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Review
. 2015 Feb 2;6:27.
doi: 10.3389/fpsyg.2015.00027. eCollection 2015.

Ketosis, Ketogenic Diet and Food Intake Control: A Complex Relationship

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Free PMC article
Review

Ketosis, Ketogenic Diet and Food Intake Control: A Complex Relationship

Antonio Paoli et al. Front Psychol. .
Free PMC article

Abstract

Though the hunger-reduction phenomenon reported during ketogenic diets is well-known, the underlying molecular and cellular mechanisms remain uncertain. Ketosis has been demonstrated to exert an anorexigenic effect via cholecystokinin (CCK) release while reducing orexigenic signals e.g., via ghrelin. However, ketone bodies (KB) seem to be able to increase food intake through AMP-activated protein kinase (AMPK) phosphorylation, gamma-aminobutyric acid (GABA) and the release and production of adiponectin. The aim of this review is to provide a summary of our current knowledge of the effects of ketogenic diet (KD) on food control in an effort to unify the apparently contradictory data into a coherent picture.

Keywords: appetite; brain; hunger; hypothalamus; ketogenic diet; ketones.

Figures

Figure 1
Figure 1
Concentrations of KB: acetone, BHB and acetoacetic acid (AcAc), and plasma free FAs (FFA) from the post-absorptive state to 40 days of starvation in human subjects. Y axis was expanded to better describe the great change in BHB concentration. Modified from Fukao et al. (2004), Owen (2005).
Figure 2
Figure 2
A reduced availability of dietary carbohydrates leads to an increased liver production of KBs. The liver cannot utilize KBs because it lacks the mitochondrial enzyme succinyl-CoA: 3-ketoacid (oxoacid) CoA transferase (SCOT) necessary for activation of acetoacetate to acetoacetyl CoA. KBs are utilized by tissues, in particularly by brain. KBs enter the citric acid cycle after being converted to acetyl CoA by hydroxybutyrate dehydrogenase (HBD), succinyl-CoA: 3–CoA transferase (SCOT), and methylacetoacetyl CoA thiolase (MAT). Modified from Owen (2005), Paoli et al. (2014).
Figure 3
Figure 3
Effects of ketone bodies on AMP-activated protein kinase (AMPK) actions in different tissues.
Figure 4
Figure 4
Scheme of orexigenic and anorexigenic effects of ketosis. The picture is highly schematic. For more details please see the text. AMPK, AMP-activated protein kinase; CCK, cholecystokinin; GABA, gamma-aminobutyric acid; BHB, β-hydroxybutyric acid; FFA, free fatty acids; ROS, reactive oxygen species; NPY, neuropeptide Y; AgRP, agouti gene-related protein.

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References

    1. Amen-Ra N. (2006). Humans are evolutionarily adapted to caloric restriction resulting from ecologically dictated dietary deprivation imposed during the Plio-Pleistocene period. Med. Hypotheses 66, 978–984. 10.1016/j.mehy.2005.11.013 - DOI - PubMed
    1. Benani A., Troy S., Carmona M. C., Fioramonti X., Lorsignol A., Leloup C., et al. . (2007). Role for mitochondrial reactive oxygen species in brain lipid sensing: redox regulation of food intake. Diabetes 56, 152–160. 10.2337/db06-0440 - DOI - PubMed
    1. Bortz W. M., Paul P., Haff A. C., Holmes W. L. (1972). Glycerol turnover and oxidation in man. J. Clin. Invest. 51, 1537–1546. 10.1172/JCI106950 - DOI - PMC - PubMed
    1. Bough K. J., Rho J. M. (2007). Anticonvulsant mechanisms of the ketogenic diet. Epilepsia 48, 43–58. 10.1111/j.1528-1167.2007.00915.x - DOI - PubMed
    1. Brown A. J. (2007). Low-carb diets, fasting and euphoria: is there a link between ketosis and gamma-hydroxybutyrate (GHB)? Med. Hypotheses 68, 268–271. 10.1016/j.mehy.2006.07.043 - DOI - PubMed

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