Pathogenicity of TCF7L2 gene for diabetes mellitus type 2

Type-2-diabetes mellitus (T2DM) is a complex metabolic condition characterized by insulin resistance, poorly controlled glucose metabolism, and progressive pancreatic beta cell function loss. The pathophysiology of T2DM is thought to be significantly influenced by the transcription factor 7-like 2 (TCF7L2) gene. Wnt signaling, adipoge nesis, incretin activity, beta cell apoptosis, and glucose metabolism modulation are a few of the disease features that TCF7L2 affects. Wnt signaling is disrupted by TCF7L2 gene variations, which increases adipogenesis and insulin resistance-two factors that are crucial in the development of T2DM. These variations also impact incretin function by lowering the release of the glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), which impairs glucose homeostasis. In addition, TCF7L2 gene variations are linked to beta cell malfunction and death, hastening the development of T2DM. TCF7L2 also affects glucose metabolism by controlling genes related to glucose transport, glycogen synthesis, and gluconeogenesis, which affects total glucose homeostasis. It may be possible to develop novel therapy strategies by better understanding the function of TCF7L2 in T2DM pathogenesis. The management of T2DM may benefit from focusing on TCF7L2 or similar pathways. More investigation is required to determine the precise molecular pathways driving TCF7L2-mediated pathogenicity and to examine its potential as a therapeutic target in the treatment of T2DM.