Lipids

Lipid Molecules made up of long hydrocarbon chains Fatty Acids - single chain hydrocarbons with 4 – 22 carbons Triglycerides - 3-carbon glycerol backbone with one fatty acid attached to each of the 3 carbons Diglycerides – as above with 2 fatty acids Monoglycerides – as above with 1 fatty acid Phospholipids - glycerol with fatty acids attached to carbons 1 & 2 with a phosphorous attached to the 3 rd. Cholesterol carbon & 1 5-hydrocarbon rings (modified to produce the various steroids)

EFA’s Structure of some lipids Glycerol Fatty Acids

Lipid Functions Primary storage form of energy & major substrate for energy (especially at rest) Absorption of Fat soluble vitamins (A, D, E, &K) Source of the Essential Fatty Acids Linoleic and α-Linolenic (linoleic is made into arachidonic acid, α - linolenic is made into docosahexaenoic acid & eicosapentaenoic acid which are essential for prostaglandin, thromboxane, & leukotriene synthesis) Common Food Sources (oils) linoleic: corn, safflower, soybeans, peanuts, sunflower seeds… α-linolenic: soybeans, linseed, flax, most other seed oils… Synthesize steroid hormones from cholesterol Synthesize bile from cholesterol & FFA Membrane phospholipids Essential component of PDH & α-kGDH

AI 12 & 17 g/day linoleic acid (C18:2; n6, 9 - all cis): F / M; based on on median intake 1.1 & 1.6 g/day α-linolenic acid (C18:3; n9, 12, 15 - all cis) F / M; based on median intake Or: % of total calories (9kcal/g)… so… lets see what you have to eat to… Some older texts suggested a minimum total intake of 20g/day to insure a sufficient uptake of fat soluble vitamins which greatly underestimates the actual dietary lipid requirement (RDAs are based on fatty acid intake, not TG intake and eating exactly 12g linoleic acid or 1.1 g α-linolenic acid would obviously necessitate eating more than 13g total fat since the EFA are a small minority of total FFAs) EFA Content of various foods in % of total FA Linoleicα-Linolenic% Fat by Wt Canola Oil~ Corn Oil~ Olive Oil~ %~ 1%100 Palm Oil~ ~ Peanut Oil~ ~ Flax Oil~ 14~ Beef (grain-fed-trimmed)~ 3.4~ 0.4~ 5 Beef (grass-fed-trimmed)~ 4.4~ 1.2 ~ 2.5 Chicken (skinless-breast)~ 21~ 0.9 ~ 4.5 Salmon (Norway-wild)~ 1~ 1 (2%EPA/20% DHA) ~ Human Milk~7 - 18~ 1~ Cow Milk Fat~ 2.6~ 1.6 ~ 0, 1, 2, or ~3.5 Based on the EFA content of common foods (as a percent of total fatty acids) you clearly have to eat a lot more grams of fat than the RDA (as expressed in grams for the EFA’s)

so let’s figure it out… average calories/day for adults 19 – 50 yrs: ~ 2400 F ~ 3000 M at 10% - 35% calories from fat… (240 – 840 kcal) (300 – 1050 kcal) EFA Content of various foods in % of total FA Linoleicα-Linolenic% Fat *Fat intake / kCal Fat intake / kCal Total “Food” Intake by Wt (g) (g) to meet RDA Linoleic α-Linolenic (min g/kcal) Canola Oil~ / Corn Oil~ / Olive Oil~ ~ / / /990 Palm Oil~ ~ / / /1980 Peanut Oil~ ~ / / /2475 Flax Oil~ 14~ / / /774 Beef (grain-trimmed)~ 3.4~ 0.4~ 5 353/ / /30,005 Beef (grass-trimmed)~ 4.4~ 1.2~ / /819 10,880/44,880 Chicken (skinless-breast)~ 21~ 0.9 ~ / / /11,454 Salmon - Norway - wild~ 1~ 1 ~ /10, /990 30,000/125,000 Human Milk~7 - 18~ 1~ / / / why bother Cow Milk (butter fat)~ 2.6~ 1.6~ 2 461/ /621 23,050/ “ Based on the EFA content of common foods (as a percent of total fatty acids) you clearly have to eat a lot more grams of fat than the RDA (as expressed in grams for the EFA’s) *Fat Intake calculated for an (“average”) adult female (for males, the intake would be approximately 25% higher). Calculations of total food intake are based on that single food item being the sole source of EFAs. From these values it is clear that eating less than 30% of calories from common sources of fat is a near guarantee of EFA (borderline?) deficiency. It also is clear that the fat in meats & milk is not very relevant in terms of significant contributions to total EFA intake. Fats in “spreads”, cooking oils, and cheeses seem to make the most difference… and of the added fats, cold-press, virgin olive oil (tends to be at the lower end in linoleic content) and butter/cheese from cows, along with cooked fish 2x/week and maybe a small amount of added flax oil would be the most logical frequent choices to ensure adequate intake of the EFAs as well as the anti-inflammatory omega3 FA: DHA & EPA.

Α-Linolenic EPA DHA ~ 0.2% ~ 37% ~ 63% Pawloski et al. 2001

Some of those “awesome Omega 3’s” One of those “evil” trans-fats

Steroid hormones are made from cholesterol

Bile acids are also synthesized from cholesterol...

Prostaglandins, thromboxanes, & leukotrienes are synthesized from arachidonic acid (& EPA/DHA which are synthesized from the essential fatty acids)

Digestion/Absorption - Mastication in mouth Bolus w/ saliva/mucus - Lipids break up to tiny droplets in chyme from stomach/acid action - Bile from liver bile salts & acids made from cholesterol, fatty acids, sodium, potassium & chloride -Lipases from Pancreas

-Emulsification by bile salts and bile acids -FFA, MG, PL, gycerol, CHOL, absorbed -Glycerol metabolized, lipids resynthesized and packaged into chylomicrons (apoB-48, *apoC-II, apoC-III, apoE)

Chylomicrons - Lipoprotein + lipids TG PL Chol ~85% ~9% ~4% released into lymph/blood ~ 50 : 50 ApoC-II activates lipoprotein lipase in capillaries Tissues remove FFA, PL Liver picks up chylomicron remnants

Lipoprotein content of the chylomicron changes as it circulates throughout the body - acquiring the apo E & C2 from HDL apoE & apoB-48 are ligands for liver uptake of remnants... apoCII is ligand to activate lipoprotein lipase for removal of fatty acids in tissues... Deliver dietary TG and PL to cells dietary CHOL to liver...

apoE is ligand for liver uptake & apoB-100 is ligand for tissue uptake... apoCII is ligand to activate Lipoprotein lipase for removal of fatty acids Delivers endogenous TG and PL to cells... Delivers CHOL to cells...

HDL really serves as a circulating resevoir for apoE and apoC’s for efficient removal of LDL’s and lipids from the blood Note that HDL also picks up CHOL from tissues and returns it to the liver for bile synthesis (CHOL excretion pathway) Function of these apoprotein ligands and the cellular receptors that recognize them have important implications for atherosclerosis