MCT for Health

In the  previous post , I showed you a mouse study that clearly shows that turning on pseudohypoxia, that is, activating the transcription factor HIF-1α in adipose tissue, triggers obesity and other metabolic problems. I have shown that one of the main triggers is the accumulation of succinic acid (succinate), one of the intermediates of the TCA cycle. If there are any problems with the TCA cycle (obtaining energy through oxidation), succinate builds up and triggers the HIF-1α rescue mechanism , fat cells get bigger and stop working properly. So the question is how to prevent this? How to reduce the risk of succinate accumulation? How to ensure stable and sufficient breakdown of succinate, i.e. the activity of succinate dehydrogenase (SDH)? Succinate content increases with increasing omega fat oxidation in peroxisomes (here added dicarboxylic acid DCA12). One of the main sources of succinate during fasting, i.e. between meals, are organelles called peroxisomes. They are bound directly

O mega oxidation of fat, what is it? You've probably never heard of this term before, in fact I think most professionals either don't know the term or have long since dismissed it as irrelevant information. I will try to explain here why I think that omega oxidation, or the insufficient activation of this metabolic process, is the root cause of civilizational diseases, including cancer. But let's start slowly. In one of the previous posts , I explained the activity of the fat cell. As long as it is not overloaded with excess fuel, free fatty acids (FFA / NEFA) or glucose, the cell works normally. If there is more fuel, it is stored as fat, if there is not enough, it releases fat into the bloodstream. Very useful activity. But studies on mice show us that if we give them a high-fat diet instead of a standard chow diet, the mice will get fat and become obese. Their fat cells will grow in size (left image), stop working properly, start to signal inflammation and releasing ex

I will try to follow up on several previous posts, because, as you may have already understood, inducing pseudohypoxia under conditions of relative sufficient oxygen fundamentally affects the metabolism of the cell and thus the entire organism. The main control element, the shift lever, is the presence of the transcription factor HIF-1α, which, through the control of HIF-1, turns hundreds of genes on and off to adjust the metabolism according to the current conditions. Stabilization of HIF-1α can be caused, for example, by an increased level of H2O2 or succinate (my notes in green). The termination of the T-shaped line indicates the suppression of the reaction and thus the stabilization of HIF-1α. We have also already recognized that it is not our enemy, but a helping hand. It appears whenever the cell has some problems. It typically occurs when there is a lack of oxygen, but not only that. It also occurs when there is an excess of fuel, i.e. an excess of glucose, fats, pyruvate, Acety