Effects of stanniocalcin hormones on rat hepatic glucose homeostasis under fed and fasted conditions

• Published in: General and comparative endocrinology 2021-02, Vol.302, p.113661-113661, Article 113661
• Main Authors: Khal De Souza, Samir, Sarapio, Elaine, Lopes Vogt, Everton, Schein, Vanessa, Bandeira Fabres, Rafael, Felipe Argenta Model, Jorge, Vieira Lima, Matheus, Santos Rocha, Débora, Silveira Martins Da Silva, Roselis
• Format: Article
• Language: English
• Subjects: Glucose Homeostasis; Rat Liver; Stanniocalcin
• ISSN: 0016-6480; 1095-6840
• DOI: 10.1016/j.ygcen.2020.113661

[Display omitted] •STCs modulated hepatic gluconeogenesis in fed and fasted rats.•STCs do not modify glycogen level and synthesis and glucose oxidation.•STC-2 increased Pck1 mRNA levels in fed and fasting rat livers.•Fasted state influenced the expression of Stc1 and Stc2 in rat liver.•Data confirm the conservation of STCs metabolic functions in the vertebrates. To test the hypothesis of conservation of stanniocalcin 1 and 2 (STC-1; STC-2) metabolic functions in vertebrates, we performed an in vitro study to determine if these hormones are implicated in regulation of the gluconeogenesis pathway, glycogen synthesis, and 14C-glucose conversion to 14CO2 in livers from fed and fasting rats (Rattus norvegicus). Stc1 and Stc2 gene expressions increased in the liver after fasting. STC-1 participated in the regulation of the hepatic gluconeogenesis pathway in rats when the precursor was 14C-lactate. STC-2 demonstrated variational signaling on rat hepatic gluconeogenesis activity and Pck1 gene expression, decreasing levels in the fed state when the substrate was 14C-alanine and increasing levels during fasting when the substrate was 14C-lactate. At the concentrations used in this study, STC-1 and STC-2 did not affect glycogen concentration and synthesis from 14C-glucose or 14C-glucose conversion to 14CO2 in the livers from fed or fasting rats. These findings highlight the role of stanniocalcins in the hepatic gluconeogenesis pathway in mammals and confirm the conservation of STC-1 and STC-2 metabolic functions in the vertebrates.