Mekanisme Molekuler Dari Resistensi Insulin Pada Diabetes Melitus Tipe Dua

Eva Decroli✉
DOI: https://doi.org/10.25077/mka.v45.i4.p610-618.2022

Abstract

Diabetes melitus merupakan kelainan endokrin yang paling sering ditemukan. Salah satu patofisiologi utamanya adalah resistensi jaringan target terhadap insulin. Pada tahap seluler, resistensi insulin adalah adanya kemampuan yang tidak adekuat dari insulin signaling pada reseptor insulin terhadap molekul pada proses aksi insulin. Sekuensi patofisiologi yang tepat yang menyebabkan resistensi insulin masih belum banyak diketahui. Tujuan: Untuk mengetahui mekanisme molekuler dari resistensi insulin pada diabetes melitus tipe dua. Metode: Artikel ini ditulis berdasarkan studi kepustakaan yang berhubungan dengan mekanisme molekuler dari resistensi insulin pada diabetes melitus tipe dua. Hasil:  Banyak molekul yang terlibat dalam pengolahan intraseluler dari insulin signaling yang diperankan oleh insulin, IRS-2, PKB, protein Foxo dan P85 subunit PI-3 kinase. Disfungsi-disfungsi dari molekul ini menyebabkan resistensi insulin in vivo. Identifikasi defek signaling dan pemahaman hubungan kompleks dari faktor yang berbeda dalam memodulasi sensitivitas insulin yang merupakan prasyarat penting untuk pengembangan senyawa anti-diabetes baru dan lebih spesifik. Simpulan: Dengan menjelaskan mekanisme molekuler pada insulin signaling yang bertanggung jawab untuk resistensi insulin, dapat dipahami sebagian besar dari resistensi insulin secara molekuler.

Keywords

diabetes melitus; resistensi insulin; insulin signaling; substrat insulin; reseptor insulin

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