Genomic Study of TCF7L2 Gene Mutation on Insulin Secretion for Type 2 DM Patients: A Review

Aim: This paper aims to establish whether a correlation between TCF7L2 gene mutation on insulin secretion for Type 2 DM Patients.

Background: Diabetes type 2 is the most common metabolic disorder worldwide. Beta cell dysfunction reduces insulin secretion and increases the glucose level in the blood and insulin resistance that raises the glucose production in the liver and decreases the glucose uptake to muscle, liver, and adipose tissue causing hyperglycemia (T2DM). TCF7L2 (transcription factor 7–like 2) works as a nuclear Receptor for CTNNB1(B catenin) that mediated the WNT signaling pathway (a group of signal transduction pathways made of proteins that pass signals from outside a cell through cell surface receptors to the inside of the cell) and any variation will cause the development of T2DM.

Methods: GenBank in NCBI database was used to extract the DNA sequence and mRNA sequence of the TCF7L2 gene (an accession number of the gene, number of amino acids, exons, and length of nucleotides). FASTA format was also useful to retrieve the nucleotide sequence and get the function of the protein. BLAST was used to compare the protein product of the TCF7L2gene between humans and gorillas, and pygmy chimpanzees (Pan paniscus).

Results: The accession number is NC_000010.11, the number of amino acids in the protein product is 602, the number of exons found is 20 and the gene is in chromosome 10. Finally, many organisms have the same gene as dogs, cows, mice, rats, zebrafish, and frogs.

Conclusion: There is a strong association between TCF7L2 (transcription factor 7–like 2) alleles (rs7903146) T alleles and T2DM. It was found that there is a high frequency of diabetic type two patients having TCF7L2 (transcription factor 7–like 2) alleles (rs7903146) with a high frequency of the T allele.