FBP1 promotes ABCG2-mediated uric acid excretion through activation of the PI3K/AKT/CREB signaling pathway.

ABSTRACT: Hyperuricaemia, a metabolic disorder, is characterized by abnormally elevated serum uric acid (SUA) levels. Fructose-1,6-bisphosphatase (FBPase), a key rate-limiting enzyme in gluconeogenesis, catalyses the irreversible conversion of fructose-1,6-bisphosphate (F-1,6-BP) to fructose-6-phosphate (F-6-P). In humans, FBPase deficiency disorder (OMIM #229700) is an autosomal recessive inborn error of metabolism characterized by fasting-induced hypoglycaemia, life-threatening lactic acidosis, hyperuricaemia, and hepatosteatosis. However, the exact pathophysiological mechanisms driving hyperuricaemia remain unknown. To systematically investigate the regulatory role of FBPase in urate homeostasis, we developed in vitro models encompassing major metabolic tissues-HK-2 cells (kidney), LoVo/Caco-2 ce

SUBMITTER: Bai Q 

PROVIDER: S-EPMC12680681 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature