GSH-deficiency promotes basal hyperinsulinemia in the insulin secreting cell line INS-1
This study sought to determine the impact of glutathione (GSH) synthesis on beta-cell function. To induce GSH deficiency, GCLC was inhibited in INS-1 cells using buthionine sulfoximine (BSO). The 24-hour treatment of INS-1 cells with BSO (250 uM) reduced GSH levels to 33 percent of untreated, however, glucose-stimulated insulin secretion was unchanged. The 24-hour treatment of INS-1 cells with BME-free medium containing BSO further reduced GSH levels to 9 percent of untreated and elicited significantly higher basal insulin secretion. Transcriptomic analysis was conducted to determine if transcriptional changes could explain increased basal insulin secretion. Here, after 24-hours of treatment with BME-free medium with or without BSO are compared.