To claim that the body cannot store dietary fat shows a profound ignorance of physiology

Teh fatty acid transport protein (FATP) is how it gets across the cellular membrane

A few of literally dozens (if not more) of papers appears below

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1: Proc Nutr Soc. 2004 May;63(2):259-62.

New concepts of cellular fatty acid uptake: role of fatty acid transport
proteins and of caveolae.

Pohl J, Ring A, Ehehalt R, Herrmann T, Stremmel W.

Departments of Gastroenterology and Internal Medicine, University of Heidelberg,
Bergheimer Str. 58, 69115 Heidelberg, Germany.

Efficient uptake and channelling of long-chain fatty acids (LCFA) are critical
cell functions. Evidence is emerging that proteins are important mediators of
LCFA-trafficking into cells and various proteins have been suggested to be
involved in this process. Amongst these proteins is a family of
membrane-associated proteins termed fatty acid transport proteins (FATP). So far
six members of this family, designated FATP 1-6, have been characterized. FATP
1, 2 and 6 show a highly-conserved AMP-binding region that participates in the
activation of very-long-chain fatty acids (VLCFA) to form their acyl-CoA
derivatives. The mechanisms by which FATP mediate LCFA uptake are not well
understood, but several studies provide evidence that uptake of LCFA across
cellular membranes is closely linked to acyl-CoA synthetase activity. It is
proposed that FATP indirectly enhance LCFA uptake by activating VLCFA to their
CoA esters, which are required to maintain the typical structure of lipid rafts
in cellular membranes. Recent work has shown that the structural integrity of
lipid rafts is essential for cellular LCFA uptake. This effect might be exerted
by proteins, e.g. caveolin-1 and FAT/CD36, that use lipid rafts as platforms and
bind or transport LCFA. The proposed molecular mechanisms await further
experimental investigation.

Publication Types:
Review

PMID: 15294040 [PubMed - indexed for MEDLINE]

2: Lipids. 2001 Sep;36(9):981-9.

A new concept of cellular uptake and intracellular trafficking of long-chain
fatty acids.

Stremmel W, Pohl L, Ring A, Herrmann T.

Department of Gastroenterology, Ruprecht-Karls-University, 69115 Heidelberg,
Germany. wolfgang_stremmel~med.uni-heidelberg.de

Fatty acids are the main structural and energy sources of the human body. Within
the organism, they are presented to cells as fatty acid:albumin complexes.
Dissociation from albumin represents the first step of the cellular uptake
process, involving membrane proteins with high affinity for fatty acids, e.g.,
fatty acid translocase (FAT/CD 36) or the membrane fatty acid-binding protein
(FABPpm). According to the thus created transmembrane concentration gradient,
uncharged fatty acids can flip-flop from the outer leaflet across the
phospholipid bilayer. At the cytosolic surface of the plasma membrane, fatty
acids can associate with the cytosolic FABP (FABP(c)) or with caveolin-1.
Caveolins are constituents of caveolae, which are proposed to serve as lipid
delivery vehicles for subcellular organelles. It is not known whether protein
(FABP(c))- and lipid (caveolae)-mediated intracellular trafficking of fatty
acids operates in conjunction or in parallel. Channeling fatty acids to the
different metabolic pathways requires activation to acyl-CoA. For this process,
the family of fatty acid transport proteins (FATP 1-5/6) might be relevant
because they have been shown to possess acyl-CoA synthetase activity. Their
variable N-terminal signaling sequences suggest that they might be targeted to
specific organelles by anchoring in the phospholipid bilayer of the different
subcellular membranes. At the highly conserved cytosolic AMP-binding site of
FATP, fatty acids are activated to acyl-CoA for subsequent metabolic disposition
by specific organelles. Overall, fatty acid uptake represents a continuous flow
involving the following: dissociation from albumin by membrane proteins with
high affinity for fatty acids; passive flip-flop across the phospholipid
bilayer; binding to FABP(C) and caveolin-1 at the cytosolic plasma membrane; and
intracellular trafficking via FABP(c) and/or caveolae to sites of metabolic
disposition. The uptake process is terminated after activation to acyl-CoA by
the members of the FATP family targeted intracellularly to different organelles.

Publication Types:
Review

PMID: 11724471 [PubMed - indexed for MEDLINE]

3: Biochemistry. 2004 Apr 13;43(14):4179-87.

Long-chain fatty acid uptake into adipocytes depends on lipid raft function.

Pohl J, Ring A, Ehehalt R, Schulze-Bergkamen H, Schad A, Verkade P, Stremmel W.

Department of Internal Medicine IV, Ruprechts-Karls-University, Heidelberg,
Germany.

This study investigates the role of lipid rafts and caveolae, a subclass of
lipid raft microdomains, in the binding and uptake of long-chain fatty acids
(LCFA) by 3T3-L1 cells during differentiation. Disruption of lipid rafts by
beta-cyclodextrin (betaCD) or selective inhibition of caveolae by overexpression
of a dominant-negative mutant of caveolin-3 (Cav(DGV)) resulted in disassembly
of caveolae structures at the cell surface, as assessed by electron microscopy.
While in 3T3-L1 fibroblasts, which express few caveolae, Cav(DGV) or betaCD had
no effect on LCFA uptake, in 3T3-L1 adipocytes the same treatments decreased the
level of [(3)H]oleic acid uptake by up to 55 +/- 8 and 49 +/- 7%, respectively.
In contrast, cholesterol loading of 3T3-L1 adipocytes resulted in a 4-fold
increase in the extent of caveolin-1 expression and a 1.7-fold increase in the
level of LCFA uptake. Both the inhibitory and enhancing effects of these
treatments were constantly increasing with the [(3)H]oleic acid incubation time
up to 5 min. Incubation of 3T3-L1 adipocytes with [(3)H]stearate followed by
isolation of a caveolin-1 positive detergent-resistant membrane (DRM) fraction
revealed that [(3)H]stearate binds to caveolae. Fatty acid translocase
(FAT/CD36) was found to be present in this DRM fraction as well. Our data thus
strongly indicate a critical involvement of lipid rafts in the binding and
uptake of LCFA into 3T3-L1 adipocytes. Furthermore, our findings suggest that
caveolae play a pivotal role in lipid raft-dependent LCFA uptake. This transport
mechanism is induced in conjunction with cell differentiation and might be
mediated by FAT/CD36.

PMID: 15065861 [PubMed - indexed for MEDLINE]

Woo hoo! Lyle McDonald! Hiya!

Someone want to diseminate those studies down to english for those of us that get lost in 3T3-L1 adipocytes and phospholipid bilayer's....

What roll does insulin play in the above, and does it apply to a person like Bear that stays so ketogenic....?

Haha never would have expected you (Lyle) to show up on this board.

I have two questions:

What foods create, or best support, (pardon my ignorance) ATP?

At 4'11", should I REALLY weigh 95 lbs?

lylemcd, this is all scientific jibber jabber -- plain English, please.

Exactly! Were in this jabber are the words "dietary fat"? I don't see them. I'm sure if I search medline long enough I can find a study that says monkeys can fly out of my butt too.

You submitted yourself for a study to determine if monkeys fly out of your butt? I hope you were well compensated, that doesn't sound like fun.

I can't wait for the part where it's explained to everyone in plain english how dietary fat is converted to body fat and everyone says "Oh, yeah? Prove it". Then we'll be back to the quoted studies.

ok..this should get interesting...Bear vs. Lyle McDonald vs T.S Wileys husband...*karen makes popcorn...ooops..no..no..karen makes a steak and sits back to see what happens next*

Yeah, it was a real pain in the ass!

LOL!! You are too funny. Yah, don't let them get to you.

I'm not a molecular biologist (my wife is) but I'm not reading these abstracts the same way you are. The uptake of fatty-acid chains through the cell membrane implies these fats are already circulating. Where did they come from? I don't see anything here about the consumption or digestion of fats. My understanding is that insulin in a key element in the creation of lipids. digested fats become elements of structure except in extraordinary circumstances.

Dana, there is no hard and fast formula for what a person should weigh precisely, but rather a range. Those with a higher amount of lean body mass could very well look quite good at the higher end of their weight range while another person of the same height might still look chubby at the bottom end of theirs because they have less lean body mass. Age, frame size and gender also factor in to what a good weight is at any given height.
Bottom line, a healthy weight is one that you are healthy at and feel good about yourself at.
For a chart of healthy weight ranges, see here. Based on this chart, your stated goal weight is perfectly reasonable (and a goal weight of 130 for someone who is 5' 3" tall is only 'fat' in the eyes of someone who prefers stick thin women ).

Don't you love all the might be's (like maybe) in these "definitive studies".

I guess you will say my "profound ignorance" must be showing. I prefer to call it "healthy skepticism", if you don't mind.

I love the references to proteins being "important mediators". Being the primary catalysts of all biochemical reactions, that is nothing new!

And the reference to some of these proteins serving as lipid delivery vehicles for subcellular organelles is also quite obvious... however, how many of these organelles exist in white adipose cells? Therefore, were is the relevancy?

Yes, it is true that nonesterified fatty acids are bound to serum albumin (BTW, would that be a protein? ) for transport to cells. But, primarily muscle and liver cells! (I wonder why THAT would be?). And, yes, once inside (after flip-flopping across the membrane via concentration gradient... although your three articles contradict themselves, one saying proteins aid this process, and the other ones leaving it up to concentration gradient) they are bound to fatty acid binding proteins and distributed to organelles, AND the cytosol in general... where they float around (being the most abundant substance in the cytosol of our cells). However, perhaps these albumin are not taken up by adipose tissue. These studies you have sighted don't really go into much depth about that. Rather, they are fairly simple primers to how fatty acids ARE taken up by other cells in the body. The third one addresses it more than the first two... however, it seems to suggest that there is a slight "problem" with uptake of fatty acids into fat cells. Was this your point in including this study? Didn't you want to include a study about why they are/aren't taken up by erythrocytes?

Sorry, but this IS a lot of "gibberish" that does not really address the issue at hand too well... or, put another way... get us out of our "profound ignorance" (if that indeed was the purpose of your post, Lyle... funny how it confounded most people reading it).

Rob, I'm still searching for that flying monkey study... on PudMed, did you say?

Thanks. My goal weight for now is 130 and if I should be able to surpass that, all the better. But, I think I was trying to avoid disappointment if I didn't lose beyond 130.

Oh yes, should I eat even if I'm not hungry? It's lunch time and I don't even feel like eating. I haven't had much of an appetite since going LC.

Forget low carb. I've always craved on regular low carb. After a week of eating this way I have absolutely no hunger and not a single craving for anything... ANYTHING!!!!!!!! This is UNREAL to me. When I became pregnant I turned into a food monster.. nursing seems to have me the same way, until now! What a relief, a huge burden has been lifted from me.

amber,
yes eat! you wont have much of an appetite while in ketosis..but eat your meals anyway..

Meg i am on day 4 of being a carnivore and your right..the cravings have completely gone away!! Guesss we know what was causing the CRAVINGS! ummm..CARBS! i will say when i switched from a high carb, sugar diet to Atkins ALOT of the cravings did dissipate!! BUT..even on 20 carbs a day..i still had SOME cravings. Now i have NONE on the all meat diet!! woot!

That's simple. ANIMAL FAT!

And this would be a bad thing?

I "can't wait" as well.

DITTO here!

Eat! Especially animal fat! This will help you keep things steady.

Just watch out for those caveolae lipid raft microdomains! Don't wanna fatten up any of your 3T3-L1 cells... especially during differentiation! If you have any dominant-negative mutants of caveolin-3, you could always pop some DRM I suppose... or beta-cyclodextrin!

Or just ask Lyle... he'll steer ya to the right article on PubMed!

I'm glad that I was not the only one blown away by his post, and I am a college health educator! Oh my, Oh my!

BTW, Dean...I thought your translation was very clarifying for me!! HEE HEE

I am REALLY tired of dealing with people who do not READ the thread before butting it with lengthy diatribes.

Fat in the diet does NOT enter the adipose tissue- a very tiny amount of osmotic exchange in short chain fatty acids MAY occur, however studies with radioactively tagged dietary fat and glucose show NO radio-tagged fat winds up in the tissues from fat and ALL the radiotagged glucose is found in fat in the adipose tissues. I might remind all readers that bogus claims and false data is VERY common in the scientific literature. We do not question that fatty acids enter somatic muscle cells only that it is not stored in adipose cells

If you are interested in this diet, fine, then your questions are welcome- but I have a LONG experience in this, and I do not need people who have no idea of what has been discussed and rejected injecting misinformation here- we are well along the path now. PLEASE READ THE THREAD.

I just want to make sure - which posting are you referring to?

Have you read the thread?

Yes, but I'm not clear which one he is addressing. I'm guessing it's the same one I took issue with.