1Department of Chemistry, Faculty of Sciences and Informatics, Jenderal Achmad Yani University, Jl. Ters. Jenderal Sudirman, Cimahi, 40351, Indonesia
2Department of Environmental Engineering, Faculty of Science and Technology, Sunan Gunung Jati Islamic State University, Jl. A. H. Nasution No. 105, Bandung 40614, Indonesia
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@article{JKSA76934, author = {Rahmaniar Mulyani and Rina Budi Satiyarti and Siti Nur Rizki}, title = {Detection of ATPase 6 Gene Mutations in Mitochondrial DNA of Type 2 Diabetes Mellitus Patients: A PCR-Sequencing Study}, journal = {Jurnal Kimia Sains dan Aplikasi}, volume = {29}, number = {8}, year = {2026}, keywords = {G9053A; Mitochondria; Mitochondrial Diabetes; PCR; Type 2 Diabetes Mellitus}, abstract = {Mitochondrial diabetes is a form of diabetes caused by mutations in mitochondrial DNA (mtDNA). These mutations impair oxidative phosphorylation (OXPHOS) and ATP synthesis, which reduces glucose-stimulated insulin secretion. Because its clinical features overlap with those of type 2 diabetes mellitus (T2DM), mitochondrial diabetes is often diagnosed as T2DM. The G9053A mutation in the ATPase 6 gene is a nonsynonymous mtDNA variant that has been predicted to affect ATP synthase function. In this study, a fragment of the ATPase 6 gene was amplified by the Polymerase Chain Reaction (PCR) and analyzed by Sanger sequencing. In four blood samples from T2DM patients, the G9053A point mutation (guanine to adenine) was detected in samples B21 and B22. Sample B36 carried a cytosine to thymine substitution at position 8970 (C8970T), a synonymous change at codon 148 (serine). No mutation was detected in sample B43. G9053A was the predominant variant in this small group, and both carriers had a maternal history of T2DM. A larger study with non-diabetic controls is needed to determine whether G9053A is associated with mitochondrial diabetes.}, issn = {2597-9914}, pages = {575--580} doi = {10.14710/jksa.29.8.575-580}, url = {https://ejournal.undip.ac.id/index.php/ksa/article/view/76934} }
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