الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Over 90% of worldwide diabetes cases are type 2 diabetes mellitus (T2DM). This kind of diabetes is multifactorial and polygenic due to a complex interaction of inherited and lifestyle factors. T2DM affects carbs, proteins, and lipids metabolism. Hyperglycemia results from inadequate insulin release by pancreatic β-cells, insulin resistance (IR), or both.
Early-onset type 2 diabetes mellitus (EOD), diagnosed in those under 40, has increased globally along with T2DM. EOD is associated with worse health outcomes. EOD patients are also more likely to have macrovascular and microvascular issues, cardiovascular disease, microalbuminuria, and pancreatic β-cell loss. To prevent and control EOD and monitor pancreatic β-cell function, early and active risk factors must be identified.
The intronic SNP rs10830963 of the MTNR1B gene may be linked to T2DM in young adult Egyptians aged 30–39. The individuals were subjected to intravenous whole blood samples to measure T2DM-related physiological markers. Each sample underwent extensive molecular biology investigations. Genomic DNA was extracted from EDTA-tubed whole blood. PCR amplified the MTNR1B partial intronic sequence. Agarose gel electrophoresis separated the incomplete gene sequence for DNA sequencing. The T-coffee online program detected nucleotide changes in samples compared to the NCBI reference sequence. The Vienna RNA secondary structure online tool predicted the samples’ RNA secondary structure in respect to minimum free energy (MFE).
Our cohort of young adult diabetic Egyptians under 40 may have the MTNR1B rs10830963 risk G allele, which may contribute to T2DM. The NCBI reference sequence and sequences solely carrying the risk G allele had little difference in RNA secondary structure. The difference may explain rs10830963’s effect on the MTNR1B gene expression.
In summary, the risk G allele may contribute to the early onset of T2DM in our young Egyptian group. RNA splicing efficiency may also affect how the rs10830963 mutation causes T2DM. Egyptians and other populations need more replication studies on the risk G allele and EOD.