Exogenous ketones lower blood glucose level

Abstract

Certain disease conditions, involving inflammation and oxidative stress, are accelerated by high blood glucose levels. The safe reduction of blood glucose levels is difficult due to their regulation by powerful homeostatic mechanisms. The ketogenic diet (KD) induces a metabolic shift towards fatty acid oxidation and hepatic ketogenesis, elevating the ketone bodies acetoacetate (AcAc), β‐hydroxybutyrate (βHB), and acetone in the blood, which serve as alternative metabolic substrates to glucose. However, patient compliance to KD can be low; therefore, exogenous ketones provide an alternative method to establish and maintain elevated blood ketone levels. In this study, we tested the changes in blood glucose and ketone (βHB) levels in response to acute, sub‐chronic and chronic administration of one or more ketogenic compounds in either a post‐exercise or rested state. Rodent models with (WAG/Rij rats, WR and GLUT1Deficiency Syndrome mice, GLUT1D) and without (Sprague Dawley rats, SPD) pathology were tested. Experimental groups included either KD, standard diet with water (control, C) or in combination with the following ketogenic compounds: 1,3 butanediol (BD), beta hydroxybutyrate ketone mineral salt (KS), KS with medium chain triglyceride (KSMCT), BD acetoacetate diester (KE), KE with MCT (KEMCT), and KE with KS (KEKS).In SPD rats without exercise, KD, KS, KE and KSMCT significantly reduced blood glucose levels, compared to control. After exercise blood glucose was significantly lower in the KEMCT group, compared to control. In WR rats KE, KS, KSMCT, KEKS and KEMCT groups had lower blood glucose than control, in both a rested or post‐exercise state. In GLUT1D mice without exercise, KD and KS resulted in significantly lower glucose levels. These results indicate that ketogenic compounds were efficacious in reducing blood glucose levels in and outside the context of exercise.Support or Funding InformationUniversity of South Florida Foundation, GLUT1 Deficiency Syndrome Foundation, National Development Agency of HungaryThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.