So when dietary fats are in the small intestine, they are emulsified by bile salts in order for action by lipases to occur. Lipases degrade the triacylglycerols into monoacylglycerols, diacylglycerols, free fatty acids, and glycerol, and these are taken up by intestinal epithelial cells. Once taken up, these are reformed into triacylglycerols.
My question: why do these have to be broken down in order to be absorbed, and what is the driving force for reformation of triacylglycerols once absorbed?


Your question does not have a clear answer yet, as stated in Metabolic regulation: a human perspective / Keith N. Frayn. – 3rd ed (2010) on page 39.

There is still debate about how fatty acids cross cell membranes.

On that page they claim that a simple diffusion transport is possible through a 'flip-flop' mechanism, where the fatty acid inserts itself in the membrane and then experiences a reversal movement. The kinetics of the process seem to be in agreement with the observed utilization rates.

Also, it is claimed that there is growing evidence specific fatty acid transporters like FAT and FATP (fatty acid translocase and transport protein) play a key role in the process. They might join forces with the fatty acyl-CoA synthase, consuming ATP. ATP consumption activates them, i. e provides energy, for the acyl-CoA formation (not in order to move against gradient). The activated state would enable them to both move into the cell and regenerate a triacylglycerol.

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Why do these (triacylglycerols) have to be broken down in order to be absorbed?

I would say that the hydrolyzed products (fatty acid and glycerol) are more readily internalized because their structure is simpler. Fatty acids can perform the flip flop mechanism, but whole triacylglycerols might not (I am not sure). There is a fatty acid binding protein that may help maintain the fatty acid importation gradient too.

What is the driving force for reformation once absorbed?

It is the secretion of chylomicrons loaded with regenerated triacylglycerols. Since they are secreted, they don't pile up inside the enterocyte (intestine cell) and the equilibrium in the synthesis route (the monoacylglycerol esterification pathway) favors the production of triacylglycerols.

Remarkably, not all fatty acids are reesterified, those of short length (< 14 carbons) are not compatible with the acyl-CoA synthase and enter the plasma in a free state. That happens when digesting dairy products.


I'd like to just add on with some more detail. According to this, gastric lipase cleaves 15-20% of fatty acids in the stomach. The rest is completed in the duodenum by lipases secreted by the pancreas. Bile salts, phospholipids and cholesterol coat these lipid particles to prevent them from coalescing. The reason is because lipases have adapted to oil-water interfaces. Therefore breaking down dietary fact into "into an emulsion of fine oil droplets enhances the action of lipases. The smaller fat globules have an increased surface area and are more easily accessible to active pancreatic enzymes for further breakdown."

As for your question on the driving force of why they are reassembled, "several enzymes reassemble the fatty acids and monoacylglycerides to reconstitute triglycerides. Subsequently, the enterocytes package the reconstituted triglycerides with proteins and phospholipids into chylomicrons." These chylomicrons travel into the blood stream through the lymph system where they go to adipose tissue and muscle cells for further breakdown.

Barbara E. Goodman Advances in Physiology Education Jun 2010, 34 (2) 44-53; DOI: 10.1152/advan.00094.2009


Triglycerides are "huge" molecules relatively speaking compared to carbohydrates like glucose or amino acids like alanine. Within the intestinal lumen they are broken down by lipases and solubilized by bile for absorption, which also enhances the activity of pancreatic lipase. So, to get into the enterocytes of the small intestine they need to be broken down. However, once they are reformed you can't just excrete them into the venous circulation because there are exceedingly hydrophobic and can't circulate in their native form. In fact, they first pass into the intestinal lymphatics before entering the arterial circulation. Before this happens, though, triglyceride particles and other lipids like cholesterol are packaged onto lipoprotein molecules for their transport. These lipoprotein molecules are still large, but they have proteins (i.e. Apo-B48) that act as signals to the peripheral tissues for particle uptake into the muscle, adipocytes, etc.

  • $\begingroup$ Thanks for your contribution. References are appreciated at Biology.SE. I think it is a great answer, but without references no one can follow up on your information. $\endgroup$ – AliceD Jun 19 '15 at 1:12
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    $\begingroup$ Yes, many answers come from the top of my head too, but everyone can claim to be an expert and start selling nonsense :) Like in your previous answer I simply added a wiki link. Personally I don't like wikis and prefer primary literature instead of open-source stuff, but if you are reluctant adding primary literature, some links to credible sources are an easy alternative $\endgroup$ – AliceD Jun 19 '15 at 1:23

Could the reason that triglycerides being neutral and non-polar, require the aid of additional proteins for their transportation but when broken into glycerol and free fatty acids, the individual components being polar are more easy to transport. Also, in terms of storage, the triglyceride form is better because of its non-polar properties and that it would remain relatively inert in the cytosolic environment.

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    $\begingroup$ Some points that you mention have already been covered in other answers. Can you please edit your answer to add some more details so that your answer provides additional information? $\endgroup$ – WYSIWYG Jan 9 '19 at 10:20
  • $\begingroup$ Welcome. Answers need to be founded on credible sources. Please cite relevant references to allow other users to background read on your material. $\endgroup$ – AliceD Jan 9 '19 at 20:22

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