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SIRT7 - villain or key to longevity?

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I am following up on a previous post in which a study indicating the possibility of heart damage with a ketogenic diet was mentioned. The result of the search for the cause was the finding that the ketogenic diet reduces the activity of histone deacetylase 2 (HDAC2), which controls the deacetylase SIRT7. So SIRT7 is activated, which is supposed to be the problem. I did some googling and found that SIRT7 activation seems to be generally very good.  For example, it suppresses (pseudo)hypoxia, i.e. chronic inflammation .  I found a number of studies that consider the activation of SIRT7 to be very beneficial, they are looking for different drugs that would activate SIRT7, but they do not tell us that it is β-hydroxybutyrate or even the short-chain fatty acids acetate/vinegar and butyrate that activate SIRT7 through HDAC2 suppression. All these substances are considered very beneficial. So we have a rather fundamental contradiction here. Does SIRT7 activation have positive or negative ef
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Does the ketogenic diet destroy the heart?

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The ketogenic diet is based on the strict restriction of carbohydrates in the diet, quite popular now. There are groups of people in the world who strongly promote the ketogenic diet as a cure for obesity, type 2 diabetes and other diseases. The very first known and documented therapeutic use of the ketogenic diet is for childhood epilepsy. Since then, the number of diagnoses suitable for the application of a ketogenic diet has greatly expanded. Therefore, it is highly desirable to investigate how the composition of fats affects the effectiveness, but mainly the safety, of this diet. The main component of the ketogenic diet is fat. And there are many different types of fats from different sources. Some can harm, others help. A ketogenic low-carbohydrate diet reduces body weight, MCT oils reduce the amount of adipose tissue, thus preserving more lean tissue. Recently, a number of studies have been published showing the potential danger of heart damage on the ketogenic diet. Let's lo
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What do lactate and fish oil have in common? They suppress obesity! Why?

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Lactate is a product of glucose fermentation, usually thought to cause muscle fatigue and problems, but probably not at all. Fish oil is known for containing a large amount of omega-3 fats, we will mainly be interested in the longest omega-3, i.e. DHA. What could these two substances have in common, that they suppress the development of obesity. Attention! Let's distinguish suppressing of obesity development from treatment, i.e. let's distinguish prevention of obesity from elimination of already existing obesity, these are two completely different disciplines ! Let's first look at the study with fish oil, i.e. with DHA . Here we have a mouse model study that includes four types of high fat diet. Control low-fat (Con, 10% fat), high-fat diet with lard (HFD, 60% fat), high-fat diet with lard and safflower oil (SO, 30%+30%), high-fat diet with lard and safflower oil and fish oil (SF , 30%+15%+15%), and finally a fatty diet with lard and fish oil (FO, 30%+30%). Fish oil (SF, FO
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How to increase the feeling of satiety and lose weight (theoretically)?

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I can't help myself, I have to theorize. In the previous post , we saw how easy it is to get fat, i.e. in the rat model. We also saw how to achieve weight loss again, feel free to take a look. It all follows from the fact that if we frequently change the macrobiotic ratios of the diet, i.e. the ratio of long-chain fats in relation to carbohydrates plus proteins together, the body cannot respond to the changes and derives the feeling of satiety from how quickly it fills the liver's glycogen reserves.  During the entire period of adaptation to the new food composition, the body will overeat.  The speed of adaptation of the metabolism to the new composition of the diet depends on the amount of short and medium fats in the food. The more of them the consumed fat contains, the faster the adaptation will take place. The lower will be the risk of overloading fat cells  (or rather their poisoning with endotoxin LPS from the digestive system )  and their probability of switching to pseu
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Who will tell us that we have eaten enough food?

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How is food consumption controlled? You may think that our will decides this. Perhaps, sometimes. But animals probably have no such will and yet know when they have had enough and how much to eat. They know better than we do! That's a surprise. So how do they know when they've had enough to eat or not yet?   I haven't delved too much into this issue yet , so it might not be as well thought out as it should be. But it doesn't matter, it has to start somehow. What led me to this problem is this picture from a study on laboratory rats and also an excellent blog written by Peter . We are seeing several step changes in their diet. First, at the very beginning, a change from a standard rat diet to a high-fat, human-like western diet. We first see an interesting transitional event there, when fats are not a food for rats, which would relieve them of hunger. They cannot oxidize them for energy. Only over time will they learn to process them and can therefore gradually reduce e
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Do AMPK phosphorylation and ATP level control vascular calcification?

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The strengthening and hardening of soft tissues by calcification is a very interesting phenomenon. The same process takes place in the strengthening of bones, but is usually undesirable in the case of soft tissues. Actually, it is not calcium as such at all, but calcium phosphate ( hydroxyapatite, HA, Ca10(PO4)6(OH)2 ), which strengthens soft tissues. It is the very same material that is missing from the bones in osteoporosis, while it builds up and damages the soft tissues. The driving force of calcification is therefore not calcium at all, but phosphorus, or inorganic phosphate (Pi). And to make it not so simple, it depends on its form. Inorganic phosphate (Pi) accelerates calcification, inorganic pyrophosphate (PPi) protects against calcification. The difference or ratio between the levels of these two forms of inorganic phosphorus is stabilized and balanced by a group of enzymes called alkaline phosphatases (ALP/TNAP). These break down the pyrophosphate into two phosphate molecules
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