Diets low in carbohydrates and proteins and enriched in fat stimulate the hepatic synthesis of ketone bodies (KB). These molecules are used as alternative fuel for energy production in target tissues. The synthesis and utilization of KB are tightly regulated both at transcriptional and hormonal levels. The nuclear receptor peroxisome proliferator activated receptor α (PPARα), currently recognized as one of the master regulators of ketogenesis, integrates nutritional signals to the activation of transcriptional networks regulating fatty acid β-oxidation and ketogenesis. New factors, such as circadian rhythms and paracrine signals, are emerging as important aspects of this metabolic regulation. However, KB are currently considered not only as energy substrates but also as signaling molecules. β-hydroxybutyrate has been identified as class I histone deacetylase inhibitor, thus establishing a connection between products of hepatic lipid metabolism and epigenetics. Ketogenic diets (KD) are currently used to treat different forms of infantile epilepsy, also caused by genetic defects such as Glut1 and Pyruvate Dehydrogenase Deficiency Syndromes. However, several researchers are now focusing on the possibility to use KD in other diseases, such as cancer, neurological and metabolic disorders. Nonetheless, clear-cut evidence of the efficacy of KD in other disorders remains to be provided in order to suggest the adoption of such diets to metabolic-related pathologies.

Ketogenic Diet : a New Light Shining on Old but Gold Biochemistry / R. Longo, C. Peri, D. Cricri', L. Coppi, D. Caruso, N. Mitro, E. De Fabiani, M. Crestani. - In: NUTRIENTS. - ISSN 2072-6643. - 11:10(2019 Oct 17), pp. 2497.1-2497.22. [10.3390/nu11102497]

Ketogenic Diet : a New Light Shining on Old but Gold Biochemistry

R. Longo
Primo
;
C. Peri;D. Cricri';L. Coppi;D. Caruso;N. Mitro;E. De Fabiani;M. Crestani
Ultimo
2019

Abstract

Diets low in carbohydrates and proteins and enriched in fat stimulate the hepatic synthesis of ketone bodies (KB). These molecules are used as alternative fuel for energy production in target tissues. The synthesis and utilization of KB are tightly regulated both at transcriptional and hormonal levels. The nuclear receptor peroxisome proliferator activated receptor α (PPARα), currently recognized as one of the master regulators of ketogenesis, integrates nutritional signals to the activation of transcriptional networks regulating fatty acid β-oxidation and ketogenesis. New factors, such as circadian rhythms and paracrine signals, are emerging as important aspects of this metabolic regulation. However, KB are currently considered not only as energy substrates but also as signaling molecules. β-hydroxybutyrate has been identified as class I histone deacetylase inhibitor, thus establishing a connection between products of hepatic lipid metabolism and epigenetics. Ketogenic diets (KD) are currently used to treat different forms of infantile epilepsy, also caused by genetic defects such as Glut1 and Pyruvate Dehydrogenase Deficiency Syndromes. However, several researchers are now focusing on the possibility to use KD in other diseases, such as cancer, neurological and metabolic disorders. Nonetheless, clear-cut evidence of the efficacy of KD in other disorders remains to be provided in order to suggest the adoption of such diets to metabolic-related pathologies.
cancer; epigenetics; epilepsy; ketogenic diet; ketone body regulation; metabolic disorders; neurological disorders
Settore BIO/10 - Biochimica
   Control of metabolic and inflammatory pathways by nuclear receptor
   NR-NET
   EUROPEAN COMMISSION
   FP7
   606806

   Health and Understanding of Metabolism, Aging and Nutrition
   HUMAN
   EUROPEAN COMMISSION
   FP7
   602757

   Histone deacetylase 3 in adipose tissue: a link between immuno-metabolic dysfunctions and obesity and type 2 diabetes
   FONDAZIONE CARIPLO
   2015-0641

   Novel pharmacological approaches to increase ketone bodies availability in Glut1 deficiency syndrome
   FONDAZIONE TELETHON ETS
   GEP14129
17-ott-2019
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/683601
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