In this second part of “Oil. It’s What’s for Dinner!” we begin the journey of oils/fats/lipids as they enter your mouth. These molecules present special problems to digestion, firstly because they don’t like water and we’re made of 55-90% water. Secondly, our cells cannot directly absorb TAGs, the main source of fat in a Western style diet. The body overcomes the solubility issue by allowing the fats to self associate or by coating them with detergents like cholesterol/bile acids. It overcomes the TAG problem by launching special enzymes called lipases to chew them up. These smaller pieces can then be absorbed by your cells. The actual hydrophobic chain of the FFAs are not broken down until later, as I will discuss in the next installment.

The digestion of lipids actually begins in your mouth with an enzyme called lingual lipase. This enzyme has a greasy pocket on one side that easily grips the TAG and another side that removes a FFA from the TAG leaving behind a diglyceride and a FFA. Lingual lipases even continue working while in the extreme pH of your stomach, chewing up almost 30% of the digested lipids before entering the small intestines. Just past the stomach, any FFA’s that are 6-12 carbons long have the benefit of self associating into small particles along with bile salts. These particles are then easily absorbed by the intestines and shuttled directly into the small intestinal capillaries where they may bind to carrier proteins in the blood. The FFAs of our earlier olive oil example (oleic, palmitic, and linoleic acid) are longer (18, 16, and 18 respectively)and therefore less soluble in blood, they must first be processed before they can enter the blood stream.

The larger FFAs and TAGs are given a coat of cholesterol/bile salts and packed into little suitcases called micelles. The hydrophobic carbon chain of the TAGs forms the inside of the micelle while the acid side creates a hydrophilic shell.

The cholesterol/bile salts act as a glue to help hold the micelle and lipids together. These micelles help break up any large aggregates of lipids into smaller and smaller blobs, therefore increasing their surface area. It’s at the micelle oil/water surface interface that the other 70% of TAGs not broken down by lingual lipase are clipped by yet another lipase called pancreatic lipase. Pancreatic lipase, and its helper called colipase, do not have greasy pockets like lingual lipase and must work together at the micelle interface to break down the TAGs into monoglycerides and FFAs.

This is where it gets a little weird: When all that’s left are micelle rafts of degraded FFAs and monoglycerides surrounded by cholesterol/bile salts they easily cross the intestinal cell walls where they are re-formed into TAGs. What? Why break everything down into small bits, just to make them into big bits again? It’s all because TAGs cannot cross any of your cell walls. It’s kind of like the ship-in-the-bottle problem. All together the ship can’t fit through the narrow neck of the bottle, but disassemble it, pass the smaller pieces through the neck, then reassemble it inside. Your cells also do this because a TAG is one of the most efficient ways you can store lipids. It’s a very stable molecule that enables you to store three fatty acids in one place. Kinda like measuring spoons.

Finally, the re-gifted TAGs are collected into another larger blood soluble suitcase called a chylomicron. The chylomicrons contain cholesterol and lipid transport proteins called apolipoproteins, ApoA and ApoB.

The chylomicrons, now fully loaded with almost 85-95% TAGs, are exported out of the intestinal cell walls and into the lymphatic system where they eventually make it into a large vein above your heart. Once in the bloodstream the TAGs are sent to either liver, fat or muscle cells where they have one of two fates: storage or energy. But I’ll save that for the next edition…

We often think only of bacteria as attacking us, but they are also constantly under siege by organisms called phage. Using a supercomputer, Michael Deem, a professor at Rice University’s Department of Biochemical and Genetic Engineering, has been studying the ways that bacteria adapt to survive these phage attacks.

Viruses work by injecting their DNA into your cell, their DNA becomes incorporated into your DNA and then literally “hijacks” your cell’s protein machinery into making more viruses. Bacteria have a special section of their genome called CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) that stores pieces of phage DNA from previous attacks. Upon a phage assault, a bacterium reads through CRISPR, finds the piece of DNA that matches from a previous attack from this same phage, and creates a complementary copy of the DNA that binds to the new phage DNA, blocking and destroying it before its incorporation.

Past work had shown that in between each section of phage DNA in CRISPR is a kind of bookmark of repeated DNA sequences (i.e. AAAAA or ACACACAC) at different lengths that the bacterium uses to recognize specific phage DNA. Previous researchers had also shown that within a bacteria population the chance of two bacteria having the same DNA in the same position increased as you went along the CRISPR sequence. Deem and his team wanted to know if this bookmarking and the sequential phage DNA in the CRISPR was due to the bacteria’s exposure to different phage during it’s lifetime.

Wielding some fancy computational power, they developed equations that may describe what is going on: In a colony of bacteria and phage, almost all the bacteria will have the current attacking phage DNA at the oldest part of the CRISPR, while the newest parts can vary from bacteria to bacteria. This conservation of the oldest part is not only because all of the bacteria have asexually reproduced from the other, and therefore transferred CRISPR, but because of selective pressure on the bacteria to keep the gene or die. The variability allows for when a new phage arrives, some bacteria will have immunity, while the other will perish.

If this all sounds familiar, it’s because it’s very similar to our own adaptive immune system, i.e. once we get chicken pox we don’t get it again. What’s amazing is that bacteria are billions of years old.

I was recently reading an article about oil eating bacteria and began thinking, “Why can’t we eat oil?” Yes, too much caffeine and a slow work day allows me to think crazy thoughts. Anyway, below is what I found out and it’ll be a three-part “Whatever Wednesday” series. Bon appetit!

“Oil” means many things, but technically it is a hydrocarbon (molecules that consist only of hydrogen and carbon) that is a viscous liquid at room temperature (~70-75F, ~20-22C) and does not mix with water. Oil can have animal, mineral, or synthetic sources. Since a synthetic source is usually just a copy of an animal or mineral source made in a lab, lets just look at the first two.

Mineral sources of oil, such as petroleum, are organic material that have been converted by geological processes and found in a mineral source such as porous rocks. It varies in consistency depending on its location, but a usual sample of petroleum contains a mixture of hydrocarbons, mostly alkanes such as octane (oct = eight carbons, ane = alkane), and cycloalkanes. Octane is a linear saturated alkane, meaning that it is not branched and all the carbons have single bonds.

Cyclooctane is just a circular version of octane and is always saturated. This configuration gives it different energy abilities than the linear one.

Organic sources of oil are found in plants and animals and are used as an energy storage source. Olive oil is an excellent example of an organic oil. It’s made up of a mixture of molecules called fatty acids (FAs), mainly: oleic acid, palmitic acid, and linoleic acid. Olive oil molecules resemble the alkanes seen in petroleum, but have an “acid” group on one end. This acid group makes them reactive and allows living things to enzymatically combine the oil with other molecules that are required for storage or energy. Other names for FA’s are lipids, free fatty acids or carboxylic acids.

Palmitic acid is a linear unsaturated hydrocarbon structure like octane, but with twice as many (16) carbons.

Oleic (means “from an olive”) acid has eighteen carbons, but has a kink at carbon number nine (as counted from the acid part). The kink is caused by a double bond because carbon nine is missing a hydrogen and oleic acid is therefore called a monounsaturated fatty acid (MFA).

Linoleic acid is also eighteen carbons long, but has two carbons missing hydrogen at carbon number nine and twelve. It’s therefore called a polyunsaturated fatty acid (PUFA).

Strictly speaking, oil is not to be confused with fat. Fat is usually not a liquid at room temperature, oil always is. Fat is three FA molecules attached to a glycerol backbone and they are called triacylglycerides (TAGs). This is a TAG with oleic, palmitic, and linolenic acid attached:

When the FAs are not attached to anything the are called “free” fatty acids (FFAs). The combination of different oil molecules attached to the backbone makes it either a solid or a liquid at ambient temps. To make this all even more confusing, fats and oils are under the umbrella term of “lipids.”

Next Wednesday I will describe how humans digest then store or burn the oil!