After a few days of fasting, or of drastically reduced carbohydrate consumption (below 50 g / day), glucose reserves become insufficient both for normal fat oxidation via the supply
of oxaloacetate in the Krebs cycle (which gave origin to the phrase «fat burns in the flame of carbohydrate») and for the supply of glucose to the central nervous system (CNS).4
As I mentioned in the Definitive Guide, dietary protein, along with glucose, is a source
of oxaloacetate.
It's the absence
of oxaloacetate that inhibits ATP generation via Krebs» cycle and necessitates ketone production.
Not exact matches
This pathway allows glutamine to be converted into a variety
of metabolic intermediates such as aspartate, asparagine, citrate and
oxaloacetate and pyruvate [103].
Upstream ORFs and ATF4 - binding sites are found in many genes, but for the purposes
of this review genes that carry out biosynthesis
of non-essential amino acids (ASNS, alanine aminotransferase 2, PSAT, serine hydroxymethyltransferase 2, pyrroline -5-carboxylate reductase and glutamate -
oxaloacetate transaminase) and genes encoding amino acid transporters (cat1, ASCT1, ASCT2, SNAT2, SNAT7, LAT1, EAAT5 and xCT) are notably abundant [83,120].
Since
oxaloacetate is formed from pyruvate (a metabolite
of glucose), a certain level
of carbohydrate is required in order to burn fats.
Ketones are produced when there is no longer enough
oxaloacetate in the mitochondria
of cells to condense with acetyl CoA formed from fatty acids.
But if you look at the recent data on utilising ketones during exercise, giving a small supply
of glucose provides some substrate for anapleurosis (i.e. regenerating
oxaloacetate) to allow you to use the Acetyl - CoA coming from ketones or beta - oxidation
of fats.