2024
DOI: 10.1016/j.tem.2023.10.001
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Common and divergent molecular mechanisms of fasting and ketogenic diets

Antonio Paoli,
Grant M. Tinsley,
Mark P. Mattson
et al.
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Cited by 9 publications
(4 citation statements)
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“…Therefore, to prevent extensive loss of lean mass, it is most important that the brain, a significant consumer of glucose, switches its energy source from glucose to ketone bodies produced through increased fat oxidation [22]. Ketone bodies not only function as an alternative energy substrate but can also activate the enzyme AMP-activated protein kinase (AMPK), which increases the mitochondrial oxidation of fa y acids while simultaneously inhibiting the mechanistic target of rapamycin complex 1 (mTORC1) in skeletal tissue [23]. mTORC1 plays a crucial role in integrating growth and metabolism by responding to nutrient levels and growth signals [24].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Therefore, to prevent extensive loss of lean mass, it is most important that the brain, a significant consumer of glucose, switches its energy source from glucose to ketone bodies produced through increased fat oxidation [22]. Ketone bodies not only function as an alternative energy substrate but can also activate the enzyme AMP-activated protein kinase (AMPK), which increases the mitochondrial oxidation of fa y acids while simultaneously inhibiting the mechanistic target of rapamycin complex 1 (mTORC1) in skeletal tissue [23]. mTORC1 plays a crucial role in integrating growth and metabolism by responding to nutrient levels and growth signals [24].…”
Section: Discussionmentioning
confidence: 99%
“…mTORC1 plays a crucial role in integrating growth and metabolism by responding to nutrient levels and growth signals [24]. The inhibition of mTORC1 aims to suppress energyconsuming protein synthesis in skeletal muscle tissue during glucose scarcity [23]. In summary, following a ketogenic LCHF diet impacts both fat and lean mass through hormonal changes and the molecular effects of elevated ketone bodies.…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, adiponectin could increase liver glycogenase activity, which also enhances NADH production via glycolysis, indirectly activating AMPK [82]. As a final point, intermittent fasting and ketogenic diets may also activate AMPK and/or inhibit the mTOR pathway, contributing to the suppression of oxidative stress and/or inflammation levels through boosting mitochondrial plasticity [83].…”
Section: Some Molecules Involved In the Regulation Of Ampkmentioning
confidence: 99%
“…Additionally, the KD was initially employed for managing refractory epilepsy and has progressively extended its application to encompass other neurological disorders [ 84 ], such as Parkinson’s disease and Alzheimer’s diseases. With the advancement of medical technology and sports science, there are several studies that have demonstrated the potential of this dietary pattern in enhancing sports performance in some ways [ 85 , 86 , 87 ]. Nevertheless, this diet still has some limitations; for example, the ability of muscle to use glycogen for oxidation is impaired after long-term ketoadaptation, leading to an inability to utilize the available glycogen, which provides a more effective energy source when the oxygen supply becomes limiting.…”
Section: The Influence Of Several Typical Dietary Patterns On the Gut...mentioning
confidence: 99%