Can ketones be stored?

#1

I just want to get this right. So this is my question: can ketones be stored for energy or is any surplus eliminated through the urine? I ask because this would mean that eating an excess of fats would not be stored in the body- and we would not gain weight. Sugars on the other hand are transformed to fat reserves by insulin. So glucose can be transformed to stored fat whereas ingesting fats themselves will create ketones for energy and any excess will be removed from the body?

(Bunny) #2

Excess dietary fat will be stored as fat[2] in the fatty acid turnover pool[1] i.e. in adipose tissue.

Ketones are oxidized fatty acids, lipids stored in adipose tissue or dietary fats[6][7].

Excess glucose is not always stored as fat, the bigger your skeletal muscle volume is, to adipose tissue or subcontaneous adipose tissue (s.c.) ratio is? Will translate into more mitochondria in skeletal muscle fibers which will oxidize (aminoisobutyric acid - BAIBA[3][4]/CPT-1[5]) excess glucose[3][4] (dietary carbohydrates) rather than storing it as fat or a lipid droplet within the adipose cell.

References:

[1] ”…For regular dietary fats, once they are digested, they enter the circulation and participate in what is called ‘fatty acid turnover.’ Whether fed or fasted, the body is always releasing, burning, and storing fat. When insulin is high, storage predominates, but turnover continues. When insulin is low, release and oxidation predominate. If you eat fat along with a lot of carbohydrates, it is prone to be stored. When fat is consumed in the context of a well formulated ketogenic diet, it—along with fat released from adipose stores—is prone to be burned. But once digested and absorbed, dietary fat and stored fat enter the ‘turnover pool’ and are in a constant state of mixing. …” …More

[2] “…The capacity to store lipid within the s.c. (SUBCUTANEOUS) tissue is the key to facing famine and limited caloric supply on the one hand and to handling excess calories on the other. In cases where s.c. fat reaches a threshold beyond which it can store no more, lipids may be shunted to other depots. In that scenario, lipids may be stored in less advantageous compartments such as the intra-abdominal (visceral) compartment, and in insulin-sensitive tissues that are prone to deposition of lipid in specific clinical scenarios. This may cause deposition of lipid within skeletal muscle and the liver, affecting their normal metabolic pathways. …” …More

[3] “…BAIBA increases the expression of brown adipocyte-specific genes in white adipocytes and β-oxidation in hepatocytes both in vitro and in vivo through a PPARα-mediated mechanism, induces a brown adipose-like phenotype in human pluripotent stem cells, and improves glucose homeostasis in mice. …” …More

[4] “…In this review, we discuss the metabolic roles of the recently discovered myokine β-aminoisobutyric acid (BAIBA), which is produced by skeletal muscle during physical activity. In addition to physical activity, the circulating levels of BAIBA are controlled by the mitochondrial enzyme alanine: glyoxylate aminotransferase 2 (AGXT2), which is primarily expressed in the liver and kidneys. Recent studies have shown that BAIBA can protect from diet-induced obesity in animal models. It induces transition of white adipose tissue to a “beige” phenotype, which induces fatty acids oxidation and increases insulin sensitivity. While the exact mechanisms of BAIBA-induced metabolic effects are still not well understood, we discuss some of the proposed pathways. …” …More

[5] “…Carnitine palmitoyltransferase I (CPT I) deficiency is a condition that prevents the body from using…carnitine palmitoyltransferase 1 attaches long-chaing fatty acid (acyl CoA) to carnitine…” …More

[6] “…Ketone bodies are readily transported into tissues outside the liver and converted into acetyl-CoA, which then enters the citric acid cycle and is oxidized in the mitochondria for energy. In the brain, ketone bodies are also used to make acetyl-CoA into long-chain fatty acids. …” …More

[7] “…The production of ketone bodies is then initiated to make available energy that is stored as fatty acids. Fatty acids are enzymatically broken down in β-oxidation to form acetyl-CoA. …Deaminated amino acids that are ketogenic, such as leucine, also feed TCA cycle, forming acetoacetate & ACoA and thereby produce ketones. …” …More

(mole person) #3

No, ketones aren’t stored.

This is incorrect. Most fat that you eat is not converted to ketones but ends up as fatty acids in your blood. Your cells take up fatty acids for fat storage much easier than it makes fat from glucose.

This is a confusion that I see reiterated a lot. Although glucose makes us fat it’s not because it turns into fat. The body’s rate of lipogenesis from glucose is actually very, very low even in carb eaters. Less than 10% of your daily fat storage is from glucose. It’s a difficult metabolic process.

Almost all fat stored comes from ingested fats. This is why vegans, who eat almost entirely carbohydrate diets tend to be thin. The fat content of their diet can often be super low. This is also why all ultra low fat diets work, as awful as they are.

Here is why a ketogenic diet works. When you eat carbs your blood glucose quickly rises to levels that would be toxic if not burned for fuel. So the body must stop burning the fatty acids floating happily in your blood waiting to be a fuel source. So the body screams for insulin which pushed the fats back into the fat cells and allows the glucose primacy as the fuel source.

In short, the body makes almost all of its fat from fat but it needs insulin to keep from burning that fat as well.

It’s worth keeping in mind too that carbs are not the only things that raise insulin. It’s very important but it’s not alone and is why many people can still struggle on this diet even while keeping carbohydrates very low. Being low carb is not a sufficient condition for weight loss in many people and in some it won’t even prevent weight gain without other manners of insulin control. This is why most people eventually stall out. Your body make insulin in response to everything that you eat. At some point your body reaches a balance point where the insulin produced by the current diet is enough to maintain the fat still on the body. The only way past this are dietary tweaks to lower insulin further or years of waiting for the body’s cells to respond with lowered insulin resistance.

This is where the idea of the Phinney weight comes from. It’s basically the weight an individual body will achieve through carb restriction alone.

(Bunny) #4

…and carbohydrates:

”…‍If dietary saturated fat intake has little to do with saturated levels in our blood, then what does? There is, in fact, sound evidence that dietary carbohydrate is a major determinant of serum saturated fat levels. We know this because two respected research groups [16,17] fed humans carefully measured, weight-maintaining diets either high in carbohydrate or moderate in carbohydrate. In both studies, blood levels of saturated fats went up dramatically on the high carb diets, even though they were very low in fat. We [18] performed a weight loss study during which we fed diets varying from 32 up to 84 grams of saturated fat per day, with “healthy carbohydrate” making up the energy difference when dietary fat was reduced. In blood triglycerides and cholesteryl esters, saturated fat levels trended upwards when the high carbohydrate, very low fat diet was consumed, despite the diet being energy restricted, causing ongoing body fat loss. …” …More

…excess glucose being stored as a lipid droplet in the adipose cell then converted back into saturated fat and released into the blood stream before being oxidized as glucose?

But if your metabolically fit, that saturated fat in the blood will be turned into ketones especially when you sleep? Even on a high carbohydrate diet?

So what I’m looking at is a smaller fatty acid turn over pool?

And is 70-80% of dietary fat in calories (not volume) excessive or perfect for the human body to metabolize appropriately if your trying to oxidize body fat?

#5

@atomicspacebunny I am now curious, what are your personal eating habits?

(mole person) #6

@atomicspacebunny That article is about the lack of a relationship between dietary saturated fats and the amount of saturated fats in your blood. It’s says nothing about the rate of lipogenesis from glucose.

As I said above, de novo lipogenesis does occur but it is a much smaller source of fat storage than direct storage of fatty acids, approximately 10% of fat storage in normal individuals.

I found this interesting though:

" By contrast, triglycerides synthesized via de novo lipogenesis was significantly higher in high liver-fat group, compared to low liver-fat group. This study suggests that, while adipose derived free fatty acids contribute the largest proportion of liver triglycerides in subjects with normal liver-fat, the contribution of this pathway does not increase in NAFLD subjects, whereas hepatic de novo lipogenesis does increase in this patient population. When taken together, the data from this study indicate that the primary difference in nutrient homeostasis in individuals with and without NAFLD is attributed to hepatic de novo lipogenesis."

So for people with fatty livers the contribution from carbohydrates directly to fats can be as high as 23%. Very interesting.

(Bunny) #7

But it does discuss a low and high ”healthy carbohydrate” being converted from glucose into a lipid inside the adipose cell and then released back into the blood stream as a saturated fatty acid in the fatty acid turn over pool (i.e. “rate”) and possibly into a ketone depending on metabolic flexibility?

“Healthy Carbohydrate” meaning Whole Foods?

I also think it is important to note the other differences as you pointed out between a metabolically fit person and a person as you describe with a NAFLD fatty liver, insulin resistance, diabetes etc. or degrees in variations of metabolic fitness and metabolic dysregulation variables ± 23% conversionary rate of carbohydrates to fat storage in adipose tissue?

Thank gawd there are limitations on that for most people or we humans would all blow up like balloons within short amounts of time with all the highly concentrated and refined carbohydrates out there?

Not enough mitochondria in the skeletal muscle fibers to oxidize all those refined carbs?

(Ken) #8

We’re missing a step. The role of Glycogen. Fat storage does not happen unless Glycogen levels in the liver are full. It is only when the receptors are downgraded that this occurs, both for excess glycogen and de novo lipogenesis using glucose.

Not much of a concern with the VLCHF eating pattern, not understanding this often causes the Demonization of limited or occasional carb consumption. It takes quite a few cars to fill up the liver, certainly eating more than a Day’s worth within an overall keto pattern.

(Bunny) #9

In my case that’s a given and if you don’t know that, you cannot know the latter?

A no brainer?

You can easily release glycogen from storage by eating ONLY a little bit of protein (and nothing else) with a quickness!

(mole person) #10

You keep saying this but it flies in the face of all the evidence. There is a constant state of fatty acid flux at adipocytes. Whether or not we gain or lose fat is entirely dependent on the whether the net of that flux is positive or negative. People can and do gain weight on strict ketogenic diets.

We’ve had this conversation before so I will leave the link here for anyone interested.

(Ben ) #11

Just put another log on the fire.