada kondisi )esistensi insulin insulin tidakPada kondisi )esistensi insulin insulin tidak
*a*pu *engge)akkan u*la$ GL' 6 %ang cukup*a*pu *engge)akkan u*la$ GL' 6 %ang cukup
ke pe)*ukaan selke pe)*ukaan sel
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OvereatingInactivity
SmokingDiabetogenic drugs
regnancy!ndocrine diseasesDiabetogenic drugs
"alnutrition in utero
#nkno$n #nkno$n
%& cell defectsInsulin resistance
Genetic &acto)sGenetic &acto)s
Glucose to'icity
Hyperglycaemia
(orsening %&cell functions ) Amyloid deposition"alnutrition in utero
I*pai)ed glucose
tole)ance
*IDD"
Envi)on*ental &acto)sEnvi)on*ental &acto)s
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KOMPLIKASI KRONIK DMKOMPLIKASI KRONIK DM
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)omplications:)omplications:
• !hort term ompli%ations:!hort term ompli%ations: (metaboli%)(metaboli%)
*$pogl$%emia*$pogl$%emia
Diabeti% etoa%idosisDiabeti% etoa%idosis
&on etoti% h$perosmolar diabeti% %oma&on etoti% h$perosmolar diabeti% %oma +a%ti% a%idosis+a%ti% a%idosis
• +ong term ompli%ations:+ong term ompli%ations:(mi%roangiopath$)(mi%roangiopath$)
'ngiopath$, Retinopath$, &ephropath$, 'ngiopath$, Retinopath$, &ephropath$,&europhath$&europhath$
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)#ronic )omplications:)#ronic )omplications:
*ngiopat#y *ngiopat#y
• Ma%ro 'ngiopath$Ma%ro 'ngiopath$ 'theros%lerosis 'theros%lerosis
!troke - M!troke - M
• Mi%ro 'ngiopath$Mi%ro 'ngiopath$ *$aline*$aline
arteriolos%lerosisarteriolos%lerosis
Diabeti% pathies/0Diabeti% pathies/0
• mmunosuppressimmunosuppression.on. nam, nfe%tions,nam, nfe%tions,
• Retinopath$Retinopath$ Mi%roaneur$sms,Mi%roaneur$sms,
Dot blot hemorrhagesDot blot hemorrhages
*ard and soft eudates*ard and soft eudates
otton 3ool infar%tsotton 3ool infar%ts Proliferati4e retinopath$.Proliferati4e retinopath$.
• &ephropath$&ephropath$ &odular&odular
glomerulos%lerosisglomerulos%lerosis
• &europath$&europath$• Dermopath$Dermopath$
&e%robiosis, gangrene&e%robiosis, gangrene
5rannuloma5rannuloma
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("&)'>#%&#)
)ET"+'P#T?
+EP?)'P#T? )D"'('P#T?
+E)'P#T?
#T'+'("& )D"#&
,#%T)"&
)',E+"T#
D( &'(P"T"'+%
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D( &'(P"T"'+
(#&)'>#%&#)
&?D R'S/ 2 0 $
D)-TH ≥ 4
&E)E$)'>#%&#)
S TR*/) ( $
PE)"P?E)# >D$ 0 5 4 N*N6 TR-,7-T'C -7P,T-T'*N
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MAKROANGIOPATI(Komplikasi Pembuluh Darah Besar)
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FAKTOR-FAKTOR PER!KAAN ENDOTE
$ Pe"i"#ka$a" ka%ar #ula%arah
$ Kelai"a" lemak
$ Teka"a" %arah $i"##i
$ Merokok
Resis$e"si i"suli"
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BAGAIMANA TER&ADIN'A KOMPIKAIPADA PEMB!! DARA BEAR
Pembe"$uka" sel busa
$ Perlukaa" e"%o$el
Ter*a%i"+a plaka$erosklerosis
Plak +a"# mu%ah
pe,ah
Plak +a"# pe,ah
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BAGAIMANA TER&ADIN'A KOMPIKAI PADAPEMB!! DARA KEI
Pe"i"#ka$a" ka%ar #ula %arah
Pe"ebala"membra"a basalis
ila"#"+a sel-sel epi$el.peri,+$e
Kerusaka" sel-sel e"%o$el
Pe"u$upa" pembuluh %arahKerusaka" pembuluh %arah
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DiabeticDiabetic
Microangiopat#y Microangiopat#y
Normal Capillary
Diabetic
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Neuropat#y Neuropat#y
• !ensor$!ensor$ Motor (m$elin)Motor (m$elin)
• Peripheral &europath$Peripheral &europath$ 6ilateral, s$mmetri%6ilateral, s$mmetri%
Progressi4e, irre4ersibleProgressi4e, irre4ersible Paraesthesia, pain, mus%leParaesthesia, pain, mus%le
atroph$atroph$
• 7is%eral neuropath$ 7is%eral neuropath$
ranial ner4e diplopia, 6ellranial ner4e diplopia, 6ellpals$pals$
589 %onstipation, diarrhoea589 %onstipation, diarrhoea
7! orthostati% h$potension7! orthostati% h$potension
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KAIFIKAI NE!ROPATI DIABETIK
/0 NE!ROPATI FOKA Mo"o"europa$i - "europa$i kra"ial - ra%ikulopa$i.pleksopa$i E"$rapme"$ s+"%rome - ,arpal $u""el s+"%rome - ul"ar "er1e e"$rapme"$ - pero"eal "europa$h+
20 NE!ROPATI DIF! Neuropa$i mo$orik proksimal Poli"europa$i sime$rik %is$al
30 NE!ROPATI OTONOMIK is$em kar%io1askuler is$em pe",er"aa" is$em perke",i"#a" u%omo$or kaki $i%ak berkeri"#a$
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&;R"P'8 D'68
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)#ronic Polyneuropat#y )#ronic Polyneuropat#y
Claw foot – Dermopaty ! Neuropaty
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Diabetic *myotrop#y Diabetic *myotrop#y
Painful muscle wastin"
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Neuropat#ic ulcer Neuropat#ic ulcer
Callus formation
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Nep#ropat#y Nep#ropat#y
• Most %ommon %ause ofMost %ommon %ause ofmorbidit$ # mortalit$.morbidit$ # mortalit$.
• Deposition of
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DiabeticDiabetic
+lomerulosclerosis+lomerulosclerosis
Hyaline nodulesHyaline nodules
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DiabeticDiabetic
+lomerulosclerosis+lomerulosclerosis
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PERKEMBANGAN NORMO-MAKROAB!MIN!RIA
NORMA MIKROA- MAKROA- INDROM B!MIN!RIA B!MIN!RIA
NEFROTIK
/4 34 344
M#.hari
Pro$ei"uria±544 m#.hari
Mikroalbumi"uria 34-344 m#.h a$aurasio albumi"6krea$i"i" uri" 7 2 8 25 m#.mmol pa%a laki-laki 3 8 34 m#.mmol pa%a 9a"i$a
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DERA&AT NEFROPATI DIABETIK
Dera*a$ / 6 Pembesara" #i"*al %a" pe"i"#ka$a" :u"#si
Dera*a$ 2 6 esi pa%a #i"*al $a"pa $a"%a-$a"%a kli"is
Dera*a$ 3 6 Mikroalbumi"uria DMT2 saa$ %ia#"osis $er*a%i pa%a /;=?< Fu"#si #i"*al mulai $uru"
Dera*a$ ? 6 Ne:ropa$i %iabe$ik kli"is ;< DMT2 saa$ %ia#"osis Pro$ei"uria @4=3 #.h :u"#si semaki" $uru"
Dera*a$ 5 6 Ga#al #i"*al $ermi"al :u"#si semaki" $uru" Perlu $erapi pe"##a"$i (%ialisis)
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Retinopat#y Retinopat#y
• Mi%roaneur$sms,Mi%roaneur$sms,
• Dot blot hemorrhagesDot blot hemorrhages
• *ard and soft*ard and soft
eudateseudates
• otton 3ool infar%tsotton 3ool infar%ts
• &eo4as%ulari>ation &eo4as%ulari>ation
Proliferati4eProliferati4e
retinopath$.retinopath$.• ?ibrosis?ibrosis
• Retinal deta%hment.Retinal deta%hment.
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Normal RetinaNormal Retina
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Diabetic Retinopat#y Diabetic Retinopat#y
+otton $ool spots
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Diabetic Retinopat#y Diabetic Retinopat#y
Dot blot – #emorra"es $ Microaneurysms
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Diabetic Retinopat#y Diabetic Retinopat#y
Pre retinal #emorra"e
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Diabetic +angreneDiabetic +angrene
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"!ND*(I +,(*"!ND*(I +,(*
D*R*-D*R*-P!NTIN+N* "!ND*(I +,(*P!NTIN+N* "!ND*(I +,(*
D*R*- *N+ PTIM*(D*R*- *N+ PTIM*(
ID- 0P"B0HO Dia(etes Guidelines 2
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''e)apie)api
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@A
+lucose Tolerance+lucose Tolerance
)ategories)ategories
Diabetes
Mellitus
I0+
Normal
Diabetes
Mellitus
I+T
Normal
0asting P+ 2$# P+n +TT
324
mg9d(
335 mg9d(
255 mg9d(
375 mg9d(
f 5l8 f 5l i
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8argets for 5l$%emi%8argets for 5l$%emi%
ontrolontrol
.6< *gBdL
835 **olBL
.>; *gBdL
83; **olBL :
2$) postp)andial
?*gBdL@
..< *gBdL
=3. **olBL
.
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PERKENI6 Ti#h$ #l+,emi, $ar#e$
A/, (05A/, (05
FBG (m#.%l) ;4-/44FBG (m#.%l) ;4-/44
2-hpp (m#.%l) ;4-/??2-hpp (m#.%l) ;4-/??
f i l #P f i l # T
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@B
• !et treatment goals!et treatment goals
• 'ssess the Cualit$ of diabetes 'ssess the Cualit$ of diabetestreatment pro4idedtreatment pro4ided
• dentif$ areas 3here moredentif$ areas 3here moreattention or self9managementattention or self9managementtraining is neededtraining is needed
• Dene timel$ and referral patternsDene timel$ and referral patternspatients to appropriate spe%ialistpatients to appropriate spe%ialist
Professionals #o TreatProfessionals #o Treat
People it# DiabetesPeople it# Diabetes
Means To ;Means To ;
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@
Management PlanManagement Plan
• !tatement of short9 and long9term goals!tatement of short9 and long9term goals
• Medi%ation (insulin "*',Medi%ation (insulin "*',
antih$pertensi4e, lipid9lo3ering agents,antih$pertensi4e, lipid9lo3ering agents,
aspirin therap$, and othersaspirin therap$, and others• ndi4iduali>ed nutritionndi4iduali>ed nutrition
re%ommendationre%ommendation
• Re%ommendations for appropriateRe%ommendations for appropriatelifest$le %hangeslifest$le %hanges
• Patient and famil$ edu%ationPatient and famil$ edu%ation
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@E
(aboratory Tests(aboratory Tests
• ?asting plasma glu%ose,?asting plasma glu%ose, 2 hPP,2 hPP, *b' *b' 11
• ?asting lipid prole total9 (total?asting lipid prole total9 (total
%holesterol), *D+9, +D+9, 85%holesterol), *D+9, +D+9, 85
(trigl$%erides)(trigl$%erides)
• !erum %reatinine (if proteinuria present)!erum %reatinine (if proteinuria present)
• ;rinal$sis glu%ose, ketones, protein,;rinal$sis glu%ose, ketones, protein,
sedimentsediment
• 8est for mi%roalbuminuria8est for mi%roalbuminuria• 55
• ;rine %ulture, and others if an$ indi%ations;rine %ulture, and others if an$ indi%ations
*D*9!*SD )onsensus *lgorit#m*D*9!*SD )onsensus *lgorit#m
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*D*9!*SD )onsensus *lgorit#m *D*9!*SD )onsensus *lgorit#m
#tdia6nosis/i;estyle @(et;ormin
i;estyle @(et;ormin@ $asal inslin
i;estyle @(et;ormin
@ %l;onylrea
i;estyle @(et;ormin@ "ntensi:einslin
Tier 1/8ell6vali&ate& therapies
%TEP 1 %TEP 2 %TEP
&all to action i; ?b#1c is ≥7
Tier 2:+ess 3ell 4alidatedtherapies
i;estyle @(et;ormin@ Pio6litaAoneNo hypoglycaemiaOedema/CHF Bone loss
i;estyle @met;ormin@ ,P-1 a6onistNo hypoglycaemiaWeight loss
Nausea/vomitingNathan D7, et al. Diabetes Care 29:32 193623.
Hb- re;ects
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Hb-1c re;ects
"P< an& mealtime glucose spi!es
Relative contributions o "P< an& mealtime glucose spi!es to 2$6hourglycemic control
C. Diabetes Care 199:13(=0>.
3
2
1
P l a s m a g l u c o s
e ? m g @ & l A
am 12 pm pm 12 pm am
Time o &ay
7ealtimeglucosespi!es
"astinghyperglycemia
Normal
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$E)D#%#)B#+ T#),ET+# TE)#P" D(
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$E)D#%#)B#+ T#),ET+# TE)#P" D(D#P#T D",''+,B#+ (E+C#D"
1. Post Pan&rial hipergli!emia B mis DietB Rapi&-cting 'nsulinB acarboseB meglitini&B
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,#SICS O- 'YPE2 DM 'HE"#PY
.
DIE'
2
EE"CISE
HYPOGLYCEMIC
6
.
EDC#'ION
ISLE' '"#NSPL#N'
;
Sit & # ti & C t O#D
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)e& ve)sion 23.
Sites o& #ction o& Cu))ent O#D
GL#+OS!
,OD#+-IO*
M+SCLE
!,IH!,AL GL#+OS!
#-A.! / #-ILI0A-IO*
I*S#LI* S!+,!-IO*
#DIPOSE 'ISS+E
LI!E"
Mo7ifie7, Ann Intern Me7 %'''(%3%,)5%
IN'ES'INE
GL#+OS! A%SO,-IO*
&glucosidase in1ibitors
P#NC"E#S
-1iazolidinedionesia%ide'
%iguanides
()iazolidi%edio%e'
Glucose
Sulp1onylureas
"eglitinides
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#+T" D"#$ETE%#(# /
1. Sulonilurea
– !lorpropami&
– gliben!lami&
– glipisi&
– gli!asi& – glimepiri&
– gli!ui&on
2. 7etormin
3. glu!osi&ase inhibitor
$. 'nsulin
$#)
1. meglitini&
2.
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%l;onilrea /
e!erEa &engan cara memacu sel eta Pan!reas untu!menghasil!an insulin
Relati cepat menurun!an !a&ar gula &arah
+ebih &ituEu!an untu! basal hipergli!emia
/ebutuhan insulin !urang &ari 2 , per hari
elum pernah mengalami !etoasi&osis &an berat ba&an normal
atau lebih Ti&a! &ianEur!an untu! terapi D7 &engan !ompli!asi yg berat
(ET
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(ET4
2. 7engurangi pro&u!si gula hati.3. 7ening!at!an gli!olisis yang anaerobe
$. 7enurun!an glu!oneogenesis.
5. 7enghambat absorpsi glu!ose &i usus.
$i6anide tida menrnan 6la dara pada oran6normal
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"+D"B#%" PE+,,+##+ (ET
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B'+T)#"+D"B#%" (ET
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#carbose
-carbose menghambat pencernaan &ari !arbohi&ratrantaipanEang &i bagian atas EeEunum sehingga !arbohi&rattersebut&icerna sepanEang usus halus. Pengaruh utamanya
a&alahmenurun!an glu!osa &arah sesu&ah ma!an.
-carbose &apat menurun!an glu!osa &arah postpran&ial
36 mg4 B glu!osa &arah puasa 1562 mg4 &an Hb- 1cB561 4.
)epa6linid
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)epa6linid
Repaglini& a&alah &erivat &ari carbamoyl methyl benoic acid.
*bat in ee!nya serupa &engan nateglini&B yaitu memacuse!resi insulin secara cepat &an a!sinya Euga hilang &engan cepat.
penggunaannya tepat sebelum ma!an ?one meal one dose, nomeal no dose!
)!sresinya terutama le8at saluran empe&u &an hanya sebagian
!ecil le8at urin.
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+ate6linide
Nateglini&e a&alah &erivat asam amino D6phenylalanine
Nateglini&e menyebab!an pelepasan insulin yang cepat &arisel β pan!reas &an a!sinya Euga hilang &engan cepat
Cara !erEanya menyerupai sulonilureaB yaitu melalui -TP&epen&ent !alium channel.
Penggunaannya a&alah tepat sebelum ma!anB &an &apatmenurun!an terutama glu!osa &arah postpran&ial.
Pacuan terha&ap se!resi insulin hanya terEa&i saat a&anyahipergli!emiB sehingga resi!o hipogli!emi sangat !ecil.
TiaAolidinedione
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TiaAolidinedione
memperbai!i resistensi insulin.
teri!at pa&a "ero#isome "roli$erator%&ctivated 'eceptor(""&')!
&eerensiasi prea&iposit → sel lema! mata!
a!tivasi trans!ripsi gena → e!spresi protein spesiF! → regulasi/.H. K lipi& 6 a!si insulin ↑
a&a 2 ( trogglitaone K pioglitaone.
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'egunaan 'linis Thia"oli$ine$ione
Troglitaone menurun!an !ebutuhan isulin pa&a D7 tipe62yang
men&apat insulin ?use &!!. 19>>A.
Perubahan prea&iposit → sel lema! matang &isub!utan 6troglitaone bl ratio lema! visceral@sub!utan ↓ ?7ori
&!!B 1999A
Pioglitaone 6 sensivitas insulin &i hepar K Earingan ↑
?7iyaa!i&!!B 21A.
Plasma glucose multihormonal
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Plasma glucose multihormonalregulation o glucose
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'nlacin
8 7a&e in 'n&onesia
8 7emperbai!i resistensi insulin
8 7engin&u!si e!spresi gen PP-R y pa&ating!at mRN-
8 7ening!at!an epresi
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Summary o glucose lo8ering interventions
"nter:ention dec#1&
#d:anta6es Disad:anta6es
Tier 1( 8ell6vali&ate& core
Step 1( initial therapy
+iestyle to&ecrease8eight an&
increaseactivity
1.62. roa& beneFts'nsu%cient or most
8ithin Frst year
7etormin 1.62. Leight neutral
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TDs .561.$
'mprove& lipi&proFle?pioglitaoneAB
potential &ecreasein 7'?pioglitaoneA
"lui& retentionB H"B8eight gainB boneracturesB epensiveBpotential increase in 7'?rosiglitaoneA
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T)R-P'
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$ +-N
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"*/,S
8
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R)/*7)ND-S'
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8 /olesterol ( Q 263 mg
8 Protein ( 1 62 4
8 -l!ohol ( Q 3 g ?+AB Q 15 g ?LA?-D-A
/-R*H'DR-T
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/-R*H'DR-T8 7empengaruhi respon gli!emi!
6 umlah /H
6 'n&e gli!emi!
6
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"-/T*R "-/T*R J< 7)N)NT,/-N/),T,H-N /-+*R'
1. enis /elamin
2. ,mur
3. -!tivitas Fsi!
$. /ehamilan @ la!atasi
5. /ompli!asi
. Tinggi &an berat ba&an
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/),T,H-N )N)RB5622B5
/,R,S Q ' 0 14 Q 1>B5
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ondisi Penambaan ener6i
b lebih 1 4
b gemu! 2 4
b !uran 3 4
Stres metaboli! 1634
Hamil trimester i &an ii 3 !alori
Hamil trimester ''' 5 !alori
)N'S -/T'#'T-S "'S'/
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)N'S -/T'#'T-S "'S'/
ati:itas conto Penambaanener6i
R'N
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Tips ;or ealty cooin6
8 &oo o; boil meat insted o;;ryin6
8 Tae te sin o; cicen be;orecooin6
8 se less salt and s6ar enpreparin6 ;ood
8 #:oid ;at
Tips ;or ealt cooin6
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Tips ;or ealty cooin6
8 se ;res or ;roAen ;rit and:e6etables en eatin6 or in
beteen meals8 se lo ;at cesse instead o; re6lar
cesse
8 se lo ;at mil 8 Drin ;rit jice instead o; poder jice
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hysical Activity
To control diabetes the
recommendation is to increase
physical activity, preferably
every day for 20-60 minutes.
< 20 min : no effect
60 min : prone to in!uryand disease attac"
'NT)NS'TJ
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#$% a'imum $eart %ate( 220 )
A*e
T$% &Tar*et $eart %ate( 60 ) +0 ,
#$% &-0,(
'NT)NS'TJ
/9/RCIS/
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/9/RCIS/
8 C , continuous
8 R , rytmical
8 I , inter:al
8 P , pro"ressi:e
8 / , en7urance
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hysical Activity
.enefits:
/oers *lucose levels in blood
1mproves blood circulation in the
entire body
ontributes to ei*ht loss
1mproves physical and mental
ellbein*
$elps the body to utili3e insulin
more efficiently
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T E ) " ( # B # % " ?