Who will tell us that we have eaten enough food? (2)

I have a free continuation of my thoughts on how food intake is controlled in animals, and I assume that the same mechanism will work similarly in humans. If you haven't read it yet, I recommend it here and here. I have a feeling that we have not yet fully exploited the possibilities offered by the use of glucose as a dietary supplement. This is probably because it is glucose that increases insulin in the blood, and therefore, it is the main culprit that we must avoid. Really? Well, that is, of course, true if we undergo, for example, an oral glucose tolerance test (OGTT). Then yes, the culprit will be fully manifested here. But that is not what I mean. We already know that the main negative factor is the rate of intake. We know this from Dr. Richard Johnson and others. It is enough to finely grind or dissolve carbohydrates and mice will start to gain weight on their standard diet, just as they do on a human high-fat diet. So the speed of flooding the liver is decisive.

How not to overeat? Excess proteins (amino acids) will adequately reduce food intake. Excess carbohydrates (glucose) and fats (lipids) will not.

While searching the internet, I happened to come across a study on rats, where scientists investigated how a separate infusion of glucose, amino acids, or fats would affect appetite and overall caloric intake.

Do rats know that they have added calories to their system through another route, directly into the blood? Yes, they do, but not for all food components in the same way. Let's take a look, but first I'll repeat my hypothesis from the first post about who tells us that we've eaten enough. The principle I formulated there is that during the active phase of the day, we try to fill our liver glycogen (stored carbohydrates) to a certain level so that we feel well-fed for the period of resting when we go to bed. The level of filling of liver glycogen stores, therefore, determines how many calories we have to eat during the day. If something is being stored elsewhere, it means that we need to eat more calories. It's probably as simple as that.

Proteins do not cause overeating, and the quality of compensation of the infusion by reducing food intake is striking.

Look at the results of the study. The most interesting result is the amino acid supplementation. Do you see the precision with which the additional intravenous calorie intake is compensated by reducing food intake? Why so precise? Excess amino acids are apparently immediately converted to glucose in the liver and stored directly in glycogen. The process is slow enough for everything to be stored in liver glycogen and not stored anywhere else. 

Not so with intravenous glucose. It is also stored in muscle glycogen, which is not counted! So glucose is only compensated for about half. What about fats? They are stored outside the liver in adipose tissue, and on the first day, they are not counted at all! This exactly corresponds to my hypothesis. First, hepatic de novo lipogenesis (DNL), i.e. the conversion of glucose into fat in the liver, must be reduced so that the glucose that is not used up as fat can be stored in glycogen. However, this takes time, several days, and even then the compensation is not perfect. The precision of all these processes is astonishing. Why has no one thought of it yet? I am not aware of any similar explanation, anything comparable, a calculation of the intake of food needed to satisfy hunger, anywhere in any work.

Glucose infusion is compensated by reducing food intake by only about half.

Fat infusion does not reduce food intake immediately but gradually, as de novo lipogenesis decreases and more glucose is available in the liver for glycogen formation.

Let's now return to glucose/dextrose as a food supplement. I have a hypothesis that if we were to supplement a little bit of glucose evenly throughout the day, we would increase the amount of liver glycogen. The problem is again in the rate, this time in the rate of glycogen formation in the liver. A large amount of carbohydrates in one meal will not adequately increase the amount of liver glycogen, the glucose will overflow from the liver to the whole body and be stored elsewhere. But slow, systematic support for glycogen formation with slightly increased glucose levels throughout the day? Wait, we would actually support a mechanism that the body probably uses itself. It forces us to eat, that is, eat more glucose or proteins, which we do not understand and we also take in more sugar/fructose and fats, which then cannot be burned for energy. Glucose, for example, in coffee or water, could reduce feelings of hunger and reduce caloric intake, it goes directly to the liver through the portal vein. And unlike regular sugar/fructose, glucose does not block fat burning in any way, the missing energy could easily be replenished from fat stores. Isn't that a paradox? Maybe glucose as a food supplement will eventually be the solution to obesity.


Addition

I get asked quite often how hunger is suppressed on a ketogenic diet. How is it possible for people to go a long time without food and how does the body know when it has had enough.

The principle is actually simple, if you switch to a low-carb or ketogenic diet, every cell in your body, if it can, tries to get energy from burning fat or ketones. There are cells that can't do this, they have to process glucose (e.g. red blood cells or some brain cells), but other cells "go" to fat. This will significantly reduce the need for glucose obtained from liver glycogen. It is not depleted as quickly and the body feels safe, feelings of hunger do not arise. However, this is conditional on sufficient fat burning. If you somehow prevent it, for example with fructose, which suppresses CPT1A, fats will not get into the mitochondria, you'll reduce your glycogen stores and you will soon get very hungry.

On a ketogenic or low-carb diet, it is advisable for fats to contain enough short- and medium-chain fatty acids as a direct source of energy. This will avoid a decrease in metabolic rate, and the body will not start to conserve energy. Short- and medium-chain fats support thermogenesis and the waste of energy from food, thus supporting weight loss, are significantly ketogenic and essentially replace glucose in the combustion process. However, they cannot create liver glycogen, for this purpose glucose from the diet or created by gluconeogenesis (GNG) from glycerol, lactate or proteins is needed. Here it is necessary to be careful that in obese people, protein metabolism is often switched to the formation of fats, so glycogen is not created and proteins then do not reduce hunger. In such a case, a low-protein diet can help.

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References:

Differential effects of intravenous glucose, amino acids, and lipid on daily food intake in rats

Diet-induced obesity in ad libitum-fed mice: food texture overrides the effect of macronutrient composition


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