| Ketosis | |
|---|---|
| Other names | Ketonemia |
 | |
| Ketone bodies: acetone, acetoacetic acid, and beta-hydroxybutyric acid | |
| Pronunciation | |
| Specialty | Endocrinology |
Ketosis is a metabolic state characterized by elevated levels of ketone bodies in the blood or urine. Physiological ketosis is a normal response to low glucose availability. In physiological ketosis, ketones in the blood are elevated above baseline levels, but the body's acid–base homeostasis is maintained. This contrasts with ketoacidosis, an uncontrolled production of ketones that occurs in pathologic states and causes a metabolic acidosis, which is a medical emergency. Ketoacidosis is most commonly the result of complete insulin deficiency in type 1 diabetes or late-stage type 2 diabetes. Ketone levels can be measured in blood, urine or breath and are generally between 0.5 and 3.0 millimolar (mM) in physiological ketosis, while ketoacidosis may cause blood concentrations greater than 10 mM.[1]
Trace levels of ketones are always present in the blood and increase when blood glucose reserves are low and the liver shifts from primarily metabolizing carbohydrates to metabolizing fatty acids.[2] This occurs during states of increased fatty acid oxidation such as fasting, starvation, carbohydrate restriction, or prolonged exercise. When the liver rapidly metabolizes fatty acids into acetyl-CoA, some acetyl-CoA molecules can then be converted into ketone bodies: pyruvate, acetoacetate, beta-hydroxybutyrate, and acetone.[1][2] These ketone bodies can function as an energy source as well as signalling molecules.[3] The liver itself cannot utilize these molecules for energy, so the ketone bodies are released into the blood for use by peripheral tissues including the brain.[2]
When ketosis is induced by carbohydrate restriction, it is sometimes referred to as nutritional ketosis. A low-carbohydrate, moderate protein diet that can lead to ketosis is called a ketogenic diet. Ketosis is well-established as a treatment for epilepsy and is also effective in treating type 2 diabetes.[4]
- ^ a b Cite error: The named reference
:6was invoked but never defined (see the help page). - ^ a b c Ward C (2015). "Ketone Body Metabolism". Diapedia. doi:10.14496/dia.51040851169.29 (inactive 1 November 2024). Archived from the original on 2018-11-11. Retrieved 30 September 2019.
{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)[self-published source?] - ^ Mattson MP, Moehl K, Ghena N, Schmaedick M, Cheng A (2018). "Intermittent metabolic switching, neuroplasticity and brain health". Nature Reviews. Neuroscience. 19 (2): 63–80. doi:10.1038/nrn.2017.156. PMC 5913738. PMID 29321682.
- ^ Westman EC, Tondt J, Maguire E, Yancy WS (15 September 2018). "Implementing a low-carbohydrate, ketogenic diet to manage type 2 diabetes mellitus". Expert Review of Endocrinology & Metabolism. 13 (5): 263–272. doi:10.1080/17446651.2018.1523713. PMID 30289048. S2CID 52920398.