Intake of medium chain fatty acids (notably 12:0 and 14:0) from human milk in Antigua is not related to growth and does not cause energy wasting due to excessive beta-oxidation - abstract

The effect of postnatal intake of medium chain fatty acids (MCFA; C6-C14) from human milk on excessive beta-oxidation and growth was studied in Antigua. On day 23-28 a mean estimated intake of 8.9 g(range:3.8-16.6) of MCFA (notably 12:0 and 14:0) per litre did not cause excessive beta-oxidation, as derived from urinary excretion of ketone bodies and beta-hudroxybutyric acid. MCFA intake was not related to growth in the first 23-28 days. Intakes of as low as 2.7 g MCFA (notably 8:0 and 10:0) per litre from semisynthetic medium chain triglycerides are known to produce excessive beta-oxidation and urinary excretion of dicarboxylic acids (Rebouche et al, Am J. Clin. Nutri. 1990;52:820-824). It is concluded that, from a metabolic point of view, 12:0 and 14:0 from human milk belong to an intermediate subclass of MCFA that resembles long chain fatty acids greater than or equal to 16). Their uptake into adipose tissue may prevent hepatic oxidation, despite conceivable transportation of free 12:0 via the portal vein (AU)

Biochemical aspects of ketogenesis, a review

Ketogenesis occurs only under certain physiological conditions, the physiological substrate for the process being long chain fatty acids. The condition for ketogenesis arises if the long chain fatty acid levels are high enough to render the liver incapable of metabolising all the acetyl CoA, formed as a result of hepatic oxidation of long chain fatty acids, via the tricarboxylic acid cycle to yield water and carbon dioxide. The state in which unesterified fatty acid levels are high enough to cause ketogenesis can be arrived at if there is a lack of insulin or a condition of starvation. Biochemical regulation, pathological condition and relative levels of ketone bodies are also reviewed. It was found that maximum ketonemia reflects not only increased production but also decreased use. The determination of urine or plasma 3-hydroxybutyrate may be of more importance than a simple urinary test upon ketone bodies in diabetic persons

An investigation into anti-ketogenic bodies

Many oxidizable substances, for example glycerol and sorbitol, decrease the formation of ketone bodies in rat liver slices, but as yet little is known of the mechanism by which these compounds exert their antiketogenic action. During a survey of potential antiketogenic compounds it was found that glyco-aldehyde is known to break down initially through oxidation by aldehyde dehydrogenase to glycollate and this in turn is oxidized to glyoxylate by glycollate oxidase. Glyoxylate can form glycine by transamination or it can be oxidized to Formalin and Carbon Dioxide. Evidence was presented in this paper suggesting that glyoxylate is responsible for the apparent decrease in the formation of acetoacetate by rat liver slices when glycoaldehyde is the added substance and the decrease is due to the non-enzymic condensation of aceto-acetate and glyoxylate (AU)