How MCTs work

Medium Chain Triglycerides (MCT Oils) are medium chain fatty acids attached to three arms of a small molecule called glycerol. MCT Oils sources include coconut, palm kernel oil and camphor tree drupes.

MCT Oils benefits include weight loss, increased energy expenditure, epilepsy and Alzheimer’s disorders. MCT Oils have found use in the treatment of a variety of malabsorption ailments and in parenteral nutritional emulsions. MCT Oils are known among athletes specifically desiring extended workouts or greater endurance. The safety of MCT Oils, up to levels of 1g/kg, has been confirmed in several clinical trials 1 in humans. MCT Oils side effects include a mild laxative effect and cause nausea and gastric discomfort when consumed more than 20g at a time.

MCT oils are hydrolyzed quickly, completely, and are absorbed mostly as free fatty acid. After consumption, MCT Oils are hydrolyzed (broken down by) by pancreatic lipase (an enzyme) to respective medium chain fatty acids (MCFAs). The MCFAs, the products of MCT hydrolysis, are absorbed faster than those of long chain triglycerides (LCTs) like beef tallow, and as fast as glucose 2. In case of pancreatic lipase or bile salts deficiency, they are still absorbed but as triacyl glycerol and broken down by intestinal lipases 3. The majority of the MCFAs are retained in the liver till they undergo oxidation 4, and only a small amount appears in the peripheral blood for a short period of time.

MCFAs can cross the mitochondrial membrane very rapidly without the need for carnitine unlike longer chain fatty acids. MCFAs are acylated and enter the liver mitochondria, where they undergo an important method of fat burning called β-oxidation, to form ketone bodies. Ketone bodies are small lipid-derived molecules that serve as a circulating energy source for tissues in times of fasting or prolonged exercise. There are three distinct ketone bodies molecules, acetone, acetoacetic acid, and β-hyrody butyrate (β-OHB). Among them the β-OHB is the most important.”

Since the liver can’t use ketone bodies in any form, they are released into the bloodstream to be used by other organs including visual system, and non-hepatic tissues. In the blood, ACA and BHB are transported from the vascular lumen to the brain interstitial space, and to both glia and neurons by monocarboxylic acid transporters (MCTs). MCT-1 is the principal carrier localized to the vascular endothelium 5. The ketone body BHB crosses the blood-brain barrier and is then taken up by neuronal cells. Ketones are used in a concentration-dependent manner in the adult human brain 6 - 7.

Once the circulating concentrations reach approximately 12 mM, the oxidative machinery is saturated 8. Within neurons, both ACA and BHB are transported directly into mitochondria, and then converted to acetyl-CoA through several enzymatic steps. BHB is converted to ACA through D-β- hydroxybutyrate dehydrogenase, and ACA undergoes subsequent conversion to acetoacetyl-CoA through a succinyl-CoA transferase enzyme. Finally, acetoacetyl-CoA-thiolase converts acetoacetyl-CoA to two acetyl-CoA moieties which then enter the TCA cycle and generate ATP, as well as increase pools of acetyl-CoA and acetylcholine. Neuronal system of the retina can use ketone bodies even in the presence of abundant glucose. In fact, ketone bodies have been shown to reduce brain glucose consumption 9 - 10.

  1. Traul KA, et al, Review of the toxicologic properties of medium-chain triglycerides. Food Chem Toxicol. 2000;38:79-98.
  2. Iber F. Relative rates of metabolism MCT, LCT and ethanol in man. In: Kaunitz H, Lang K, Fekl W, eds. Mittelkettige Triglyceride in der Diat. Z Ernhrungswiss 1974; 17(suppl):9- 16.
  3. Valdivieso V. Absorption of medium-chain triglycerides in animals with pancreatic atrophy. Am I Dig Dis 1972; 17:129-36.
  4. Bach AC, et al. Medium-chain triglycerides: an update. Am J Clin Nutr. 1982;36(5):950-962.
  5. Susan A. Masino, Jong M. Rho, Mechanisms of Ketogenic Diet Action, Jasper’s basic mechanism of epilepsy, 4th Edison
  6. Laffel L. Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev. 1999;15(6):412-426.
  7. Morris AA. Cerebral ketone body metabolism. J Inherit Metab Dis. 2005;28(2):109-121
  8. Mayes PA. Oxidation of fatty acids: ketogenesis. In: Murray RK, Granner DK, Mayes PA, Rodwell VW, eds. Harper’s Biochemistry. New York, NY: McGraw-Hill; 2000.
  9. Freeman J, Veggiotti P, Lanzi G, Tagliabue A, Perucca E. The ketogenic diet: from molecular mechanisms to clinical effects. Epilepsy Res 2006; 68:145–180.
  10. Sucher KP. Medium chain triglycerides: a review of their enteral use in clinical nutrition. Nutr Clin Pract. 1986; 1(3):146-150.


Before starting any diet, you should speak to your doctor. You must not rely on the information on this website as an alternative to medical advice from your doctor or other professional healthcare provider. If you have any specific questions about any medical matter, you should consult your doctor or other professional healthcare provider. If you think you may be suffering from any medical condition, you should seek immediate medical attention. You should never delay seeking medical advice, disregard medical advice or discontinue medical treatment because of information on this website.