Peter’s latest post on his blog Hyperlipid is simply incredible; if you’re science-minded at all (or fancy yourself idiot savant in biochemistry) check it out.
For the rest of you, here’s a summary:
A question – If insulin acts as a gatekeeper for fat storage (by increasing levels of alpha glycerol phosphate), then how is it possible to gain weight on a low-carb diet (where insulin levels are automatically kept low via diet)?
A proposed answer – ASP (Acylation Stimulating Protein). This enzyme stimulates fat storage by fat cells and while it does seem to be associated with insulin levels, seems to do its job independent of insulin, mostly in the period after meals.
If this is the case, it opens up a pathway for fat storage aside from high insulin levels, explaining why it’s possible to gain fat on a high-calorie low-carb diet.
All this is just highfalutin’ science stuff for me to geek on; the implications to someone looking to lose weight are unchanged – that is, that omitting grains, sugars, and starches from your diet doesn’t give you the license to pig out on bacon and pork rinds. You still have to watch your caloric intake. You’re just more likely to taste success with a low-carb approach because:
- You won’t be stimulating insulin secretion, so you’ll be minimizing appetite
- You’ll be more sated due to higher fat content in the diet (i.e., not as hungry)
- You’ll be eating foods that are more nutrient dense (meat, vegetables, fruit) in lieu of foods that are less so (carbs).
To repeat – if you want to save yourself a headache – if you overconsume calories on a low-carb regimen, it is possible to gain weight, so don’t do it.
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{ 10 comments… read them below or add one }
I also have some head ache before when I make a low carb diet. I also suspect that is the culprit why having this head ache.
Not necessarily. You could be underconsuming calories, or underconsuming water as well.
It’s also possible that you’re extremely carb-adapted and that you’ll just have to wait out the couple of days of feeling crappy until your body switches over to fat for energy.
thanks alot
thanks alot
What about type one diabetics who cannot produce insulin? They certainly cannot retain proper amounts of fat tissue with just ASP.
Katie,
That’s right, and they don’t. Type 1 diabetics don’t get fat – unless, of course, they take insulin.
So what does that say about ASP? It isn’t regulated by insulin, as far as I know, so how would it store fat in anyone else?
Katie,
Because the body doesn’t work in a linear fashion (akin to a computer with punchcards – input—>output), it is regulated by feedback loops.
This is how Richard Feinman explained it to me (using insulin as the example): You could say that high levels of insulin cause fat accumulation because it causes energy (from food) to be shifted away from utilization to storage. But that’s not exactly how it works. Insulin is regulated not only by blood sugar level, but by glucagon concentration and enzymatic function. If you were to look at it in schematic form, it looks like more like a causal loop diagram (http://upload.wikimedia.org/wikipedia/commons/5/52/Causal_Loop_Diagram_of_a_Model.gif) where all the parts influence one another. Sugar (glucose) just happens to be the key to the whole loop because without sugar it’s hard to create enough alpha glycerol phosphate to shift the whole system towards fat storage.
As far as ASP goes, insulin does regulate ASP (http://www.endocrine-abstracts.org/ea/0016/ea0016p527.htm), so it’s a contributing factor. But because it works independently of insulin, it’s probably what’s causing fat gain when insulin (and alpha glycerol phosphate, presumably) is low. Since I’m no PhD, it’s safe to say that there are probably other regulatory factors that are pushing fat into fat cells when calorie consumption is too high but I haven’t the foggiest what they would be.
Thank you for your response. This does help as I have been a bit confused on it lately. I appreciate the research and time that went into your second response. I am training to be a PT and I am a pre-med undergraduate. It seems my teachers can’t answer the question either.
Here’s another perspective on it. When I originally read about ASP I thought of it as a regulatory factor that minimized fat loss. If you think about it from an evolutionary perspective, it doesn’t make a whole lot of sense to carry ultra-low levels of body fat (decreases chances of survival in event of famine conditions). So what ASP might do is to prevent fat levels from dropping past some sort of “red-line” warning zone (similar to how muscle spindles cause the stretch reflex to occur when fibers are stretched past a certain percentage of baseline).
You’re welcome, and if you find a biochemist who can answer your question, please pass it along:)
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