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The last reaction in this metabolic pathway, which involves the conversion of {{nowrap|<small>D</small>-β-}}({{nowrap|<small>D</small>-β-hydroxybutyryloxy}}){{nowrap|-butyrate}} into {{nowrap|<small>D</small>-β-hydroxybutyrate}}, is catalyzed by the [[hydroxybutyrate-dimer hydrolase]] enzyme.<ref name="Butyrate metabolism" /> |
The last reaction in this metabolic pathway, which involves the conversion of {{nowrap|<small>D</small>-β-}}({{nowrap|<small>D</small>-β-hydroxybutyryloxy}}){{nowrap|-butyrate}} into {{nowrap|<small>D</small>-β-hydroxybutyrate}}, is catalyzed by the [[hydroxybutyrate-dimer hydrolase]] enzyme.<ref name="Butyrate metabolism" /> |
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The concentration of β-hydroxybutyrate in human blood plasma, as with other [[ketone bodies]], increases through [[ketosis]].<ref name="Medscape2015">{{Cite journal |url= https://emedicine.medscape.com/article/2087381-overview#a4|title = Beta-Hydroxybutyrate |vauthors = Perelas A, Staros EB |date=October 30, 2015 |website= Medscape |publisher = WebMD LLC. |access-date= February 8, 2017}}</ref> This elevated β-hydroxybutyrate level is naturally expected, as β-hydroxybutyrate is formed from acetoacetate. The compound can be used as an energy source by the brain and skeletal muscle when [[blood glucose]] is low.<ref>{{cite journal | vauthors = Owen OE, Morgan AP, Kemp HG, Sullivan JM, Herrera MG, Cahill GF | title = Brain metabolism during fasting | journal = The Journal of Clinical Investigation | volume = 46 | issue = 10 | pages = 1589–1595 | date = October 1967 | pmid = 6061736 | pmc = 292907 | doi = 10.1172/JCI105650 }}</ref><ref>{{cite journal | vauthors = Evans E, Walhin JP, Hengist A, Betts JA, Dearlove DJ, Gonzalez JT | title = Ketone monoester ingestion increases postexercise serum erythropoietin concentrations in healthy men | journal = American Journal of Physiology. Endocrinology and Metabolism | volume = 324 | issue = 1 | pages = E56–E61 | date = January 2023 | pmid = 36449571 | pmc = 9870573 | doi = 10.1152/ajpendo.00264.2022 }}</ref><ref>{{cite journal | vauthors = Cahill GF | title = Fuel metabolism in starvation | journal = Annual Review of Nutrition | volume = 26 | issue = 1 | pages = 1–22 | date = 2006-08-01 | pmid = 16848698 | doi = 10.1146/annurev.nutr.26.061505.111258 }}</ref><ref>{{cite journal | vauthors = Mikkelsen KH, Seifert T, Secher NH, Grøndal T, van Hall G | title = Systemic, cerebral and skeletal muscle ketone body and energy metabolism during acute hyper-D-β-hydroxybutyratemia in post-absorptive healthy males | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 100 | issue = 2 | pages = 636–643 | date = February 2015 | pmid = 25415176 | doi = 10.1210/jc.2014-2608 | doi-access = free }}</ref> [[Diabetic]] patients can have their ketone levels tested via urine or blood to indicate [[diabetic ketoacidosis]]. In [[alcoholic ketoacidosis]], this ketone body is produced in greatest concentration. Ketogenesis occurs if [[oxaloacetate]] in the liver cells is depleted, a circumstance created by reduced carbohydrate intake (through diet or starvation); prolonged, excessive |
The concentration of β-hydroxybutyrate in human blood plasma, as with other [[ketone bodies]], increases through [[ketosis]].<ref name="Medscape2015">{{Cite journal |url= https://emedicine.medscape.com/article/2087381-overview#a4|title = Beta-Hydroxybutyrate |vauthors = Perelas A, Staros EB |date=October 30, 2015 |website= Medscape |publisher = WebMD LLC. |access-date= February 8, 2017}}</ref> This elevated β-hydroxybutyrate level is naturally expected, as β-hydroxybutyrate is formed from acetoacetate. The compound can be used as an energy source by the brain and skeletal muscle when [[blood glucose]] is low.<ref>{{cite journal | vauthors = Owen OE, Morgan AP, Kemp HG, Sullivan JM, Herrera MG, Cahill GF | title = Brain metabolism during fasting | journal = The Journal of Clinical Investigation | volume = 46 | issue = 10 | pages = 1589–1595 | date = October 1967 | pmid = 6061736 | pmc = 292907 | doi = 10.1172/JCI105650 }}</ref><ref>{{cite journal | vauthors = Evans E, Walhin JP, Hengist A, Betts JA, Dearlove DJ, Gonzalez JT | title = Ketone monoester ingestion increases postexercise serum erythropoietin concentrations in healthy men | journal = American Journal of Physiology. Endocrinology and Metabolism | volume = 324 | issue = 1 | pages = E56–E61 | date = January 2023 | pmid = 36449571 | pmc = 9870573 | doi = 10.1152/ajpendo.00264.2022 }}</ref><ref>{{cite journal | vauthors = Cahill GF | title = Fuel metabolism in starvation | journal = Annual Review of Nutrition | volume = 26 | issue = 1 | pages = 1–22 | date = 2006-08-01 | pmid = 16848698 | doi = 10.1146/annurev.nutr.26.061505.111258 }}</ref><ref>{{cite journal | vauthors = Mikkelsen KH, Seifert T, Secher NH, Grøndal T, van Hall G | title = Systemic, cerebral and skeletal muscle ketone body and energy metabolism during acute hyper-D-β-hydroxybutyratemia in post-absorptive healthy males | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 100 | issue = 2 | pages = 636–643 | date = February 2015 | pmid = 25415176 | doi = 10.1210/jc.2014-2608 | doi-access = free }}</ref> [[Diabetic]] patients can have their ketone levels tested via urine or blood to indicate [[diabetic ketoacidosis]]. In [[alcoholic ketoacidosis]], this ketone body is produced in greatest concentration. Ketogenesis occurs if [[oxaloacetate]] in the liver cells is depleted, a circumstance created by reduced carbohydrate intake (through diet or starvation); prolonged, excessive alcohol consumption; and/or insulin deficiency. Because oxaloacetate is crucial for entry of [[acetyl-CoA]] into the TCA cycle, the rapid production of acetyl-CoA from fatty acid oxidation in the absence of ample oxaloacetate overwhelms the decreased capacity of the TCA cycle, and the resultant excess of acetyl-CoA is shunted towards ketone body production.{{citation needed|date=June 2016}} |
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{{Leucine metabolism in humans|note=yes|align=left|caption=Acetoacetate, the metabolic precursor of β-hydroxybutyrate, is a metabolite of [[fatty acid]]s, [[ketogenic amino acid]]s such as [[leucine]]<ref name="HMG biosynthesis" /> and [[isoleucine]],<ref name="HMG biosynthesis">{{cite web|title=Valine, leucine and isoleucine degradation - Reference pathway|url=http://www.genome.jp/kegg-bin/show_pathway?map00280+C00356|website=Kyoto Encyclopedia of Genes and Genomes|publisher=Kanehisa Laboratories|date=27 January 2016|access-date=1 February 2018}}</ref> and [[beta-Hydroxy beta-methylbutyric acid|{{nowrap|β-hydroxy}} {{nowrap|β-methylbutyrate}}]]}}{{clear}} |
{{Leucine metabolism in humans|note=yes|align=left|caption=Acetoacetate, the metabolic precursor of β-hydroxybutyrate, is a metabolite of [[fatty acid]]s, [[ketogenic amino acid]]s such as [[leucine]]<ref name="HMG biosynthesis" /> and [[isoleucine]],<ref name="HMG biosynthesis">{{cite web|title=Valine, leucine and isoleucine degradation - Reference pathway|url=http://www.genome.jp/kegg-bin/show_pathway?map00280+C00356|website=Kyoto Encyclopedia of Genes and Genomes|publisher=Kanehisa Laboratories|date=27 January 2016|access-date=1 February 2018}}</ref> and [[beta-Hydroxy beta-methylbutyric acid|{{nowrap|β-hydroxy}} {{nowrap|β-methylbutyrate}}]]}}{{clear}} |
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