Ketolysis: Difference between revisions
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Ketogenesis occurs primarily in the [[liver]], whereas ketolysis occurs in non-liver cells, especially in the [[heart]], [[brain]], and [[skeletal muscle]].<ref name="pmid28178565">{{cite journal | vauthors=Puchalska P, Crawford PA | title=Multi-dimensional Roles of Ketone Bodies in Fuel Metabolism, Signaling, and Therapeutics | journal=[[Cell Metabolism]] | volume=25 | issue=2 | pages=262-284 | year=2017 | doi = 10.1016/j.cmet.2016.12.022 | pmc=5313038 | pmid=28178565 }}</ref> The [[OXCT1|SCOT]] enzyme is required for ketolysis, and is present in the [[mitochondria]] of all mammalian cells except for [[hepatocyte]]s.<ref name="pmid28178565" /> |
Ketogenesis occurs primarily in the [[liver]], whereas ketolysis occurs in non-liver cells, especially in the [[heart]], [[brain]], and [[skeletal muscle]].<ref name="pmid28178565">{{cite journal | vauthors=Puchalska P, Crawford PA | title=Multi-dimensional Roles of Ketone Bodies in Fuel Metabolism, Signaling, and Therapeutics | journal=[[Cell Metabolism]] | volume=25 | issue=2 | pages=262-284 | year=2017 | doi = 10.1016/j.cmet.2016.12.022 | pmc=5313038 | pmid=28178565 }}</ref> The [[OXCT1|SCOT]] enzyme is required for ketolysis,<ref name="pmid24706027">{{cite journal | vauthors=Fukao T, Mitchell G, Aoyama Y | title=Ketone body metabolism and its defects | journal=[[Journal of Inherited Metabolic Disease]] | volume=37 | issue=4 | pages=541-551 | year=2014 | doi = 10.1007/s10545-014-9704-9 | pmid=24706027 }}</ref> and is present in the [[mitochondria]] of all mammalian cells except for [[hepatocyte]]s.<ref name="pmid28178565" /> |
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Although [[Pulmonary_alveolus#Type_II_cells|type II cells of the pulmonary alveolus]] possess [[monocarboxylate transporter]]s to transport of [[beta-Hydroxybutyric acid|beta hydroxybutyrate]] precursors into the cytoplasm, the absence of ketolytic enzymes results in the cells being unable to catabolize the beta hydroxybutyrate.<ref name="pmid33014275">{{cite journal | vauthors=Bradshaw PC, Seeds WA, Curtis WM | title=COVID-19: Proposing a Ketone-Based Metabolic Therapy as a Treatment to Blunt the Cytokine Storm | journal=[[List_of_Hindawi_academic_journals#O|Oxidative Medicine and Cellular Longevity]] | volume=2020 | pages=6401341 | year=2020 | doi = 10.1155/2020/6401341 | pmc=7519203 | pmid=33014275}}</ref> |
Although [[Pulmonary_alveolus#Type_II_cells|type II cells of the pulmonary alveolus]] possess [[monocarboxylate transporter]]s to transport of [[beta-Hydroxybutyric acid|beta hydroxybutyrate]] precursors into the cytoplasm, the absence of ketolytic enzymes results in the cells being unable to catabolize the beta hydroxybutyrate.<ref name="pmid33014275">{{cite journal | vauthors=Bradshaw PC, Seeds WA, Curtis WM | title=COVID-19: Proposing a Ketone-Based Metabolic Therapy as a Treatment to Blunt the Cytokine Storm | journal=[[List_of_Hindawi_academic_journals#O|Oxidative Medicine and Cellular Longevity]] | volume=2020 | pages=6401341 | year=2020 | doi = 10.1155/2020/6401341 | pmc=7519203 | pmid=33014275}}</ref> |
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[[Category:Medical terminology]] |
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Revision as of 16:07, 29 April 2022
Ketolysis is the process of catabolizing ketones, the opposite of ketogenesis which is the process of synthesizing ketones. Ketolysis provides more energy for ATP synthesis than fatty acid oxidation (beta oxidation). [1]
Ketogenesis occurs primarily in the liver, whereas ketolysis occurs in non-liver cells, especially in the heart, brain, and skeletal muscle.[2] The SCOT enzyme is required for ketolysis,[3] and is present in the mitochondria of all mammalian cells except for hepatocytes.[2]
Although type II cells of the pulmonary alveolus possess monocarboxylate transporters to transport of beta hydroxybutyrate precursors into the cytoplasm, the absence of ketolytic enzymes results in the cells being unable to catabolize the beta hydroxybutyrate.[4]
The cardioprotective effects of SGLT2 inhibitors have been attributed to the elevated ketone levels and increased ketolysis.[1]
References
- ^ a b Kolb H, Kempf K, Martin S (2021). "Ketone bodies: from enemy to friend and guardian angel". BMC Medicine. 19 (1): 313. doi:10.1186/s12916-021-02185-0. PMC 8656040. PMID 34879839.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b Puchalska P, Crawford PA (2017). "Multi-dimensional Roles of Ketone Bodies in Fuel Metabolism, Signaling, and Therapeutics". Cell Metabolism. 25 (2): 262–284. doi:10.1016/j.cmet.2016.12.022. PMC 5313038. PMID 28178565.
- ^ Fukao T, Mitchell G, Aoyama Y (2014). "Ketone body metabolism and its defects". Journal of Inherited Metabolic Disease. 37 (4): 541–551. doi:10.1007/s10545-014-9704-9. PMID 24706027.
- ^ Bradshaw PC, Seeds WA, Curtis WM (2020). "COVID-19: Proposing a Ketone-Based Metabolic Therapy as a Treatment to Blunt the Cytokine Storm". Oxidative Medicine and Cellular Longevity. 2020: 6401341. doi:10.1155/2020/6401341. PMC 7519203. PMID 33014275.
{{cite journal}}: CS1 maint: unflagged free DOI (link)