Kelompok 8

• Terapi DM terbaru
• Glukagon sebagai agent terapetik
• Pembahasan Kasus
Nama Anggota Kelompok
1. Arif Setiawansyah
2. Elliya Rosyada
3. Febriza Risti W
4. Hapsari Yurismawati
5. Melisa Widyani
6. Yusnandhi Iin Pratiwi
 Newest Therapy for DM
Jurnal :
1. Glucagon-like peptide-1 mimetics, optimal for Asian type 2 diabetes
patients with and without overweight/obesity: meta-analysis of
randomized controlled trials
Publish : 22 Nov 2017
2. Update on the treatment of type 2 diabetes mellitus
Publish : 15 September 2016
Jurnal 1
Penggunaan obat Dm selama ini memiliki efek samping, dan mahal. Oleh karena itu,
penyelidikan rejimen antidiabetes baru, dengan efek samping yang kurang dan lebih murah,
merupakan tantangan utama bagi para peneliti.

Pada jurnal ini terdapat beberapa rencana treatmen dalam pengobatan DM dan salah satunya
adalah Basal insulin analogs with glucagon-like peptide-1 mimetics. Kombinasi dari GLP1
mimetics dengan insulin basal mengurangi risiko hipoglikemia dan kenaikan berat badan yang
diinduksi untuk regimen insulin intensif pada pasien DM Tipe 2. Bukti awal menunjukkan bahwa
penambahan insulin basal ke GLP1 mimetik dengan atau tanpa terapi oral, memberikan
perbaikan pada basal dan postprandial. kontrol glukosa, dengan berat badan yang lebih sedikit,
mengurangi risiko hipoglikemia dan meningkatkan kepuasan.
Jurnal 2
 Pada jurnal ini mengatakan, penggunaan Glucagon-like Peptide-1
Mimetics (GLP1M) pada penyakkit diabetes terutama pada pasien
dengan berat badan berlebih (obesitas). Tujuan dari penelitian ini
adalah membandingkan apakah GLP-1RAs menunjukkan penurunan
glukosa yang berbeda antara pasien diabetes tipe 2 Asia dengan dan
tanpa kelebihan berat badan (obesitas).
 GLP-1 berkontribusi terhadap penurunan berat badan dengan mengurangi asupan makanan
dan meningkatkan pengeluaran energi. Dilaporkan bahwa pada subjek dengan berat badan tidak
berlebih, infus supraphysiological dari GLP-1 meningkatkan pengeluaran energi tetapi terkendali oleh
tingkat insulin fisiologis. Pada subjek obesitas, dosis supraphysiological dari GLP-1
mengurangi nafsu makan dan asupan makanan, yang kemudian menginduksi penurunan berat
badan, mengurangi resistensi GLP-1, dan meningkatkan sensitivitas insulin. Karena peningkatan BMI
merusak sekresi GLP-1 dan memperburuk resistensi insulin, infus supraphysiological dari
GLP-1 dapat bertindak sebagai sinyal umpan balik pada pasien obesitas untuk meningkatkan
sensitivitas insulin dan mengurangi obesitas kronis.
Mekanisme penggunaan GLP-1 ini masih belum banyak diketahui dan dipahami, tetapi
beberapa studi sebelumnya pada intervensi liraglutide melaporkan bahwa pasien dengan BMI
yang lebih tinggi mencapai penurunan berat badan yang lebih besar, sedangkan pada pasien
dengan BMI yang tidak tinggi menunjukkan bahwa GLP-1RAs menjamin pemeliharaan berat
badan yang stabil.
Glukagon sebagai agent terapetik

Skema peran exenatide dan

CEACAM1 dalam insulin serapan
de novolipogenesis. Exenatide
mengikat reseptor GLP-1
(GLP-1R) mengaktifkan
pensinyalan GLP-1R, memulai
transkripsi dimediasi PPARc dari
CEACAM1 mRNA. Aktivasi
CEACAM1
secara bersamaan menghambat
de novolipogenesis dengan
mengikat FASN dan
meningkatkan ambilan insulin
dan izin, mencegah
perkembangan ke NAFLD
Exenatide telah terbukti menekan nafsu makan dan meningkatkan sekresi insulin
yang distimulasi glukosa. Ini efek dimediasi melalui aktivasi GLP-1 sinyal reseptor di
sistem saraf pusat dan pancreaticbcells. Temuan penting dari penelitian ini adalah
efek positif yang exenatide pada izin insulin di hepatosit, yang belum dibuktikan
sebelumnya. Selain itu, exenatide dapat menekan hati de novolipogenesis melalui
pengikatan CEACAM1 ke FASN, yang menghambat aktivitas FASN. Sebagai
tambahannya peningkatan sekresi dan sensitivitas insulin, peningkatan pembersihan
insulin dan penghambatan de novo lipogenesis oleh exenatide secara kumulatif
berpartisipasi dalam mencegah perkembangan NAFLD. Meskipun CEACAM1
memainkan peran penting dalam pembersihan insulin, kadar trigliserida hati yang
berkurang oleh CEACAM1 dimediasi melalui penghambatan FASN aktivitas.
Ini mungkin independen dari promosi CEACAM1-dimediasi izin insulin.
Pembahasan Kasus
Soal Kasus
1. Apa tindakan seluler dan molekuler insulin?

2. Apa etiologi diabetes mellitus, dan bagaimana diabetes mellitus tipe l

berbeda
dengan diabetes mellitus Tipe II?
3. Apa makna kadar glukosa darah dan HbA1c dari diabetes Ny. S?
Adakah situasi di mana satu parameter dinaikkan dan yang lain bisa normal?

4. Selain meringankan poliuria dan polidipsia, mengapa penting untuk

mengontrol
diabetes Ny. S (yaitu, apa komplikasi akut dan kronis yang bisa timbul)?

5. Apa mekanisme kerja dari berbagai agen farmakologis yang digunakan

untuk
mengobati diabetes: inhibitor a-glukosidase, sulfonilurea, meglitinides,
tiazolidinedion, biguanides, dan GLP-1 mimetics? Apakah metformin
merupakan terapi yang
 1. Apa tindakan seluler dan molekuler insulin?
Molekuler
Setelah berinteraksi dengan reseptornya,
rekrutmen ini dan memfosforilasi terutama
dua protein yang beradaptasi: IRS,mediator
utama tindakan metabolisme insulin, dan
SHC, yang memediasi proliferasi sel dan
tindakan pertumbuhan. Jalur utama yang
dimediasi IRS termasuk jalur PI3K / Akt,
yang memainkan peran sentral dalam
aktivasi dan pengaturan beberapa proses
metabolisme,
termasuk glukosa stimulasi transportasi,
glikogen dan sintesis protein dan
adipogenesis. Dalam kasus SHC, ini terkait
dengan jalur MAP kinase aktivasi untuk
mengatur fungsi-fungsi proliferatif dan
pertumbuhannya.
 Mekanisme asam lemak yang berakibat resistensi insulin
Seluler
pada otot rangka. Peningkatan konsentrasi asam lemak
mengakibatkan tingginya asetil KoA yang
intramitochondrial/CoA dan NADH/NAD+ rasio, dengan
inaktivasi dari piruvat dehidrogenase menyebabkan
meningkatnya konsentrasi
sitrat dan menyebabkan penghambatan fosfofruktokinase.
Setelah konsentrasi intraseluler glukosa-6-fosfat meningkat
akan menghambat aktivitas heksokinase II, yang akan
mengakibatkan peningkatan intraseluler konsentrasi
glukosa dan penurunan otot pengambilan glukosa.
Peningkatan perpindahan dari asam lemak ke otot atau
penurunan metabolisme intraseluler asam lemak
menyebabkan peningkatan intraseluler metabolit asam
lemak seperti diasilgliserol, lemak asil KoA, dan
ceramides. Metabolit ini mengaktifkan serin/treonin
kinase cascade (mungkin diprakarsai oleh protein kinase
Cq) menyebabkan fosforilasi serin/treonin situs pada
substrat reseptor insulin (IRS-1 dan IRS-2), yang pada
gilirannya mengurangi kemampuan substrat insulin
reseptor untuk mengaktifkan PI 3-kinase. Sebagai akibatn
ya, glukosa transportasi kegiatan dan lainnya peristiwa
hilir reseptor insulin signaling berkurang
2. Apa etiologi diabetes mellitus, dan bagaimana diabetes mellitus tip
e l berbeda dengan diabetes mellitus Tipe II?
Perbedaan DM tipe 1 dan DM tipe 2
 3. Apa makna kadar glukosa darah dan HbA1c dari diabetes
Ny. S? Adakah situasi di mana satu parameter dinaikkan dan
yang lain bisa normal ?

• Pada kasus tersebut, kadar glukosa meningkat yakni 240 mg / dL

( normal : <140 mg/dl ), dan HbA1c juga meningkat yakni 9,2 %
( normal : 3,5-5 % ), HbA1c menunjukkan komponen minor dari hemoglobin
yang berikatan dengan glukosa komponen minor dari hemoglobin yang
berikatan dengan glukosa, HbA1c menunjukkan kadar glukosa rata-rata
selama 3 bulan.

• Pada kasus tersebut, belum menemukan adanya parameter yang

menunjukkan satu parameter bisa dinaikann sedangan yang lain normal,
karena terpadat peningkatan kadar kolesterol, glukosa, dan HbA1c yang
meningkat pada kasus.
 4. Selain untuk meringankan efek poliuria dan polidipsia, mengapa penting
untuk mengontrol diabetes Ny. S. Komplikasi akut dan kronis seperti apa
yang dapat timbul?

Untuk mempertahankan kadar gula darah, kadar HbA1c dan profil lemak dalam
rentang normal, serta untuk mencegah atau meminimalkan kemungkinan terjadinya
komplikasi.

Komplikasi Akut:
Ketoasidosis Diabetik (KAD)
Status Hiperglikemik Hiperosmolar (SHH)
Hipoglikemia
Komplikasi Kronik:
Mikroangiopati
Pembuluh darah jantung: PJK
Pembuluh darah tepi: Ulkus iskemik pada kaki
Pembuluh darah otak: Stroke iskemik atau stroke hemoragik
Makroangiopati
Retinopati
Neuropati
Nefropati
5. Mekanisme obat-obat peningkat sekresi insulin
• Sulphonylureas berikatan dengan sulfonilurea reseptor
(SUR) -1  kanal kalium kir 6.2 tertutup mengurangi e
fflux Kalium terjadi depolarisasi sel dan membuka sal
uran masuk kalsium yang tergantung voltase. Peningkat
an kalsium intraseluler menghasilkan pelepasan insulin.
Mekanisme α-Glucosidase Inhibitors
• α-Glucosidase Inhibitors secara kompetitif me
nghambat aktivitas enzym α-Glucosidaseme
ncegah pemecahan disakarida normal dan su
bstrat aboligosakarida menjadi monosakarida
sebelum penyerapan mengalangi pencernaa
n karbohidrat hingga lebih jauh di sepanjang s
aluran usus penundaan penyerapan glukosa
Mekanisme Bi
guanid
1. Biguanid menghambat komplex 1 mencegah produksi AT
Prasio ADP:ATP dan AMP:ATP meningkat mengaktifka
n AMPK
2. Atau AMPK dapat diaktifkan melalui mekanisme lisosom (m
embutuhkan axin (aktivator LAMTOR 1).
3. Rasio AMP:ATP meningkatfruktosa - 1,6-bifosfatase terh
ambatterjadi penghambatan akut glukoneogenesis
4. sementara juga menghambat adenilat siklase dan menurun
kan produksi cAMP
Mekanisme Thiozolidindiol
• Thiozolidindiol menstimulasi PPARγme
mpromosikan terjadinya diferensiasi pread
iposit yang disertai terjadinya lipogenesis
efek insulin meningkat
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