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So in theory, insulin hormone is the one that tells the body "eat more. don't burn body fat". Alongside with glucose blood level regulation and turning excessive glucose into liver (which later goes into muscles as glycogen or into fat cells). Fats are the only thing that do not provoke insulin secretion. 0 glycemic index.

So in theory, if I eat 2 or 3 times more worth the energy I spend during the day, I'll never store body fat because of 0 glycemic index?

Or will I still gain because such huge fat intake will make liver into making glucose from fats & proteins?

Surely u'll never find a sustainable product to eat that is 100% fat, but just a few examples are butter, lard, heavy cream. This is just a theoretical question, where the proteins/carbs intake is so low that it is not count.

Could you please clarify it since I got lost.

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    $\begingroup$ Interesting question! I would guess adipose fatty uptake and esterification would increase with higher fat ingestion, regardless of insulin levels, simply because there is more fat around. The body cannot make glucose from fat, so fat accumulation via glucose is not a possible. (Which is also a reason why such a diet would be lethal.) $\endgroup$ – Roland Jun 14 '15 at 7:58
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    $\begingroup$ @Roland how come it can't? It can. en.wikipedia.org/wiki/Gluconeogenesis $\endgroup$ – knitevision Jun 14 '15 at 8:05
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    $\begingroup$ Gluconeogensis from fat doesn't work due to stoichiometric problems. With only acetyl-CoA from fatty acids, the TCA cycle cannot function, because oxaloacetate used for gluconeogenesis cannot be replenished. Organisms that can turn fat to sugar use something called the glyoxylate cycle, which doesn't exist in humans. See any major biochemistry textbook, like Stryer's. $\endgroup$ – Roland Jun 14 '15 at 8:22
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    $\begingroup$ As for "lethality". 80% energy from fat (which sounds like a lot to me) corresponds to 65% fat in your diet (by weight). So you are still taking in 35% carbs and protein. Your hypothetical 100% fat diet would be more like drinking oil and eating nothing else. $\endgroup$ – Roland Jun 14 '15 at 8:55
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    $\begingroup$ Agree with @Roland - any basic biochemistry textbook (i.e. Stryer) will tell you that you can't make sugar from fat. That is, you can't make glucose from fatty acids because the reaction catalyzed by pyruvate dehydrogenase is irreversible. When someone goes on a high fat diet (i.e. Atkins diet), they force themselves to become ketotic - which means the body begins making a significant amount of ketone bodies from the breakdown of fatty acids. The body is trying to 'hold on' to its glucose reserves by burning ketone bodies, which can cross the blood brain barrier for brain energy metabolism. $\endgroup$ – Vance L Albaugh Jun 20 '15 at 19:58
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There are a couple of reasons why this approach doesn't work quite as well as you might hope.

First, insulin doesn't go away after a high-fat meal. This paper reports changes in serum insulin following pure-sugar and pure-fat meals. Although there is much less of an increase in insulin following the pure-fat versus the pure-sugar meal, you will notice in Figure 1 that the insulin levels following the pure-fat meals (panel A) are higher than the levels during a fast (panel B). So even if high insulin were the only signal for fat storage, your dream of eliminating insulin with a high-fat meal is not realistic.

Second, when a high-fat diet is designed for medical purposes, a good deal of care is required to avoid significant potential adverse effects. Adequate protein intake is still required, and amino acids from the protein can be converted to glucose. Furthermore, ketoacids are produced when fatty acids from ingested fat are in excess. (As noted in comments, humans do not convert fatty acids to glucose.) Although ketoacids can be excreted in the urine (admittedly, heading toward your goal of not storing all the calories you consume), the net metabolic effect on the body when you excrete ketoacids is increased acidification, which in turn can lead to difficulties with potassium regulation and thus, in severe cases, with heart function. In the extreme if this were continued for a long time, you may face a problem of life-threatening ketoacidosis as occurs in type-1 diabetics (low/no insulin) whose disease is not being managed.

That said, your basic idea is similar to the arguments for low-carbohydrate diets. How well they work and, if they do, through what mechanisms are still somewhat controversial, as I understand. Insofar as they work through excreting some of the ingested fat through urinary loss of ketoacids, however, the associated risks need to be considered.

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