Navarro, Juan ADecara, JuanMedina-Vera, DinaTovar, RubénSuarez, Juan|Pavón, Francisco-JavierSerrano, AntoniaVida, MargaritaGutierrez-Adan, AlfonsoSanjuan, CarlosBaixeras, ElenaFonseca, Fernando Rodríguez de2024-02-122024-02-122020-07-08http://hdl.handle.net/10668/15920http://hdl.handle.net/20.500.12105/18074To characterize the metabolic actions of D-Pinitol, a dietary inositol, in male Wistar rats, we analyzed its oral pharmacokinetics and its effects on (a) the secretion of hormones regulating metabolism (insulin, glucagon, IGF-1, ghrelin, leptin and adiponectin), (b) insulin signaling in the liver and (c) the expression of glycolytic and neoglucogenesis enzymes. Oral D-Pinitol administration (100 or 500 mg/Kg) resulted in its rapid absorption and distribution to plasma and liver compartments. Its administration reduced insulinemia and HOMA-IR, while maintaining glycaemia thanks to increased glucagon activity. In the liver, D-Pinitol reduced the key glycolytic enzyme pyruvate kinase and decreased the phosphorylation of the enzymes AKT and GSK-3. These observations were associated with an increase in ghrelin concentrations, a known inhibitor of insulin secretion. The profile of D-Pinitol suggests its potential use as a pancreatic protector decreasing insulin secretion through ghrelin upregulation, while sustaining glycaemia through the liver-based mechanisms of glycolysis control.engVoRhttp://creativecommons.org/licenses/by/4.0/AKTD-PinitolGhrelinInsulinInsulin resistanceLiverPhosphorylationAdministration, OralAnimalsDepression, ChemicalFabaceaeGhrelinGlucagonGlycogenGlycogen Synthase Kinase 3GlycolysisInositolInsulin SecretionLiverMalePhosphorylationProto-Oncogene Proteins c-aktPyruvate KinaseRats, WistarAttribution 4.0 International3265057912710.3390/nu120720302072-6643Nutrientsopen access