RT Journal Article
T1 Insulin controls clock gene expression in the liver of goldfish probably via Pi3k/Akt pathway
T2 La insulina controla la expresión del gen del reloj en el hígado de los peces de colores, probablemente a través de la vía Pi3k/Akt
A1 Saiz Aparicio, Nuria
A1 Velasco, Cristina
A1 Pedro Ormeño, Nuria De
A1 Soengas, José Luis
A1 Isorna Alonso, Esther
AB The liver circadian clock plays a pivotal role in driving metabolic rhythms, being primarily entrained by the feeding schedule, although the underlying mechanisms remain elusive. This study aimed to investigate the potential role of insulin as an intake signal mediating liver entrainment in fish. To achieve this, the expression of clock genes, which form the molecular basis of endogenous oscillators, was analyzed in goldfish liver explants treated with insulin. The presence of insulin directly increased the abundance of per1a and per2 transcripts in the liver. The dependency of protein translation for such insulin effects was evaluated using cycloheximide, which revealed that intermediate protein translation is seemingly unnecessary for the observed insulin actions. Furthermore, the putative interaction between insulin and glucocorticoid signaling in the liver was examined, with the results suggesting that both hormones exert their effects by independent mechanisms. Finally, to investigate the specific pathways involved in the insulin effects, inhibitors targeting PI3K/AKT and MEK/ERK were employed. Notably, inhibition of PI3K/AKT pathway prevented the induction of per genes by insulin, supporting its involvement in this process. Together, these findings suggest a role of insulin in fish as a key element of the multifactorial system that entrains the liver clock to the feeding schedule.
PB MDPI
SN 1661-6596
YR 2023
FD 2023-07-25
LK https://hdl.handle.net/20.500.14352/105668
UL https://hdl.handle.net/20.500.14352/105668
LA eng
NO Saiz N, Velasco C, De Pedro N, Soengas JL, Isorna E. Insulin Controls Clock Gene Expression in the Liver of Goldfish Probably via Pi3k/Akt Pathway. IJMS. 2023;24(15):11897
NO Ministerio de Ciencia e Innovación (España)
NO Xunta de Galicia
NO Universidad Complutense de Madrid
DS Docta Complutense
RD 6 oct 2024