However, it is logical that a "similar statement, without any explanation, could be misleading, especially to all those who do not have the necessary knowledge to understand the topic."
From one extreme to the other, there are many who misunderstand this "new mantra" and or use it as an excuse to promote yet another alternative nutritional system.
In this article we will try to understand what it means that fats burn on the fire of carbohydrates but above all how this concept would affect the slimming process.
However, we anticipate that the "only slimming method recognized as" correct "is the balanced one, that is, that respects all the trappings of the case. ", we specify that: with the same calories, all the breakdowns of energy macronutrients (carbohydrates, proteins and fats) offer more or less the same results; what matters is the caloric balance, which must obviously be negative.
However, there are significant differences in terms of applicability and athletic performance, especially in the performance of endurance sports, in the preservation of lean mass in those of strength and in bodybuilding etc.
But what does it really mean that fats burn on the fire of carbohydrates? Simply that, biochemically speaking, the cellular oxidation of fatty acids cannot do without glucose. However, we must not overlook some details which we will not fail to explain as clearly as possible below.
For further information: Ketogenic Diet (ATP), which we could define as the "only true container and distributor of" pure energy ".
In fact, each separation of a phosphate from adenosine (ATP-> ADP, by hydrolysis of the enzyme ATPase) results in a significant release of energy, a reaction exploited for all the cellular processes of the organism. Therefore, regardless of the type of substrate and by metabolic route, albeit in a slightly different way (so to speak of course), the ultimate goal of energy production is always the recharge of ATP (ADP-> ATP)
But how is the ATP recharged? The road is long but, since we started from the end, we will retrace everything in reverse.
you depend). On the other hand, for this to happen, the electron transport chain or respiratory chain must first be completed.NADH and FADH2, enzymes enriched with H + during the Krebs cycle (which we will see below), electrons are discharged thanks to the so-called cytochromes. After the oxidation of NADH and FADH2 to NAD + and FAD, these conduct and release electrons to specific enzymes, capable of pumping the residual H + ions across the membrane and generating a proton gradient. The reentry of these ions is regulated by the enzyme itself. ATP synthase which exploits its electrochemical potential for recharging the ADP.
and oxaloacetate cycle, is an essential step in energy production in the presence of oxygen. In addition to synthesizing the elements necessary for oxidative phosphorylation (NAD + and FAD -> NADH and FADH2), it also participates in other fundamental processes for the cell.
Note: this is called a "cycle" because it does not actually have a beginning and an end but should continue perpetually.
The main substrate of the Krebs cycle is acetyl-CoA (acyl group + Coenzyme A), which in turn derives from anaerobic glycolysis (glucose catabolism) and beta-oxidation of fatty acids. We recommend that you pay close attention to this. passage, because it is essential to the understanding of the subject matter.
The entry of Acetyl-CoA into the Krebs cycle occurs through its condensation with oxaloacetate, generating citrate.
ATTENTION! Oxaloacetate is a molecule that can be produced exclusively from glucose; its lack jeopardizes the condensation of Acetyl-CoA to citrate, therefore the entry into the Krebs cycle, and determines the accumulation of Acetyl-CoA. The union of two Acetyl-CoA gives rise to a ketone body.
At the end of the cycle itself, the two carbon atoms released by the acetyl-CoA will be oxidized into two CO2 molecules, regenerating again oxaloacetate capable of condensing with acetyl-CoA.
In energy terms, what happens is the generation of a molecule of guanosine triphosphate (GTP) - used to immediately recharge an ADP into ATP) - three molecules of NADH and one of FADH2 (initially NAD + and FAD). As we have seen above, these act as transport of electrons until their oxidation and transfer of the same to the cytochromes that will allow the functioning of the ATP synthase.
We then come to the production of Acetyl-CoA.
, intermediate of anaerobic glycolysis. In the mitochondrion, thanks to the multi-enzyme complex of pyruvate dehydrogenase, this is converted into acetyl-CoA.The synthesis of acetyl-CoA can also occur from fatty acids. These, activated in the cellular cytoplasm (by binding with a molecule of Coenzyme A, forming the acyl-CoA complex), then enter the mitochondrial matrix thanks to the "action of L-carnitine. Thus begin the beta oxidation which will have the final result l" acetyl-CoA.
Protein amino acids (AAs) can also be used for the production of acetyl-CoA; acetyl CoA is obtained directly by deamination of the ketogenic AAs, while intermediates of the Krebs cycle are obtained from the glucogenic AAs.
in the liver and muscles. Its lack is compensated, at least in part - it depends on the severity of the nutritional deficiency and the level of physical activity - by neoglucogenesis, a hepatic process that uses glycerol, lactic acid and glucogenic amino acids to obtain glucose. For this reason, despite a low intake of total carbohydrates, many high-protein diets do not allow the condition of ketosis to be established (only insufficient levels of oxaloacetate can be reached). However, nitrogen residues are very high and this imposes an increase in the workload for the liver and kidneys; in the healthy subject, this hardly causes pathologies proper, but it is however not recommended to maintain these diets for too long.The absence of oxaloacetate determines the accumulation of Acetyl-CoA which the cells remedy with the synthesis of ketone bodies. Fortunately, ketone bodies can also be used for energy purposes and any excess in the healthy organism is compensated by urinary excretion, sweat and pulmonary ventilation. This does not mean that the body functions at full capacity, especially in the presence of considerable motor activity.
Moreover, even if these undoubtedly determine a partial suppression of appetite - see the article on the ketogenic diet - this benefit is nullified by the side effect of reducing the cellular use of fatty acids.
On the other hand, in sick subjects, such as type 1 diabetics, kidney or liver failure, etc., the onset of severe pathological keto-acidosis is likely.
To learn more: Exogenous Ketones for Weight Loss: Do They Work?
