I read that this morning, too. I wonder how people reconcile the apparent benefits of adipose DNL with the belief that we should "keep insulin low" for health purposes. Added to the fact that the more damaging liver DNL is not substantial compared to the DNL in adipose tissue, so it would seem the general benefits of spiking insulin outweigh the "risks".
De novo lipogenesis and stearoyl-CoA desaturase ... [J Biol Chem. 2010] - PubMed - NCBI
"DNL may not act primarily to increase fat stores but may serve as a key regulator, in tandem with elongation and desaturation, to maintain cell membrane fluidity and insulin sensitivity within the human adipocyte."
One more: Modulation of palmitate-induce... [Am J Physiol Endocrinol Metab. 2011] - PubMed - NCBI
"Overall, these data support the hypothesis that enhanced MUFA synthesis via upregulation of SCD2 activity can protect β-cells from elevated saturated FAs, as occurs in prediabetic states. Overt type 2 diabetes is associated with diminished islet expression of SCD and Elovl6, and this can disrupt desaturation of saturated FAs to MUFAs, rendering β-cells more susceptible to saturated FA-induced ER stress and apoptosis."
Yep yep. I was wondering why the research on DNL seemed to drop off after 2004. It didn't drop off, it just branched off. My only question is how this all relates to dietary palmitate.
I thought that might be what prompted ya . I really will have to study it a bit. After reading the article a few times I'm getting what they are saying to a degree, but I definitely need to do some further reading for my own understanding. I do note that liver DNL is bad (fructose/PUFA overload?) but peripheral white adipose tissue upregulation of DNL is good. The upregulation of DNL in caloric restriction kinda confuses me though.....as they point out this is counterintuitive. I'll read your links there, but my question to you is does a low insulin diet upregulate or downregulate DNL at the adipose tissue? And we would have to agree on what we call "low insulin" though. Are we talking ketogenic diet, IF'ing, or general low carb. Sort of cumulative vs insulin highs sort of question? I know what I might think it does, but I was wrong in the case of caloric restriction.
I mean we could have a "low insulin diet" based on cumulative amount of insulin by only eating one meal a day even if that meal contained plenty of carbohydrate right? In fact many argue that this is part of the reason higher carb societies have no issue...they only eat a couple times a day vs. persistently spiking several times and keeping levels elevated.
Last edited by Neckhammer; 01-04-2013 at 12:47 PM.
Just read this Hyperlipid: Protons: de novo lipogenesis. I think if your looking for a "how do you reconcile this...." then this would be part of it. I'm not saying one way or another. I do know that there are plenty of other physiological indicators for longevity and health though. Its vastly complex and no I don't think you can boil it all down to only insulin either.
Everything our bodies can do benefits us. It's just whether those things are happening in excess or deficit or somehow incorrectly that is the problem.
Female, 5'3", 50, Max squat: 202.5lbs. Max deadlift: 225 x 3.
"To summarise: Palmitoleate is released by adipocytes when glucose and insulin are plentiful. Palmitate is released when glucose is sparse and insulin is low.
The sh!t hits the fan when glucose and insulin are plentiful but adipocytes are so distended that they THINK glucose and insulin are low. When both insulin and glucose are high you want palmitoleate. If your adipocytes give you palmitate under these circumstances you had better have a pancreas of steel or diabetes here you come."
I'll respond in full later, but that blog of Peter's didn't reconcile anything. He said adipose DNL makes you fat. Perhaps in a mouse it does because DNL is a more significant pathway, and I have a study saved on my computer that says as much. Would anyone like to read it? Maybe if Gary Taubes had read it he wouldn't have proposed his ridiculous alternative hypothesis.
Evelyn blogged on this as well. The Carb-Sane Asylum: De Novo Lipogenesis ~ Another Case of an Undeserved Bad Reputation?
Last edited by Timthetaco; 01-04-2013 at 03:56 PM.
Then there is your one article that seems to imply eating saturated fats up-regulates DNL. Would this be the same set of circumstances? Paul Jamminet shows that many supercentenarians tend to eat diets high in SFA. Is this a portion of why that seems to promotes longevity? He actually even makes the comment in Carb-Sanes blog........ "Palmitoleic acid is made from palmitate. Palmitate can be obtained either from dietary saturated fat that is 16-carbons or fewer, or from DNL. So I guess you would conclude it is the 18-carbon or longer saturated fats that deprive the body of palmitoleate."
Until we can hash out the difference in the different states of up-regulation and what the effects are I'm really just kinda sitting back and soaking it in. It is very interesting and wasn't really on my radar before, so thanks for the post.