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What is atherosclerosis?

What is atherosclerosis?



What is atherosclerosis?

∙ What is atherosclerosis? 

o Thickening of arterial walls causing decreased blood flow

 Primarily affects arteries

∙ Coronary arteries supply myocardium

∙ Vessels in lower extremitiesPAD (peripheral artery  


o Can cause cramping, numbness, feeling cold in  


 Leads to coronary artery disease (CAD) 

o Atherosclerotic Plaque Formation 

 Endothelial damage

∙ Endothelium – single layer of cells lining lumen

∙ Can be physical, caused by free radicals, etc.

 LDLs penetrate endothelium

Where are most tg’s located in the body?

∙ More damaged or older LDLs or just a high number of  

LDLs flow aroundmore likely to be dropped off in  

vascular system

 Aggregation of platelets, monocytes, and t-lymphocytes

∙ Macrophages take up LDLs

∙ Growth factors released from platelets and macrophages

∙ Growth factors stimulate smooth muscle cell growth and  

attract more macrophages

∙ Smooth muscle cells

∙ Fatty streaks form

 Arterial narrowing We also discuss several other topics like Which one of the following will decrease the net working capital of a firm?

∙ Decreased blood flow

∙ Increased blood pressure

 Vessels compensate by vasodilation

Where are the majority of our phospholipids?

∙ Eventually it can’t vasodilate anymore

 Increased pressure causes cracks in plaque, more endothelial  damage

∙ If it occurs in the brainmost damage

∙ More platelet aggregation (cyclic process)

 Platelet aggregation

∙ Continued narrowing of vessels

∙ If loose=blood clot, can get stuck in narrowed vessels

 Total blockage by plaque

∙ Myocardial infarction (heart attack)

∙ Stroke (in brain)

∙ Poor circulation in lower extremities

∙ Can cause tissue/cell death (no blood flow)Don't forget about the age old question of What physical and motor developments are seen in 12- to 18-monthold children?

 Fatty streaksearly plaque formationarterial  

narrowinglocalized slowing of blood flowcracks in  

plaqueplatelet recruitment 

o Treatment (surgery) 

 Stent 

∙ Medicated or non-medicated

∙ Dilated balloon catheter

∙ Lasts about 10 years; get it checked out and it can either  stay in or may have to change it

∙ Presses plaque against artery walls

∙ Medications: antiplatelet aggregation meds help prevent  more plaque more building around stent

∙ Balloon angioplasty – inflate then take out


∙ “coronary artery bypass graft” We also discuss several other topics like How do we look to shareholders?

∙ AKA open heart surgery (obviously very invasive)

∙ Going in and removing the plaque

∙ Use a bypass graft from a vein and it is then used to go  around a blockage

∙ This helps reduce the pressure on the blockage and helps  supply the myocardium

∙ Can be done multiple times if needed (e.g. – triple bypass  surgery=3 grafts)

o Possible causes of endothelial damage 

 Foam cells erupt

 Oxidized LDLs

∙ Damaged LDLs-more likely to deposit cholesterol on  


 High blood pressure

∙ Increases especially when foam cells are already present  Smoking  

∙ Increased endothelial damage

∙ Accelerates atherosclerotic lesion formation We also discuss several other topics like What defines our solar system?

∙ Source of free radicals

∙ Secondhand smoke can cause problems as well

∙ Smoking decreases nitric oxide (helps  

vasodilate)increased blood pressure

o Serum Cholesterol 

 Total cholesterol

∙ Tells value of all cholesterol in blood

∙ Recommendation: <200 mg/dL

 LDL: recommendation <100 mg/dL

 HDL: recommendation >60 mg/dL

∙ A negative risk factor (cancels out/counteracts LDLs)  Total/HDL ratio: should be 3.8 or lower

∙ Better indicator than just total cholesterol values  TopHat: Who has healthier cholesterol? Bill or Jill? ∙ Bill –  

o Total Cholesterol=230 Don't forget about the age old question of How does this mean we are progressing as a human race?
Don't forget about the age old question of What are the most common myths about communication?

o LDL=150

o HDL=65

o TC/HDL ratio230/65=3.5

∙ Jill -  

o Total cholesterol=190

o LDL=100

o HDL=35

o TC/HDL ratio190/35=5.4

∙ Answer: Bill does because his TC/HDL ratio is below 3.8  (higher HDL count than Jill).

 How to modify cholesterol 

∙ HDL – increase by  

o Exercise

o Moderate alcohol intake of red wine (1 glass/day –  women; 2 glasses/day – men)

∙ LDL – want to decrease:

o Fat intake

 Saturated

 Polyunsaturated

 Monounsaturated

o Weight loss

 It’s been shown that any method of weight  

loss will result in decreased LDLs

∙ Dietary approaches: 

o Lower saturated fats

o Lower trans fats

o High fiber

o Role of antioxidants

∙ Replace SFA (sat.) in diet with: 

o SFA (sat. f.a.’s) in diet with:

o CHO (simple)=no decreased risk of CHD

o PUFA (polyunsat.)=reduction in CHD

 Omega-3: decreased risk of CVD

∙ EPA, DHA – fish

∙ ALA – flax, canola, walnuts

 Omega-6: decreased risk of CHD?

∙ Depends; we need more omega-6’s  

than omega-3’s but if there is a big  

difference between the two and we  

have too many omega-6’s, it can come

with an inflammatory response

∙ Comes from plant oils (corn oil,  

soybean oil, nuts, seed, flax)

o MUFA (monounsat.)=reduction in blood cholesterol  but doesn’t decrease risk of CHD

 Sources: olive oil, canola oil, avocados

∙ TopHat: Sources of Omega-6 fatty acids include… o Answer: sunflower oil (plant oils)

∙ Decrease trans fats: 

o Trans fats with increase LDLs and decrease HDLs o Sources:

 Naturally occurring: meats, dairy products

 Chem. Processed: cis to trans configuration  during hydrogenation

o Labeling laws

 2006-trans fats must be included on label

 Rounded to nearest 0.5 g if less than 5 g

 Rounded to nearest g if over 5 g

 If total fat is less than 0.5 g, can state 0 g of  trans fats

o US Dietary Guidelines: <2g/day 

∙ Fiber: 

o Fermented in colon – short chain fatty acids  Acetic acid

 Butyric acid

 Propionic acid

o Functions of short chain FAs

 Stimulates water and sodium absorption into  mucosal cells

 Provide colonocytes with energy

 Enhanced immune function

∙ Stimulates immune cells (most of  

immune system is in gut)

∙ Stimulates good bacteria production

 Decreased atrophy of the gut

∙ Atrophy leads to gaps between  

cellsinflammation (e.g. – IBS)

 Decreased cholesterol by:

∙ Decreasing pH of the gut=decreasing  

reabsorption (recycling) of bile (made  

from cholesterol)

∙ Inhibits cholesterol synthesis in liver?

o More research being done

o HMG CoA?

o Excreted as fecal matter

 Carries bile with it  

∙ Soluble carries more than insoluble

o Sources: veggies, fruits, whole grains

∙ Antioxidants 

o Reactive oxygen species = more ROS

o Oxidation

 Metabolic: complexes of ETC and MEOS,  lipoxygenase and cyclooxygenase pathways  External poulltants

o Oxidation of:

 Endothelium - increased deposition of  cholesterol to vascular system

 LDLs-atherosclerosis

o Antioxidants:

 Vitamins E & C

 Carotenoids (give fruits/veggies their color)  Glutathione

 Coenzyme Q

o Sources:

 Plants/plant oils

HUN 3224 Exam 3 Notes: Lipids 

 ∙     Fatty acids 

o Straight hydrocarbon chain

 4-24 carbons long

 14 or more C – nutritionally significant

 Most have even numbers of carbons

o Short chain – made from fiber

o Medium chain – found in coconut oil; metabolized differently o Long chain – omegas

 ∙     Saturation 

o Saturated fatty acids 

 All C’s are saturated with H’s

 No double bonds

 Solid at room temperature

 Typically animal fats (e.g. – fat on chicken, steak and butter,  etc.)

o Monounsaturated fatty acids 

 Unsaturated – healthier than saturated

 One double bond (C=C)

 All liquid at room temperature

 E.g. – olive oil, canola oil

o Polyunsaturated fatty acids 

 Multiple C=C bonds

 Cis is the predominant form

 E.g. – vegetable oils, nut/seed oils, omega 3, omega 6

 ∙     Hydrogenation 

o Liquidsolid

o Adding hydrogens to unsaturated fatty acids to make solid at room  temperature (e.g. – Crisco)

o Often used in commercially processed foods (e.g. – crackers, cookies) o Trans fats are usually unhealthier than cis fats

o Hydrogenationsdouble bonds left over

 Usually in trans configuration

 ∙     Nomenclature 

o Count # of carbons

o Count # of double bonds (always 3 carbons apart)

o Omega or alpha end

 Alpha: carboxyl group (Δ)

 Omega: methyl end (n)

 ∙     Essential Fatty Acids 

o We eat them; we cannot synthesize them

o Linoleic Acid (18:2w6 or 18:2Δ9, 12)

 Omega-6

 2 double bonds

o Alpha-Linolenic Acid (18:3w3 or 18:3Δ9, 12, 15)

 Omega-3

 3 double bonds

o We lack the enzymes to add C=C bonds beyond Δ9

o Both of these acids are 18 carbons long

o When we make fatty acids and add double bonds, we cannot add any  that are past Δ9 (e.g. – cannot add Δ12 or Δ15)

o When we look at fatty acids with double bonds past Δ9, we know that  they must be essential

 ∙     Eicosanoids 

o Hormone-like substance

 Modulation of:

∙ Blood pressure

∙ Platelet aggregation

∙ Immune system

∙ Nervous system

∙ Smooth muscle contraction

 Essential fatty acids are important because we metabolize them  

into eicosanoids (20 C fatty acids) and are hormone-like in  


 They function where they are made (different from other  


o Families 

 Prostacyclins

 Thromboxanes

 Leukotrienes

o Synthesized from: 

 Arachidonate acid (20:4w6)

 Eicosatrienoic acid (20:3w6)

 Eicosapentanoic acid (20:5w3)

o Omega end of a fatty acid never changes (n3 will always be n3)

 E.g. – EPA is 20:5w3  has an omega-3 end  made from alpha

linolenic acid

o Aspirin: non-steroidal anti-inflammatory drug, blocks formation of  eicosanoids to bring down fever, swelling, etc.

o *TopHat Question: EPA is a conditionally essential fatty acid, t/f.

 Answer: true – we can make EPA (eicosapentanoic acid) under  

conditions that we eat linolenic acid

Characteristics of Eicosanoids:

Eicosanoid family

Site of Synthesis

Mode of Action


Vascular endothelium

Vasodilator, platelet anti aggregation



Vasoconstrictor, platelet




Vascular contraction,  



Endothelium of a variety  of cells

Vascular smooth muscle  contraction or relaxation

 ∙     Triglycerides: 

o Glycerol backbone

 3-C chain and 3 fatty acids

 Storage – adipose tissue (similar to glycogen for storing carbs)

 ∙     Phospholipids 

o Glycerol backbone

o One or more fatty acid

o One phosphate group

 A polar head group is attached to the phosphate

 ∙     Glycolipids 

o Lipid and carbohydrate

o 2 fatty acids and 1 or more carbs

 ∙     Sterols 

o Steroid nucleus

 4 fused rings

o Cholesterol

 Bile acids

 Steroidal sex hormones

 Adrenocortical hormones

 Vitamin D

o Too much cholesterol is bad but it is still important

o Every cell can make cholesterol

o *TopHat Question: Where are most TG’s located in the body?

 Answer: adipose tissue

o *TopHat Question: Where are the majority of our phospholipids?

 Answer: cell membranes

 ∙     Lipid Digestion 

o Lingual lipase

 Secreted at base of tongue

 Stable at a low pH

 Efficient digestion of milk fat (e.g. – in infants)

o Biliary Emulsification

 In small intestine

 Emulsification:  

∙ Dispersion of fat in an aqueous solution

∙ Spreads out so everything can get digested

∙ Allows for lipase action (break down of fats)

 Bile salt – emulsifying agent

∙ Made from cholesterol

∙ Cholesterol  likes lipids

∙ Has a Na+ on one end  Na+ likes water

 o Lipolysis (via bile salts) 

 3 main enzymes

∙ Pancreatic lipase

o Breaks TG 1,2 diacylglycerol + fatty acid

o Breaks 1,2 diacylglycerolmonoglycerol + fatty  


o Breaks monoglycerolglycerol +fatty acid

o Altogether: 3 fatty acids and a glycerol

o We can absorb monoglycerols

∙ Cholesterol esterase

o Cholesterol ester free cholesterol + free fatty acid

∙ Lecithinase

o Lecithinlysolecithin + free fatty acid

 ∙     Lipid Absorption 

o Micelle formation

 Fatty elements and fat soluble vitamins surrounded by bile salts  Passive diffusion of fatty elements and vitamins at distal  

duodenum and jejunum (their enterocyte membranes)

∙ In first part(s) of SI

 Bile salts absorbed in ileum (at end of SI) and returned to liver  via EHC

o Inside enterocyte

 Long chain fatty acids (>12 C) and other fatty components  Reformation of triglycerides, cholesterol esters, and  


 Triglycerides + fatty components + proteins = chylomicron  (lipoprotein)

∙ Chylomicron – too big to fit in circulatory system; goes to  lymph

 Short-chain fatty acids  attach to albumin

 ∙     Lipoproteins 

o 5 kinds (big to small): chylomicrons, VLDL, LDL, IDL, HDL

o They are complexes which carry lipid products in the blood and lymph  to various tissues

o Has cholesterol, enzymes, etc.

o Each kind has different kinds of apoproteins

o 1 layer – phospholipid membrane

o Only a carrier proteins

∙ TopHat question: Chylomicrons are made from what?

o Answer: the fat that we eat

 ∙     Chylomicrons 

o Formation

 Synthesis in enterocytes from exogenous lipids (food we eat)  Released into lymph (thoracic ducttissues)

o Composition

 Apoproteins A, B, C, E : 1-2%

 Triglycerides: 80%

 PL and cholesterol: 15%

o Size

 The biggest lipoprotein

 90-100 nm

o Function

 Transport exogenous triglycerides to tissues

 Lipoprotein lipase (LPL)

∙ Hydrolyzes TG to free fatty acids and glycerol (both  

absorbed in tissues)

o Chylomicron Remnant

 Remains after TG hydrolysis

 Taken up by hepatocytes via receptor mediated endocytosis  ∙     Very-Low Density Lipoprotein (VLDL) 

o Formation

 Made in liver

 Released into blood

o Composition

 Apoproteins B, C: 8%

 TG: 50%

 Cholesterol: 20%

 PL: 20%

o Size: 30-90 nm

o Function:

 Transport endogenous lipid from liver to extra-hepatic tissues  Uses LPL (lipoprotein lipase)

∙ Hydrolyzes TG to free fatty acids and glycerol

∙ Free fatty acids and glycerol absorbed to tissues

 ∙     Intermediate Density Lipoprotein (IDL) 

o Formation

 From VLDL (after TG hydrolysis)

 Transient, very short-lived

o Function

 Formed into LDL after TG hydrolysis via LPL

 ∙     Low-Density Lipoprotein 

o Formation

 From IDL after TG hydrolysis

o Function

 Delivers cholesterol to non-hepatic tissues

 Uptake via RME (RME takes the whole thing wherever it needs to go)

 Susceptible to oxidation and dropping off cholesterol where it  shouldn’t go (e.g. – cholesterol in cardiovascular  


 More free LDL, that means cells are full of cholesterol

 We will always have “in transit” LDL

o Composition

 Apoproteins B-100: 21%

 TG: 9%

 Cholesterol: 50%

 Phospholipids: 23%

o Size: 20-25 nm

o Receptor Mediated Endocytosis (RME) 

 Some in liver and cell

 Receptors located in clatharin coated pits

 Receptors – specific for proteins (e.g. – LDL: apoproteins B-100)  LDL and receptor

 Receptor and LDL complex internalized vessicle forms

 Vesicle and lysosome, fuse

 Lysosome changes pH

 Apo B degraded to amino acids

 Cholesterol released into cell

 Receptor returns to surface

 Regulation

∙ HMG CoA reductase activity

o Rate-limiting enzyme for cholesterol synthesis

o More cholesterol in celldecreased enzyme activity

∙ LDL receptor synthesis

o If cholesterol level in cell are high, this will decrease

LDL receptor synthesis

∙ Therefore, high levels of dietary cholesterol in bloodmore free LDLs

o LDLs, susceptible to oxidation

o Free LDLs will drop off cholesterol in tissues like the  

cardiovascular system, etc. (e.g. – in arteries)

 ∙     High-Density Lipoprotein (HDL) 

o Formation

 Liver and intestine

o Composition

 Apoprotein (A, C, D, E): 50%

 TGs: 3%

 Cholesterol:20%

 Phospholipids: 30%

o Size: 5-25 nm (smallest lipoprotein)

o Function:

 Removal of cholesterol from non-hepatic tissues

 LCAT (lecithin-cholesterol acyltransferase)

∙ Allows HDL to pick up cholesterol from cell  

membranes/other lipoproteins

∙ Apo-A1 binds to LCAT receptor

∙ Cholesterolcholesterol ester (CE)

∙ Phospholipidlysolecithin (a phoshpholipid w/o a fatty  


∙ Lysolecithin binds to albumin

∙ HDL transport CE to liver

 High HDLs lower LDLs

 Exercise helps increase HDLs

 HDLs never actually enter cell(s), they just “pick up” cholesterol  ∙     Cholesterol 

o Synthesis

 A little more than ½ of all cholesterol in body is synthesized o Location

 Liver – 10%

 Intestine – 10%

 Every nucleated cell can make cholesterol

∙ Cytosol

∙ Endoplasmic reticulum

o Regulation of cholesterol synthesis

 HMG CoA Reductase Activity 

∙ Rate-limiting enzyme (regulates pathway)

∙ Reduced by:

o Cholesterol

o Fasting (long-term)

 Body needs energy over cholesterol so acetyl

CoA will go through Krebs cycle instead of  

cholesterol synthesis

o Glucagon

 A fasting hormone

 Acetyl CoA to Krebs cycle

o Glucocorticoid hormones  

 “fight or flight”needs energy

 Dietary cholesterol

∙ More dietary cholesterol = less synthesis

∙ Less dietary cholesterol = more synthesis in body  

∙ We eat about 600 mg/d, RDA – 300 mg/d 

∙ We get cholesterol from animal tissues, so  

vegetarians/vegans usually synthesize most of their  

cholesterol more than omnivores

o Transportation

 HDL – high density lipoprotein

∙ Transports cholesterol from tissues to liver

 LDL – low density lipoprotein

∙ Transports cholesterol from liver to tissues

o Functions

 Cell membranes

∙ Maintains fluidity

 Steroid hormones

∙ Testosterone

∙ Androgens

∙ Estrogen

∙ Progesterone

 Vitamin D

 Bile

 ∙     Bile 

o Composition

 82% water

 12% bile salts

 4% phospholipids

 0.7% free cholesterol

 Electrolytes

 Bile pigments

∙ Bilirubin, biliverdin 

∙ Give bile its yellow/green color

∙ From breakdown of heme from hemoglobin

o Volume

 Make 500-800 mL/day

o TopHat: which lipoprotein takes cholesterol to liver?

 Answer: HDL  

o Synthesis of Bile

 Hepatocytes (liver)


∙ Secretin

∙ Gastrin

 Sent to gall bladder

∙ Concentrated and stored

 CCK stimulates release from gall bladder

∙ Contraction of gall bladder

∙ Through sphincter of Oddi

∙ Into duodenum via bile duct

o Function

 Lipid emulsification

 Essential for fat digestion

 Gall stones

∙ Mixed with minerals and water leaves, concentration  


∙ Can get stuck in ductsblock secretions of liver and  


∙ Treatment: gallbladder removed

o Post-treatment: not recommended to eat a lot of fat

o Bile comes from liver now, just not as concentrated

 TopHat: what are the consequences of having the gallbladder  removed?

∙ Answer: less concentrated bile; bile is made in liver now

 ∙     Fatty Acid Synthesis 

o Synthesis

 Glucose – primary substrate

 Membrane permeability

∙ Acetyl CoA and oxaloacetate cannot cross mitochondrial  


∙ Pyruvate and citrate can cross mitochondrial membrane

∙ Majority of synthesis is in cytosol

o Fatty Acid Synthase 

 Enzyme complex (8 subunits)

∙ Thioesterase

∙ Acyl carrier protein

∙ Ketoacyl reductase

∙ Enoyl reductase

∙ Hydratase

∙ Transcyclase (2)

∙ Ketoacyl synthase

 Active Complex

∙ Dimer or 2 identical polypeptide monomers

o Altogether: 8 subunits x 2 monomers = 16 subunits

to be active

∙ Monomers connected by 2 disulfide bonds

o Desaturation 

 Occurs after we get to 16 carbons

 Addition of double bonds

 Enzyme: desaturase

 Essential fatty acids

∙ Lack enzymes Δ12 and Δ15 desaturase, which add bonds  past Δ9 position

o Double bonds – every 3 carbons

∙ 18:2 Δ9, 12

∙ 18:2 Δ9, 12, 15

 De novo fatty acids – 16 carbons long

 Must elongate then desaturate

 First double bond will be at Δ9C (n9 fatty acid)

 ∙     Beta Oxidation 

o Opposite of fatty acid synthesis

o Needs oxygen

 When we are sitting/aerobic exercisewe burn more fat (beta oxidation)

 When we are performing anaerobic exercisewe burn more carbs o Breaking down long-chain fatty acids for energy

o Energy

 Even chains

 Odd chains

o Regulation: malonyl CoA 

 High levels inhibit carnitine acyl/palmitoyl transferase 1

 Low levels allow for production of CAT-1/CPT-1

o Energy Count: Beta-Oxidation 

 Outside mitochondrial membrane

∙ -2 ATP (initiation step happens once)

 Inside mitochondrial membrane (cleavages)

∙ (each time 2 C’s are cleaved)

o +1 NADH=3 ATP

o +1 FADH=2 ATP

o =5 ATP total

 Krebs cycle (the most energy produced)

∙ (for each acetyl CoA produced – depends on length of  

fatty acid chain)

o +3 NADH=9 ATP

o +1 FADH=2 ATP

o +1 GTP=1 ATP

o =12 ATP total

 ∙     Ketones 

o After beta-oxidation there are 2 pathways for energy production from  fatty acids

 Krebs cycle (from palmitate – 129 ATP)

 Ketone production (lack of glucose)

∙ Fasting stateketosis

∙ Ketone bodies 

o Acetoacetate (from Palmitate - 33 ATP)

o Beta-hydroxybutarate (from palmitate - 21 ATP)

o Acetone (from palmitate - 0 ATP)

∙ Fasting State: 

o Blood – low glucose levels

o Adipose tissue (triglycerides) – lipolysis = fatty  

acids, glycerol

o Liver

 Glycerolgluconeogenesis = glucose

∙ Glublood stream

∙ Brings blood glucose levels up to  


∙ Taken up by other tissues (e.g. – brain)

 Fatty acidsbeta-oxidation = acetyl CoA

∙ Provides liver with more acetyl CoA  

than it can use

∙ Acetyl CoAketones

∙ Ketones enter blood stream and taken  

up by tissues (e.g. – brain)

∙ Energy (look at diagrams – Palmitate diagram)

o When do we make ketones? 

 Starvation  

∙ Low CHO

∙ Increased fatty acid oxidation (burning

fat stores)

 Low CHO diet

∙ Tricks body into ketosis

∙ E.g. – Atkin’s Diet: mimics starvation,  

not eating lots of CHO

∙ Ketosis usually sets in about 2-3 weeks o Normal if an average, healthy  

person changes food intake to  

low carbs

∙ Real starvation, ketosis sets in faster

∙ If on Atkin’s diet: weight gain can  

happen immediately when  

reintroduced to carbs, not a  

sustainable method to lose weight,  

lowers BMR

 Diabetes

∙ Insufficient insulin

∙ Uncontrolled – glucose (CHO) not  

taken up in cells, so cells think they  

are starving (glucose hanging out in  


∙ Increased beta-oxidation

o Why don’t the fatty acids go through Krebs?  Low CHO = low pyruvate  low OAA  


∙ Without OAA, we cannot run the Krebs  cycle

 More acetyl CoA than the Krebs cycle can  handle (backed up system)

∙ Large amounts of fatty acids being  


∙ Limited/no fatty acid synthesis

∙ No malonyl CoA (made from F.A.  

synthesis) to downregulate CPT1

 Energy with low CHO

∙ Proteingluconeogenesis

∙ Brain prefers glucose

o Are ketones bad for us? 

 Provide less energy than other fuel sources ∙ Will need to burn more fat to get same amount of energy  inefficient system  

 weight loss

 Kidney

∙ Dehydration/constipation can occur

∙ Body wi ll work harder to rid body  of acid

∙ Increased urine excretion

∙ If an individual has kidney  

issuesshould NOT do the Atkin’s diet

 Ketosis is bad If it is caused by real  

starvation or disease (e.g. – diabetes)

o TopHat: What end does desaturase work from?

 Answer: the carboxyl end

o TopHat: “Purpose of lingual lipase is to break fatty acids into 2 C units.”  Answer: FALSE; it goes through lipolysis (below)

o TopHat: Under what conditions will we undergo ketosis?

 Answer: all the conditions above.  

 ∙     Metabolism of Glycerol  

o Lipolysis 

 Break down of a triglyceride

 TG  3 fatty acids (which go to beta-oxidation) + glycerol  


o Esterification 

 Formation of a triglyceride

 ∙     Organ Specific Lipid Metabolism 

o Mouth

 Lingual lipase  

∙ Milk fat digestion, breaks triglycerides  

∙ Breaks 3 fatty acids off glycerol backbone

o Intestine

 Absorption of lipid from diet

 Formation of micelles 

∙ Micelles passively diffuse to enterocytes

o Enterocyte

 Chylomicron synthesis (transport/drop off)

o Liver (*does a lot with lipids)

 Bile synthesis

 Cholesterol synthesis

 Fatty acid synthesis

∙ TGs, phospholipids, oxidized

 Beta oxidation

∙ Krebs

∙ Ketone synthesis

 Lipoproteins

∙ Formation of HDL & VLDL

∙ Endocytosis of chylomicron remnant (takes it up into liver) o Adipose Tissue

 Fatty acid synthesis and storage (triglycerides)

 Insulin stimulates

∙ Glucose uptake into cells

∙ Glucose as a substrate for F.A. synthesis

∙ Lipid uptake into cells


 Leptin 

∙ Made to beat obesity

∙ Reduces appetite and increases basal metabolic rate ∙ Weight maintenance

o More adipose tissue, more leptin

∙ Tells brain you’re full when sleeping

o Not as much sleepweight gain

∙ Leptin gene mutation can lead to uncontrolled appetite  and obesity

o Very rare mutation

o Mutation comes with other physical characteristics  (e.g. – decreased pigmentation in skin)

∙ Overweight/obese individuals: excess leptin in blood  instead of cellsleptin resistant (like insulin in diabetics) ∙ Adipocyte proliferation and differentiation

o We store fat indefinitely (adipocytes)

o When the fat cells get the largest they can get,  

then more fat cells are made

o Adipocyte number cannot decrease, the cells just  shrink (losing weight)

o Adipocytes will eventually die, takes a long time  (usually die due to age)

∙ BAT vs. WAT 

o Brown adipose tissue

 More mitochondria than white adipose tissue  

(mitochondria help give the brown color)

 Uncoupling protein 1 (UCP1)

∙ Uncouples oxidation and  

phosphorylation reactions at ETC 

inefficient ETC 

∙ H+ allowed to flow back into matrix

∙ Heat and less ATP

 Infants have higher amounts of BAT than  


 Basal metabolic rate

∙ More BAT  higher BMR

∙ Obese have less BAT than leaner  


 Do muscle cells and BAT originate from the  

same stem line?

∙ Can we recruit BAT?

∙ Research says that it is very possible  

with exercise.

∙ We can get WAT to “act” like BAT.

o TopHat: If BAT has more uncoupling proteins in the  tissue, this tissue would be…

 Answer: Less efficient at making ATP than  


o Muscle

 At rest, fat is primary source of fuel (beta-oxidation)

∙ Some individuals have fat in muscles (e.g. – overweight  

individuals or endurance athletes, like distance runners)

 Exercise uses glucose as fuel

(In class, we skipped Regulation of Lipid Metabolism and will possibly bring it in to  the Heart Disease/Atherosclerosis PowerPoints)

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