Lipids

esterification

joining fatty acids to a glycerol unit

de-esterification

release of fatty acids —> result in free fatty acid chains

re-esterification

reattaching a fatty acid to a glycerol that has lost a fatty acid

triglyceride

three fatty acids

diglyceride

loss of one fatty acid

monoglyceride

loss of two fatty acids

chain length

saturation

isomerization

key features of fatty acids

long chain fatty acids

12+ carbons (ex. beef, lamb, plant oils)

transported in lymph (because they are big)

medium chain fatty acids (MCT)

6-10 carbons (ex. generally “tropical” oils: coconut and palm oils)

transported in portal system (because they are small)

short fatty acid chains (SCFA)

fewer than 6 carbons (ex. dairy products)

transported in portal system (because they are small)

MCT and SCFA

2 types of fatty acid chains that are transported by portal system due to small size

long chain fatty acids

type of fatty acid chains that are transported in lymph due to large size

saturated fatty acids

have no double bond; solid at room temp

intake increase blood levels of cholesterol

ex. red meat, high-fat dairy, coconut and palm oil

monounsaturated fatty acids

one double bond in the whole fatty acid chain; liquid at room temp

intake decreases blood levels of cholesterol

ex. olive oil, canola oil, peanut oil

polyunsaturated fatty acids

many double bonds (2+); liquid at room temp

intake decreases blood levels of cholesterol

ex. vegetable oils and fish oils

isomerization

when hydrogens on opposites of carbon are added to fatty acid chain

intake increases blood levels of LDL cholesterol

ex. margarine, shortening

trans fatty acids

straight carbon chain

produced by hydrogenation

increases cholesterol even more than saturated fat

hydrogenation

adding hydrogen to make an unsaturated fat more saturated; creates trans fatty acids

hydrogenation

turns the liquid oil into a solid, increases shelf life of the product

trans bonds

make cell membranes rigid (they stack easily), while cis bonds permit fluidity

1. count how many carbons are in the chain

2. then count how many double bonds there are between carbons (including the first one)

3. starting on the omega (methyl) end, work your way across until you get to the first double bond (ex. if it is a 3, its an omega 3)

fatty acids

oils/fats contain mixtures of ?

triglycerides

most common lipid in the body and in foods we eat (95%)

main fuel source for all cells in the body, except brain and RBCs

provides a compact energy source

insulates and protects body

aid in fat-soluble vitamin absorption and transport

functions of triglycerides

omega-3

omega-6

essential fatty acids

omega-3 fatty acids

reduces inflammation, thins blood, and reduces plasma triglycerides

found in cold water fish, walnuts, flax, canola oil

omega-6 fatty acids

regulates BP, can increase blood clotting and inflammation

found in beef, poultry, safflower oil, sunflower oil, corn oil, mayo

eicosanoids

chemical messengers that play an important role in human health

ex. immune and cardiovascular health

phospholipids

similar to triglycerides, but one fatty acid is replaced with a phosphate group

have hydrophobic (fatty acid) and hydrophilic (phosphate) ends

component of cell membrane

emulsifier

functions of phospholipids

synthesized in the body

foods: lecithin in egg yolks, wheat germ

sources of phospholipids

sterols

multi-ring structure (as opposed to fatty acids)

known as cholesterol

steroid hormones

bile

cell membranes

chylomicrons

functions of sterols

synthesized in the body

animal sterols (meat, fish, eggs, dairy)

plant sterols (fruits, vegs, and vegetable oils)

sources of sterols

plant sterols

block cholesterol absorption sites in the human intestine —> help reduce cholesterol in humans

some concern that they may block absorption of other important nutrients as well

benecol

take control

plants sterols used ot reduce cholesterol

doubled

North American fat intake has almost ? in the last century

saturated fat

trans fat

omega 6

fats that are too high in the American diet

omega-3

fats that are too low in the American diet

water, protein, air (ex. soft serve ice cream)

carbohydrates

engineered fats

types of fat replacements

fat replacers in many fat-free/reduced-fat items

ex. corn syrups, syrup solids, and high-fructose corn syrup

Olestra (items labeled as “light”)

example of engineered fat

engineered fats

synthesized from sucrose

binds with many fatty acids —> making it too large/irregular to be digested and absorbed

causes diarrhea and inhibits absorption of fat soluble vitamins

A, D, E, and K

FDA requires manufacturers to add vitamins ?, ?, ?, and ? to products made with olestra (engineered fats) to counter the effect of engineered fats

decrease saturated and avoid trans fats

increase omega 3 and monounsaturated fats

goals of a healthy diet

stomach

contains gastric lipase

gastric lipase

triglycerides are broken down into monoglycerides and free fatty acids by this enzyme

liver

produces bile

blie

emulsifies fats

gallbladder

stores bile until CCK (fat in chyme) stimulates bile release

pancreas

produces lipases that are released into SI (sphincter of Oddi)

pancreatic lipase

phospholipase

cholesterol lipase

types of lipases produced by the pancreas

small intestine (duodenum and ileum)

where most of fat digestion occurs

micelles

bile emulsifies fat to form ? that are acted upon by pancreatic lipase

phospholipase

breaks down phospholipids into free fatty acids, glycerol and phosphoric acid

cholesterol lipase

breaks down cholesterol esters into cholesterol and free fatty acids

bile emulsifies fat to form micelles

phospholipase breaks down phospholipids

cholesterol lipase breask down cholesterol esters

processes occurring in the SI for fat digestion

lipids

absorbed by absorptive cells in the duodenum and jejunum

absorptive cells

cells that absorbs lipids in the duodenum and ileum

duodenum and ileum of SI

where absorptive cells absorb lipids

short and medium chain fatty acids

fatty acid chains that are absorbed via the portal vein (“nearly” water soluble)

lipids

these are converted into triglycerides and packaged into chylomicrons and absorbed into lymphatic system

triglycerides

lipids are converted into ?

chylomicrons

lipids are converted into triglycerides and packaged into ?

chylomicrons

lipid core with a shell comprised of cholesterol, phospholipids, and proteins

enterohepatic circulation

process that recycles bile

VLDL

lipoprotein that carries lipids both taken up and made by the liver to cells

primary component: triglycerides

LDL

lipoprotein that carries cholesterol made by the liver and from other sources to cells

primary component: cholesterol

HDL

lipoprotein that helps removes cholesterol from cells and in turn excretion of cholesterol from the body

primary component: protein

chylomicron

lipoprotein that carries dietary fat from the SI to cells

primary component: triglycerides

LDL

we need some cholesterol in our cells, so ? carries and delivers it

LDL

cells with a ? receptor can absorb cholesterol

liver and other cells

cells with LDL receptors

cholesterol

protein

once LDL is inside the cell, it is broken down into ? and ?

cholesterol

used to make cell membranes or compounds into estrogen, testosterone, and vitamin D

LDL

once cell has enough cholesterol, it will “turn off” the ? receptor

blood levels

if more LDL is in the body than is absorbed, ? of LDL increase

LDL

is not supposed to be in the blood for a long period of time

it gets damaged or oxidized and causes “plaque” (negatively impacts health)

plaque

when LDL is damaged or oxidized after being in the blood for too long, it produces ?

high density lipoproteins (HDL)

protein responsible for cholesterol uptake

picks up excess cholesterol throughout the body and eventually leads to excretion (reducing total cholesterol)

blocks oxidation of LDL and reduces “plaque”

why HDL is called “good cholesterol”

aerobic exercise

how we increase HDL

plaque

1. oxidized LDL are cleaned up by special white blood cells (macrophages) —> embed themselves in blood vessels and engulf oxidized LDL

2. as cells get full and die, more cells come to take their place and eventually die, etc.

3. buildup in an artery causes ?

blood cholesterol levels

plaque

diets high in saturated and trans fats are known to increase ? and ?

atherosclerotic plaque

during the development of CVD (cardiovascular disease), ? forms in our arteries —> causes heart attack or stroke

die

clot in heart (heart attack) or clot in brain (stroke) causes tissues to ?

age, gender, race, and genetics

non-modifiable risk factors for CVD

lifesytle factors such as high dietary fat, high dietary salt, smoking, physical inactivity, obesity, and diabetes

modifiable risk factors for CVD

keep total fat to 20-35% of total calories

keep saturated fat <7% of total calories

eliminate trans fat

polyunsaturated <10% of total calories

monounsaturated <20& of total calories

don’t overdo omega-3s

limitations recommended to prevent CVD

include 2 grams of plant sterols

increase soluble fiber 20-30 g

eat fatty fish 2x/week

eat fresh meat (old meat oxidizes)

keep body weight at a healthy level

increase physical activity (raise HDL)

things to emphasize to prevent CVD