The Myth of Starving Cells II ~ Lipolysis is not rate limiting

The low carb theory on weight loss revolves on insulin's action on adipocytes.  Specifically, high insulin favors deposition (esterification to form triglycerides) in the fat cells and suppresses lipolysis (breakdown to free fatty acids).  

This of course is true.  But the problem with this discussion is that it is incomplete.  You see, lipolysis has little to do with fat burning per se.  That is beta-oxidation occurring in the mitochondria in a series of cyclical reactions commonly called the Fatty Acid Spiral, FAS.  Free fatty acids are constantly delivered to the cells and being taken up.  Those that are not oxidized for energy are re-esterified and stored as triglycerides inside the cells (e.g. IMCL or IMCT).

Now here's the rub.  As even Gary Taubes discusses in GCBC, we are continually cycling fat into and out of our fat cells with the Triglyceride/Fatty Acid Cycle.  That blog post being the first mention of that infamous 2003 Reshef et. al. paper that sort of started all the mayhem here at the Asylum.  In that article we learn that at all times, a considerable proportion of the fatty acids released by adipose tissue are taken back up and re-esterified - some by adipose tissue, some by peripheral cells.  

This, in and of itself, tells us that we are always in a state of FFA "excess" availability.  Low insulin, high insulin or everywhere in between.

The rate limiting step in fat burning is the initiating reaction of the FAS/beta-oxidation.  Simply put:  How many fatty acids are ultimately "burned" or oxidized, because these molecules only make it ultimately out of the body by this route.  

Therefore any argument focusing on lipolysis rates as relates to availability of energy substrates or fat burning capability for the individual is simply gimmickry.  What is "rate limiting" for fat loss is the degree to which your body requires fatty acids as a fuel source and the degree to which you are replenishing that which is used.


Moran Bentzur said…
So why does insulin suppress lypolysis if this has no effect whatsoever on lipid oxidation?
The effect of Insulin postprandial is to encourage clearance of glucose from the blood stream, by allowing uptake, shutting down glucagon release from the liver and suppressing lypolysis. If lypolysis is irrelevant, why is insulin affecting it?
CarbSane said…
To keep your fat stored where it's supposed to be. In the fat cells.

Lipolysis is not irrelevant, it's not determinative of the rate of oxidation. IOW when there's other fuel to burn, you want fats to stay in triglyceride form to some extent. But we don't want cells ever "starving" so there's ALWAYS a continual cycling going on.

Hope that makes sense.
Moran Bentzur said…
I agree with you that the postprandial insulin spike has little to do with fat accumulation, but as for fasting insulin levels I'm not sure. whether this is cause or effect or both is a long discussion, but for sure high fasting insulin is part of the problem.
Nigel Kinbrum said…
If fasting insulin is high, it's because target cells have become resistant to the action of insulin, resulting in more insulin needing to be secreted by classical negative feedback action.

High fasting insulin is a symptom of the problem (Insulin Resistance), not the cause.
CarbSane said…
I agree with Nigel that high FI is a symptom not the cause. It is only "part of the problem" because of why it's elevated. The IR also have elevated free fatty acids so the elevated FI is still insufficient to SUPPRESS lipolysis!
lightcan said…
Hi carbsane,

how does one know how many fatty acids one needs? obviously depends of availability of glucose, from food and reserves. Let's say I eat 80 g carbs, 50 g protein, how much fat should I get, to lose fat, considering I'm not exercising?
It kinds of ties in with Don's idea of macro housekeeping and not energy balance.
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Hi there lightcan, I've been meaning to address that post of Don's but I'm busy with revamping a few things here at the moment. He sure is making quite a splash lately, huh? In short, it is a bit of a semantics issue between mass and energy balance. And there are limits in terms of grams for carb and protein intake in terms of our glycogen stores and nitrogen pools, whereas it seems fat is seemingly limitless. I hope to get to address this fairly soon.
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