<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>Molecular Research and Diagnostic Unit Research Arm -</submitter><organism>Homo sapiens</organism><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-17412</full_dataset_link><description>Various studies have established the role of genetics in the development of type 2 diabetes mellitus (T2DM) across population groups with a reported heritability of 30–70%. These studies highlight the effect of interethnic variability in genetic susceptibility and risk for complications of T2DM. The underrepresentation of Filipinos in current global databases have prompted the goal to identify variants associated with the risk of T2DM among the population. Since the validation of variants associated with one population seems suboptimal if applied to another population, designing a specific set of genetic variants for a particular population poses a challenge.  Microarray techniques were used on extracted DNA from whole blood samples using customized microarray beadchips with selected variants from various genome repositories. Customization included candidates from both coding and non-coding regions (e.g. intergenic and intronic SNPs) with statistical evidence of associated to T2DM, its complications, treatment, diagnosis and other related conditions. Incorporation of clinical data from participants can then narrow the significant variants to the population and identify which can be valuable for developing genetic risk prediction models relevant to preventing and diagnosing the disease among Filipinos.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Sample Collection - Participants were screened using an inclusion and exclusion criteria. Ultimately, 201 unrelated participants were enrolled. Blood was collected from all enrolled participants for two purposes: 1) testing for blood lipid profile, serum creatinine, AST, ALT, alkaline phosphatase,  C-peptide levels, FBS levels, HbA1C, HDL and LDL levels; 2) DNA extraction for microarray processing.</sample_protocol><sample_protocol>Nucleic Acid Extraction - DNA was extracted using the QiaAmp DNA Blood Mini Kit following the spin protocol specified in the manufacturer’s instruction manual.</sample_protocol><sample_protocol>Labeling - The nucleic acid labelling step in the Illumina GoldenGate genotyping assay is integrated into the polymerase chain reaction (PCR) after the allele-specific extension and ligation step. First, the genomic DNA is denatured and then hybridized with two allele-specific oligonucleotides (ASOs) and a locus-specific oligonucleotide (LSO), flanking the target single nucleotide polymorphism (SNP). PCR amplification is then performed on the ligated products using universal primers which also includes allele-specific primers labelled with either Cy3 or Cy5 fluorescent dyes and an additional biotinylated primer complementary to the common sequence.</sample_protocol><sample_protocol>Scaning - Customized genotyping of candidate SNPs was performed using DNA microarray technology following the GoldenGate Genotyping and Illumina Infinium iSelect assay protocols specified in their respective manufacturer’s manual.</sample_protocol><sample_protocol>Hybridization - The nucleotide hybridization step in the Illumina GoldenGate assay begins following genomic DNA denaturation and immobilization onto paramagnetic particles. Activated single-stranded genomic DNA is incubated with a pool of assay-specific oligonucleotides in hybridization buffer, including two allele-specific oligonucleotides (ASOs) and one locus-specific oligonucleotide (LSO) designed for each target single nucleotide polymorphism (SNP). Because hybridization occurs prior to amplification, the assay minimizes amplification bias and preserves allelic discrimination accuracy.</sample_protocol><figure_sub>MIAME Score</figure_sub><figure_sub>Raw Data</figure_sub><figure_sub>Organization</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><figure_sub>Array Designs</figure_sub><data_protocol>Data Transformation - Screening for SNPs among genes clinically associated with type 2 diabetes mellitus and its complications was done by imaging beadchips on the HiScan system and utilizing the GenomeStudio v2.0 software.</data_protocol><omics_type>Metabolomics</omics_type><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><pubmed_abstract>Type 2 diabetes mellitus leads to debilitating complications that affect the quality of life of many Filipinos. Genetic variability contributes to 30% to 70% of T2DM risk. Determining genomic variants related to type 2 diabetes mellitus susceptibility can lead to early detection to prevent complications. However, interethnic variability in risk and genetic susceptibility exists. This study aimed to identify variants associated with type 2 diabetes mellitus among Filipinos using a case-control design frequency matched for age and sex. A comparison was made between 66 unrelated Filipino adults with type 2 diabetes mellitus and 121 without. Genotyping was done using a candidate gene approach on genetic variants of type 2 diabetes mellitus and its complications involving allelic association and genotypic association studies with correction for multiple testing. Nine (9) significant variants, mostly involved in glucose and energy metabolism, associated with type 2 diabetes mellitus in Filipinos were found. Notably, a CDKAL1 variant (rs7766070) confers the highest level of risk while rs7119 (HMG20A) and rs708272 (CETP) have high risk allele frequencies in this population at 0.77 and 0.66, respectively, making them potentially good markers for type 2 diabetes mellitus screening. The data generated can be valuable in developing genetic risk prediction models for type 2 diabetes mellitus to diagnose and prevent the condition among Filipinos.</pubmed_abstract><study_type>genotyping by array</study_type><species>Homo sapiens</species><pubmed_title>Genomic variants associated with Type 2 diabetes mellitus among Filipinos</pubmed_title><pubmed_authors>Molecular Research and Diagnostic Unit Research Arm -</pubmed_authors><pubmed_authors>Eva Maria C. Cutiongco-de la Paz , Jose B. Nevado Jr., Elizabeth T. Paz-Pacheco, Gabriel V. Jasul Jr., Aimee Yvonne Criselle L. Aman, Mark David G. Francisco</pubmed_authors></additional><is_claimable>false</is_claimable><name>Correlation of Candidate Genetic Variations for Susceptibility and Risk Assessment of Type 2 Diabetes Mellitus and its Related Medical Conditions among Filipinos (DM2)</name><description>Various studies have established the role of genetics in the development of type 2 diabetes mellitus (T2DM) across population groups with a reported heritability of 30–70%. These studies highlight the effect of interethnic variability in genetic susceptibility and risk for complications of T2DM. The underrepresentation of Filipinos in current global databases have prompted the goal to identify variants associated with the risk of T2DM among the population. Since the validation of variants associated with one population seems suboptimal if applied to another population, designing a specific set of genetic variants for a particular population poses a challenge.  Microarray techniques were used on extracted DNA from whole blood samples using customized microarray beadchips with selected variants from various genome repositories. Customization included candidates from both coding and non-coding regions (e.g. intergenic and intronic SNPs) with statistical evidence of associated to T2DM, its complications, treatment, diagnosis and other related conditions. Incorporation of clinical data from participants can then narrow the significant variants to the population and identify which can be valuable for developing genetic risk prediction models relevant to preventing and diagnosing the disease among Filipinos.</description><dates><release>2026-09-01T00:00:00Z</release><modification>2026-09-01T01:00:51.862Z</modification><creation>2026-07-21T01:58:37.661Z</creation></dates><accession>E-MTAB-17412</accession><cross_references><pubmed>39561140</pubmed><EFO>EFO_0002944</EFO><EFO>EFO_0003814</EFO><EFO>EFO_0003813</EFO><EFO>EFO_0002767</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003816</EFO><EFO>EFO_0003815</EFO><doi>10.1371/journal.pone.0312291</doi></cross_references></HashMap>