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Seminar Hasil Penelitian EFEK BUAH KAWISTA (Limonia Acidissima L.) TERHADAP KADAR SOD ( Superoxyde dismutase) dan MDA (Malondyaldehyde) JANTUNG TIKUS MODEL DIABETES MELLITUS TIPE II

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EFEK BUAH KAWISTA (Limonia Acidissima L.) TERHADAP KADAR SOD ( Superoxyde dismutase) dan MDA (Malondyaldehyde) JANTUNG TIKUS MODEL DIABETES MELLITUS TIPE II

Pembimbing 1: Yoyon Arif Martino. Ssi., M.KesPembimbing 2: H. Yudi Purnomo. S.si., Apt., M. KesPenguji 1 : Prof.dr. H. M. Aris Widodo, MS., SpFK., Ph.DPenguji 2 : dr. Rima Zakiyah., Sp.Rad

FAKULTAS KEDOKTERANUNIVERSITAS ISLAM MALANG2013FENY DAMAYANTI20912100311Latar BelakangDiabetes Melitus tipe 2 (DMT-2) masih menjadi permasalahan kesehatan dunia.Menurut WHO (2004), insiden DMT-2 meningkat 171 juta orang pada tahun 2000 menjadi 366 juta orang pada tahun 2030Indonesia diperkirakan akan menempati peringkat 5 dunia dengan jumlah pasien sebanyak 12,4 juta orang pada tahun 2025Gambar1: Type II (non-insulin-dependent diabetes mellitus [NIDDM], formerly called maturity onset diabetes; B) is by far the most common form of diabetes. Here, too, genetic disposition is important. However, there is a relative insulin deficiency: the patients are not necessarily dependent on an exogenous supply of insulin. Insulin release can be normal or even increased, but the target organs have a diminished sensitivity to insulin.Most of the patients with type II diabetes are overweight. The obesity is the result of a genetic disposition, too large an intake offood, and too little physical activity. The imbalance between energy supply and expenditure increases the concentration of fatty acids in the blood. This in turn reduces glucose utilization in muscle and fatty tissues. The result is a resistance to insulin, forcing an increase of insulin release. The resulting down-regulation of the receptors further raises insulin resistance.Obesity is an important trigger, but not the sole cause of type II diabetes. More important is the already existing genetic disposition to reduced insulin sensitivity. Frequently, insulin release has always been abnormal. Several genes have already been defined that promote the development to obesity and type II diabetes.Among other factors, the genetic defect of a mitochondrial decoupling protein limits substrate consumption. If there is a strong genetic disposition, type II diabetes can already occur at a young age (maturity-onset diabetes of the young [MODY]).Reduced insulin sensitivity predominantly affects the insulin effect on glucose metabolism, while the effects on fat and protein metabolism are still well maintained. Thus, type II diabetics tend especially toward massive hyperglycemia without corresponding impairment of fat metabolism (ketoacidosis, p. 288).Gambar 2: disfungsi endotel CECs>> (ec. Cedera mekanik, fx aterosklerosis, perubahan molekul adhesi sel endotel/subendotel, defek ikatan pd protein matriks anchoring, dan apoptosis seluler dg penurunan daya tahan protein sitosskeletal)Normalnya endotel sirkulasi: (:0,05/0,01), maka variansi setiap sampel sama (homogen)Jika signifikansi yang diperoleh 2 kelompok uji, parametrikUji BNT: untuk mengetahui besar perbedaan efek antar kelompok uji (dg memakai BNT 5%ad rumus khusus) & untuk mengetahui perlakuan terbaik dalam penelitian (dlm menghasilkan efek terbaik)Hasil p2 kelompok uji), dlm bentuk tabel & diagram)Uji Beda Nyata Terkecil (untuk menge-tahui perbandingaan antar perlakuan)Hasil dikatakan bermakna bila p (:0,05/0,01), maka variansi setiap sampel sama (homogen)Jika signifikansi yang diperoleh 2 kelompok uji, parametrikUji BNT: untuk mengetahui besar perbedaan efek antar kelompok uji (dg memakai BNT 5%ad rumus khusus) & untuk mengetahui perlakuan terbaik dalam penelitian (dlm menghasilkan efek terbaik)Hasil p