How does a ketogenic diet actually work, ie how does 'eating fat burn fat'?

(mole person) #21

Thank you! I appreciate it. I’ll comment after I read both.

(Edith) #22

This link may work better:

(Michael - When reality fails to meet expectations, the problem is not reality.) #23

Would someone please translate this into English. Thank you. :flushed:

(mole person) #24

I’ve looked over both those links and neither even makes the claim you are espousing that lipogenesis in adipocytes is entirely on hold as long as liver and muscle glycogen stores are not full.

(Ken) #25

How about this paragraph?

Once the storage limits are reached in the liver and muscle, your glycogen “tank” is full and no more glycogen can be stored there. When the glycogen tanks are full, the cells of your liver and muscles put up a “stop sign” to insulin. They do this by “downgrading” or desensitizing the insulin receptors on their cellular surface. Since the insulin signal is being ignored, unstored glucose starts to build up in the bloodstream, and more and more insulin must be secreted to move the glucose into the cells. Insulin levels climb very high, and you become insulin resistant. Your liver then sends the excess glucose to your fat cells to be stored as body fat. (The liver can also make the glucose into LDL cholesterol, which is why a high sugar diet is detrimental to heart health).

(mole person) #26

No, I’m sorry. Nowhere there does it say the following:

That all “excess glucose converts to Glycogen” and “only when levels are full and receptors downgrade do you get the conversion of excess to fat storage.”

Your link is talking about what happens at the liver and muscles but not what happens at the adipocytes. When insulin increases adipocytes take up glucose and fatty acids. Your claim is that they won’t when liver and muscle glycogen are depleted at all. I’ve yet to see evidence for this claim.

(Ken) #27

A quick answer. We’re essentially talking about at what point does the body switch over to storing carbs as fat. It’s important because that is key to understanding carb intake during Maintenance, as well as being able to consume some periodic carbs for metabolic purposes.

It’s my assertion that fat storage does not begin until liver glycogen is full, with additional glucose then being converted to fat. That means if you don’t eat enough carbs chronically for that to happen you never regain fat. It’s worked for me for over 15 years now.

The other view is that when we eat carbs the fat cells are able to grab glucose from the bloodstream and add fat, no matter what the glycogen levels are. That means perpetually having to eat carbs at Keto levels in order not to regain fat.

If you think about Keto backwards it makes sense, if you have to deplete glycogen to burn fat, you should have to refill it to store fat.

(Ken) #28

I think you’re stretching it a bit, and I’m not sure why. That paragraph is pretty clear and uses fairly simple language. Glycogen creation is a priority for excess glucose, much like preferentially burning carbs instead of fat. Really, the prioritization of insulin production. If the body has the ability to grab glucose and add fat at any time then why is the 20g level used? It should be zero. The reason is to deplete glucose, start glucagon secretion which enables glycogen depletion (glycogenolysis) and subsequent lipolysis. Lipogenesis is essentially the reverse of this process.

The trigger, mentioned in the paragraph, is high insulin levels. When the liver and muscles.are.“open for business” to store glycogen, insulin levels are not able to climb high enough to trigger fat storage. Once closed, insulin levels rise and the the glucose has no where else to go.

Here’s an interesting deviation regarding the Obese, but it’s more of a personal anecdote. When I was obese and essentially was without a leptin response, I probably gained fat at a higher rate when I was the heaviest. I simply could not stop eating. Whenever I cut back I would have the most terrible feelng after a day, which I know know was happening as I depleted dietary glucose as I went towards glucagon secretion and glycogenolysis. My body was demanding that I kept dietary glucose and the massive hyperinsulinemic secretions high, leading to perpetual fat gain.

Ya gotta have glycogen for that “Flight or Fight” response, so you beat the Wolf Pack to the trees. Or be able to kill that guy trying to take your Mate away.

(bulkbiker) #29

So you are actually arguing about the level of carbs you can eat before fat storage begins?
Or as an alternative …why bother to eat carbs and risk it at all ?

(Ken) #30

There is no risk at all, as long as you don’t fill up your glycogen. Eating limited carbs is a normal part of Human Evolution. The real point is is the Science, so people are not fed false information and can understand Maintenance is not really very restricted as far as food choices, just the types, amounts, and frequency of carb intake.

People can eat what they want, as long as they have actual information, not someone else’s false belief.

(Michael - When reality fails to meet expectations, the problem is not reality.) #31
(mole person) #32

I think it’s you that’s stretching. I agree the paragraph is clear. But all it’s telling us is something that we all already knew. That the liver, when depleted of glycogen, takes up glucose and that it stops doing so when it has reached its capacity.

The claim that you keep making, that I’ve yet to see any support for, is that when glycogen at the liver is not full then the adipocytes systemically, throughout the body, stop storing fatty acids and stop lipogenesis entirely.

We have glucose in our blood. If we eat an ice cream that blood glucose shoots up whether or not our liver is topped up to maximum glycogen. When insulin rises cells take up glucose and fatty acids, including the fat cells. Your claim is that this isn’t happening at the fat cells when liver glycogen is depleted. What’s the mechanism for stopping it? What’s happening at the adipocytes that makes them shut down storage completely as you repeatedly suggest on these forums?

Again, this is a surprising claim. Insulin cannot get high enough for fat storage as long as glycogen is not at capacity at muscles and liver? This sounds like a recipe for a hyperglycemic coma if I sit down to even an ice cream. Where is the evidence for this???

(Ken) #33

When the liver is saturated with glycogen, any additional glucose taken up by hepatocytes is shunted into pathways leading to synthesis of fatty acids, which are exported from the liver as lipoproteins. The lipoproteins are ripped apart in the circulation, providing free fatty acids for use in other tissues, including adipocytes, which use them to synthesize triglyceride.

(Not my words, a cut and paste)

Notice where the lipoproteins come from? Fat cells do not just “Grab” glucose from the bloodstream, although I have seen that assertion from various Gurus out there. Overall knowledge of the real role of glycogen is really lacking in the nutritional world.

I have yet to experience a hyperglycemic coma.

(Bacon is a many-splendoured thing) #34

Interesting. Your link to Ketogenic Diet Resource, in your follow-on post, doesn’t differ materially from anything I’ve posted, so I’m not sure how you think my understanding of lipogenesis differs from theirs, which you have presumably posted to enhance everyone’s understanding. (The one aspect that neither that article, nor what I’ve posted in this thread, has dealt with is the issue of de novo lipogenesis in the liver as a response to ethanol and fructose intake. I ignored it in the context of glucose storage, but it is relevant in the context of the metabolic healing promoted by a well-formulated ketogenic diet.)

My original post, with which you seemed to take issue, was merely to suggest that the storage of glucose in adipose doesn’t necessarily wait for the muscles to finish building up their glycogen stores. I don’t see how that could be controversial. Is there some mechanism you know of, by which muscle signals to adipose to wait before taking up serum glucose?

The artcile by Kreitzman et al. is very interesting, but I wish they had waited to examine their subjects till after they had keto-adapted. Four days on a very low carbohydrate diet is not very long. That would have provided more information, I suspect—information which might be more useful to people on the Ketogenic Forums. I’d also be curious to learn more about the different rates of glycogen depletion in muscle and liver. I’d actually have expected muscle to deplete sooner than liver. Do you have any references?

Apparently, this is indeed true in the case of skeletal muscle, and is one of the reasons that muscles become insulin-resistant. According to Robert Lustig, however, the liver has an essentially unlimited capacity for glycogen, and is not harmed by storing large quantities. What makes the liver insulin-resistant is apparently the quantity of fat it is storing, as a result of de novo lipogenesis. This is why fatty liver disease, whether of the alcoholic or the non-alcoholic variety, is so serious.

(Bacon is a many-splendoured thing) #35

They measured the responses of athletes to being fed carbohydrate after exercise, and observed enhanced energy efficiency during the next exercise period. They seem to have been very thorough in the various measurements they took.

This is a fascinating study, and if I were a carbohydrate-adapted athlete, I’d take it very seriously. Unfortunately, the diet of the study’s subjects is not discussed, and it appears unlikely that any of them were keto-adapted.

(mole person) #36

**My emphasis

You keep making claims about what is happening at the adipocytes but then when asked for evidence you point to what’s going on at the liver. We all know this stuff. Fatty acids don’t have to go through the liver at all. They can go straight from the intestines into the bloodstream, packaged as chylomicron lipoproteins, for take up at the fat cells and muscles.

Again lipoproteins made at the liver are not the only source of fatty acids in the blood.

“Chylomicrons transport lipids absorbed from the intestine to adipose, cardiac, and skeletal muscle tissue, where their triglyceride components are hydrolyzed by the activity of the lipoprotein lipase, allowing the released free fatty acids to be absorbed by the tissues. When a large portion of the triacylglycerol core have been hydrolyzed, chylomicron remnants are formed and are taken up by the liver, thereby also transferring dietary fat to the liver.”

“The lymphatic vessels carry the chyle to the venous return of the systemic circulation. From there the chylomicrons supply the tissue with fat absorbed from the diet. Thus, unlike the saccharides and amino acids that digestion liberates from the carbohydrates and proteins of the diet (respectively), the lipids from the diet bypass the hepatic portal system, meaning the liver does not get “first crack” at them.”

**My emphasis

Lol…yes. my point was that if our bodies worked as you think than you would have.

(Ken) #37

Hmmmm. I let this sit for awhile to see if anyone would add any additional information.you’ve pivoted away from what I’ve been talking about and gone off on a tangent about dietary fat intake. Sure, it’s easy to gain fat when eating a carb-fat pattern which causes a.synergistically increased insulin response. Of course the fatty acids come right from the digestive tract. But, that’s not what I’ve been talking about. I’ve been talking about the need to fill liver glycogen via carbohydrate intake in order to enable Lipogenesis. (From additional carb intake continuing a lipogenic hormonal secretion pattern)

I’ve been talking about this within the context of a VLCHF pattern, asserting that you can eat periodic carbs with no worries about fat.regain as long as glycogen is not overcompensated. It would not surprise me if eating carb-fat combinations could possibly lead to fat gain before total glycogen recompensation. But, that is not the issue.