Explaining Fat Loss (Part One)

Ari Snaevarsson, Features Editor and Columnist

Ari Snaevarsson, Features Editor and Columnist

By Ari Snaevarsson, Features Editor

Welcome to Part One of my two-part series dissecting the physiology of fat loss.  Enjoy!

The adipocyte

There are primarily two types of adipose tissue in the body, white adipose tissue (WAT) and brown adipose tissue (BAT).  The main purpose of WAT is storage; most fats in the body are stored in this tissue.  The main purpose of BAT is thermogenesis, or heat production.  BAT purposefully uncouples the production of ATP, the body’s energy currency, from fat oxidation, making the process less efficient, so as to produce more heat.  This means it burns more fat than the energy supply needs, so theoretically it would be advantageous for weight loss.  While the conventional knowledge is that it exists in insignificant amounts in adult humans, some newer studies have shown it is metabolically active even in older adults.  This is an excitingly revitalized field of research in nutrition science.

The WAT just under the skin is called subcutaneous fat, while that surrounding the vital organs of the abdomen is called abdominal, or visceral, fat.  Most of the fat stored in fat cells (adipocytes) is in the form of triacylglycerol, otherwise known as triglyceride.  Triglycerides are made up of three fatty acids attached to a glycerol backbone.  When fats are mobilized to begin the process of fat loss, the fatty acids are stripped from the glycerol and subsequently sent into circulation, ideally to go find tissue where they can be oxidized, or burned (alternatively, the fatty acids can sit around in the bloodstream and cause problems or be recycled back into the fat cell).

Fat loss and storage

As I have previously alluded, the fat cell can either take up or release fat, depending on its energy state.  After eating, the energy supply is high, and insulin inhibits fat release.  After fasting, hormones like epinephrine, growth hormone, and glucagon increase, causing lipases to stimulate lipolysis (fat mobilization; the fatty acids are torn from the glycerol).

The fatty acids, along with the glycerol backbone, are released into the blood.  Here we run into a problem: blood is aqueous, while fats are hydrophobic.  Therefore, we require a carrier protein, known as albumin, for transport.  Albumin carries fatty acids from circulation out to the blood vessels in skeletal muscle, where the fatty acids are detached from albumin.  Now, to get into the muscle, they must cross the cell lining that makes up the capillary, the endothelium, and then the muscle cell membrane, the sarcolemma.  This is facilitated with the help of the membrane proteins fatty acid translocase/cluster of differentiation 36 (FAT/CD36) and fatty acid binding proteins (FABPs).

Exploring the two fates

Now, a coenzyme-A (CoA) attaches to the fat to transport it further into the muscle for one of two fates.  The first is beta-oxidation, to produce energy (the fate during exercise and times of energy deficit).  For this, the fatty acid must be transported into the cell’s mitochondria, generally by way of the carnitine shuttle system.  This system uses two enzymes (carnitine palmitoyltransferase 1 and 2 [CPT1 and CPT2]) and carnitine to accomplish this.  The beta-oxidation reaction cuts carbons off the fatty acid chain.  This reaction repeats until the fatty acid has been completely reduced to acetyl-CoA.  In the case of odd chain fatty acids, it is acetyl-CoA and one propionyl-CoA.

The other fate, common when being fed, is storage.  The fatty acids are  repackaged into triglycerides and stored in cellular organelles known as lipid droplets.  Adipose tissue is not the only storage site.  Skeletal muscle can hold some fat (known as intramuscular triglycerides [IMTGs], which only make up 1-2% of fat stores), and so can some other organs, such as the liver.  Fat in the liver, however, is called ectopic, because it is not supposed to be here; this is what leads to the dangerous condition aptly named “fatty liver.”

Hopefully this little crash course on the physiology of fat loss was as fun to read and conceptualize as it was for me to write.  Stay tuned for Part Two, where we look at some of the regulation that goes on in this story.

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Author: Ari Snaevarsson

Ari Snaevarsson '17 is a Health Sciences major and Religious Studies minor, and he is the Features Editor of The Gettysburgian. He competes in bodybuilding and powerlifting and has an immense passion for dissecting the habit psychology at play in people's dieting attempts. Outside of reading and bedroom DJ-ing, he has previously maintained a health/fitness blog that also followed nutrition news, No Fluff Strength.

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