Dietary Fat v. Endogenous Fat for energy

It has become increasingly clear to me that regardless of the macronutrient composition of one's diet, dietary fat is only marginally "burnt" for energy on a given day.  The exception to this would be medium and shorter chain fatty acids that are not included in this discussion.

There's a lot of misinformation out there spread by various LC gurus regarding fat burning and storage.  Without carbs, we can still store fat and we do!  The energy substrate for "fat burning" ( is the free fatty acid (NEFA/FFA).  Where do most of these come from?

1.  Lipolysis of "lipid droplets" of stored triglycerides within the cells, often called intramyocellular triglycerides (IMTG) 

2.  Lipolysis of adipose tissue.  

3.  Lipolysis of other circulating triglyceride-carrying lipoproteins  

4.  NEFA/FFA's that "escape" the re-esterification process.

Sources 2-4 are all circulating FFA's and my research all points to the conclusion that circulating NEFA/FFA levels are highly regulated and controlled (or intended to be) by controlling release from adipose tissue (2) constituting the majority of NEFA/FFA in circulation.  The other two sources are relatively minor.  Since trained athletes have higher levels of IMTG, it can also be posited that when the need for fats arises, these stores get tapped first and the cell takes in NEFA/FFA from the blood to replenish the stores.  (This can be envisioned as analogous to using glycogen stores and taking up glucose later to replenish the stores).  In any case, the fatty acids we actually "burn" (beta-oxidation, fatty acid spiral) on any given day are almost invariably derived from stored triglycerides.  

So what happens to dietary fat?  Well ... just as those "idiots" who know nothing about nutrition and science, etc. have been saying all along, it goes into .... drum roll please .............. your fat cells!  Yep!  That's where it goes whether you eat a low fat high carb diet or a high fat low carb diet or whatever other kind of diet.  The  majority of all of your ingested fat goes directly to your fat cells.  Here's how/why.  LCFA's are relatively insoluble in blood, so while ingested carbs and proteins get broken down into glucose and amino acids and mostly go directly into circulation, ingested fats do not.  Most ingested fats are triglycerides that are broken down to FFA + glycerol in the intestine.  The FFA's are taken up by intestinal cells, re-esterified to triglycerides that are then "packaged up" with proteins to form chylomicrons.  Chylomicrons can be "seen" in the blood after a high fat meal -- they are what can lead to the centrifuged serum/plasma being cloudy.   These are released into the lymphatic system and finally enter the blood stream via the thoracic duct.  Chylos are largely cleared from the blood in a matter of an hour or so.   Chylo formation and transport is a necessary component of human nutrition, but chylo-rich blood would be more viscous (not desired).  Therefore clearance from the blood stream is a priority task.  Really ... you actually want the fat you ingest to go into your fat cells!  But I digress ....  Back to the chylos.  It turns out adipocytes have receptors that detect the presence of chylos, and the chylos stimulate the production of (something LC snake oil salesmen wish would go away) acylation stimulating protein -- ASP. ( I'll be putting up a couple of blog posts on this in coming days).  The chylos are broken down, FFA's transported into the cells, and FFA's re-esterified at the direction of ASP pretty much ASaP!  

When you think about lipid transport, why do we have different types of particles?  Why doesn't the liver scavenge up chylomicron remnants and repackage them into new chylomicrons instead of other lipoproteins?  Because our bodies do distinguish between dietary fat and endogenous fats, and I propose this is critical to regulating circulating lipids.

So ... am I trying to say that eating fat makes you fat?  Nope!  Because at any given point in time, lipolysis is going on elsewhere in the fat cell releasing some of the stored fat.  Yes, insulin regulates the release of FFA's from fat cells in a suppressive capacity.  More insulin = suppressed lipolysis, less insulin = increased lipolysis.  Ah ha!  Not so fast.  This is nothing more than insulin playing traffic cop for the heirarchy of macronutrient utilization to meet immediate energy needs.  Because carb storage is inefficient (low energy density) and limited (the average adult has the capacity for like 750g or a little more than 1.5 lbs), when dietary carbs are available, they are utilized first to meet energy needs.  But this does not last forever, and once the carbs are gone, lipoysis is ramped up.  

Does high fat vs. low fat matter?  Not really if one reads the literature and in depth studies without an agenda or books to sell.  Let's say a person's total energy expenditure is 2500 cal/day;  Person A goes on a 2000 calorie 20%protein/20% fat/60%carb diet containing about 45g fat and 300g carb; Person B goes on a 2000 calorie 20%protein/70% fat/10%carb diet containing about 155g fat and 50g carb.   Both A & B are in 500 cal/day energy deficit.  Person A will likely directly burn most of the 300g carb, perhaps converting a small amount to fat via de novo lipogenesis.  They will deposit 45g dietary fat into their stores, but in varying rates as the day goes on, they will draw about 100g of  fat out.   Person B also uses their 50g carbs first and deposits 155g fat.  They will, however draw about 210g out of the stores.

The preceding paragraphs are obviously an over-simplification.  In reality, nobody is ever utilizing just one substrate for energy, but we are "wired" to utilize that which is least efficiently stored (carbs) preferentially to that which is efficiently stored (fats).  Furthermore, the metabolic processes enhanced during fasting (or carb restriction) are glucose sparing and override this heirarchy to some extent to preserve the glucose for where it's needed most (e.g. brain).  Lastly, the amount of fat released from the stores is significantly more than is needed (in either nutritional state) with about half of mobilized fat returned to the fat cell.   

Fat and/or carbs make us fat when either or both are consumed in excess of energy needs.  Fat accumulates if we're chronically depositing more fat than we are utilizing to meet energy needs.  Fat stores diminish when we're chronically utilizing more than we deposit.