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We would like to emphasize that ketosis is a completely physiological mechanism and it was the biochemist Hans Krebs who first referred to physiological ketosis to differentiate it from the pathological keto acidosis seen in type 1 diabetes.
In physiological ketosis (which occurs during very-low-calorie ketogenic diets), ketonemia reaches maximum levels of 7/8 mmol/l (it does not go higher precisely because the CNS efficiently uses these molecules for energy in place of glucose) and with no change in p H, whereas in uncontrolled diabetic ketoacidosis it can exceed 20 mmol/l with a concomitant lowering of blood p HThere is no doubt that there is strong supportive evidence that the use of ketogenic diets in weight-loss therapy is effective; however, there are contrasting theories regarding the mechanisms through which they work.
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).
The CNS cannot use fat as an energy source; hence, it normally utilizes glucose.
After 3–4 days without carbohydrate consumption the CNS is ‘forced’ to find alternative energy sources, and as demonstrated by the classic experiments of Cahill and colleagues this alternative energy source is derived from the overproduction of acetyl coenzyme A (Co A).
This condition seen in prolonged fasting, type 1 diabetes and high-fat/low-carbohydrate diets leads to the production of higher-than-normal levels of so-called ketone bodies (KBs), that is, acetoacetate, β-hydroxybutyric acid and acetone—a process called ketogenesis and which occurs principally in the mitochondrial matrix in the liver.
This review revisits the meaning of physiological ketosis in the light of this evidence and considers possible mechanisms for the therapeutic actions of the ketogenic diet on different diseases.
The present review also questions whether there are still some preconceived ideas about ketogenic diets, which may be presenting unnecessary barriers to their use as therapeutic tools in the physician’s hand.
Despite this, there is no direct experimental evidence to support this intriguing hypothesis; on the contrary, a recent study reported that there were no changes in resting energy expenditure after a VLCKD.
The main KB produced in the liver is acetoacetate but the primary circulating ketone is β-hydroxybutyrate although the latter is not, strictly speaking, a KB because the ketone moiety has been reduced to a hydroxyl group.
Under normal conditions of adequate dietary carbohydrate, the production of free acetoacetic acid is negligible and it is rapidly metabolized by various tissues, especially the skeletal and heart muscles.
through a pathway that leads to formation from β-hydroxybutyrate of two molecules of acetyl Co A, which are used finally in the Krebs cycle.
It is interesting to note that the KBs are able to produce more energy compared with glucose because of the metabolic effects of ketosis—the high chemical potential of 3-β-hydroxybutyrate leads to an increase in the ΔG A further point to underline is, as shown in Table 1, that glycaemia, even though reduced, remains within physiological levels because of the fact that glucose is formed from two sources: from glucogenic amino acids and from glycerol liberated via lysis from triglycerides.