Lipids Flashcards
Is there any recommendation concerning cholesterol consumption, type of fat,etc.?
There is evidence to restrict cholesterol consumption to healthy people. However, there is one for people with cardiovascular diseases. CFG states that we should consume less saturated fat and eat more MUFAs and PUFAs
More omega 3 and less omega 6 ( the ratio should be 1:8, now 1:15)
Why low fat diet is not efficient?
Because our body can produce cholesterol on itself and also usually people balance lack of fats with more CHOs. As the result, consuming more calories, more obese
Name three types of lipids
1) triacylglycerol
2) phospholipids
2) sterols
How phospolipids and triacylglycerols related?
Phospholipids are the same as triacylglycerols, but one fatty acid substituted with phosphocholine
What property does phospholipids have?
Amphipathic compounds
Why plant products that claims no cholesterol on the package are not fair?
Cholesterol comes only from animal based products
Plants have phytocholesterol that we do not digest
What changes can be done to reduce fat in the diet?
To lower the milk fat percentage gradually
To trim the steak from fat, for example
In what products lecithin is found?
Eggs, mustard
What are functions of lipids in foods?
- 2 essential fatty acids
- concentrated energy
- carry fat soluble vitamins
- flavor,aroma,texture
- satiety
- emulsification
What are metabolic functions of fat in our diet?
- Adipose tissue is a concentrated energy store
- Cell membranes (phospholipid bilayer)
- Nerve impulse transmission
- Eicosanoid synthesis
What type of lipids is 99% of our diet?
Triacylglycerols
How the bond between glycerol and fatty acid is formed?
Ester bond with elimination of water( similar to glycemic bonds)
How can we use glycerol in our body (except triacylglycerols)?
To synthesize glucose
What is the reactive end and its polarity?
Carboxylic end. It is polar
What is the non-polar group in fatty acids?
Methyl end
Give the example of saturated fatty acids family and its short abbreviation
Stearic acid. 18:0
The example of MUFAs with the short name. Where can we find this fatty acid?
Oleic acid. 18:1.Omega-9 In the olive oil
What does Omega 9 mean in the naming of the fatty acid?
The position of the first double is located 9 carbons away from the methyl end.
Name 2 representatives of PUFAs class
Linolenic acid C 18:3 omega 3
Linoleic acid C 18:2 omega 6
Do we know the other positions of double bonds in linolenic acid?
Yes, as it is omega 3 and it has 3 double bonds, so the places are 3,6 and 9
For linoleic acid omega 6, so the other bond is at position 9
How do double bonds effect physical properties of lipids?
More double bonds, more liquid the fat at cooler temperatures
Why people hydrogenated fats?
For preservation
What happens to fats with double bonds on the sunlight?
Double bonds are very susceptible to oxidation( light, heat). As they are exposed to the light or heat, they turn to free radicals. These free radicals will cause other fatty acid to convert to free radicals as well. Eventually, can cause oxidative stress in the body and damage DNA, cause cancer
Hydrogenation is
Making double bonds into single bonds
What is margarine?
Hydrolyzed vegetable oil
What are the most naturally occurring fats?
Cis fats
What is the difference between trans fats and cis fats in the structure
Trans fats are more linear than cis fats
How fats can become trans fats?
Partial hydrogenation of unsaturated fats. Cis changes to trans during the reaction.
What is the consequence of different configurations of fats?
They are handled differently in the body
Why trans-fats are dangerous for humans?
In the body, trans fats are converted to peroxides. Peroxides lead to oxidation. Oxidation leads to DNA damage,cancer, cardiovascular disease
The classification of fatty acids according to the chain length
Short 2-6C
Medium 8-12(14)
Long >16
How does the solubility changes with the length of fatty acid chain?
Short fatty acids are pretty soluble
As the length increases, the solubility decreases
The classification of fatty acids, according to the double bonds (number,position,stereochemistry)
Number( saturated, MUFAs,PUFAs)
Position (omega3,omega6,omega9)
Stereochemistry (cis,trans)
What oils and fats are mostly saturated fat?
Animal fats and tropical oils (coconut,palm)
What are the best choices for oils and why ( a hint: expensive)
Flaxseed oil
Walnut oil
Because they have a lot of MUFAs and a good ratio of omega 3 to omega 6
What are the best healthy options for budget?
Canola oil for cooking
Olive oil for other purposes
A lot of MUFAs and a good ratio of n=3 to n=6
Why peanut oil is not a healthy choice?
-A lot of omega 6, no omega 3
The sources of linoleic and alpha-linolenic acids in oils
Linoleic- corn,peanut,safflower
Alpha-linoleic - canola,flax,soy
Why linoleic and alpha-linolenic acids are so-called essential?
Because when removed from the diet, there is pathology of the skin (deficiency of essential fatty acids), corrected when put back. Can not be produced form other fatty acids in our body
What is the requirement for linoleic and alpha-linolenic acids?
1 gram(linoleic) and 8 gram(alpha)
Why the consumption of these two acids are not a concern for clinical nutrition?
Because everybody on every diet does not have fatty acid deficiency
Name four families of fatty acids with the examples and short names
Saturated(stearic, 18:0)
MUFA n-9 (Oleic, 18:1)
PUFA n-6 (Linoleic, 18:2)
PUFA n-3 (Alpha-linolenic, 18:3)
Why saturated and MUFAs are not essential in our diet?
Excess of glucose will be converted to stearic FA. We have the enzyme to insert a double bond into n-9, but into 3 or n-6. That is why we can get oleic, but not linoleic or alpha-linolenic. The enzyme is called- desaturase
Why it is important to have both linoleic and alpha linolenic acids in the diet?
Both of the families use desaturase and elongase. As they are the same, one class can out-compete the other. But we need the products from two families.
At what part of the molecule does the elongaze insert carbons?
At the reactive end
What fatty acid does peanut have?
Arachidonic acid
Describe the pathway of linoleic acid
Linoleic( c18:2 n-6)->(desaturase) c 18:3 n-6 ->(elongase) c 20:3 n-6-> (desaturase) Arachidonic C20:4 n-6-> ( multiple steps-> eicosanoids n-6
What do eicosanoids do in our body?
Metabolic regulators
How do eicosanoids decipher?
Eicosa means 20 ( c20 )
Describe the pathway of alpha-linolenic to eicosanoids n-3
alpha-linolenic->(desaturase) c18:4n-3->(elongase) c20:4 n-3->(desaturase) eicosapentanoic acid(EPA) c20:5 n-3->(elongase) docosahexaenoic acid(DHA) c22:6 n-3-> eicosanoids n-3
What does eicosapentanoic and docosahexaenoic mean?
Eicosa- 20 carbons, penta- 5 double bonds
Docosa-22 carbons, hexa- 6 double bonds
Do we specifically need alpha-linolenic acid or we can get it from other sources?
We can have only EPA and DHA
In what products we can find EPA and DHA?
Fish oils. Especially, fat fish, fish form cold water.( SALMON,SARDINES,CHAR(симамасу), HERRING(сельд), MACKEREL(скумбрия),TROUT(микижа били радужная форель))
Why is it very important to eat fish for pregnant women ?
They need omega 3 for the fetus brain and retina
Why eating fish is better than eating omega-3 capsules?
Fish have protein as well, and other macro and micro-nutrients( ow in fat) that are required by our body. Can trigger imbalance of eicosanoids production in the body(excess of vit A and vit D), you do not know from what fish it came( toxic accumulation, as mercury).Fish oil is ususally 40 cal/per spoon)omega 6 are still important
How omega 3 capsules and oils should be stored?
In the dark and cool place. The risk of oxidative risk
The major eicosanoids in the body
Thromboxanes and leukotriens
The role of eicosanoids n-6
- Increasing blood clotting
- Increase of Platelet aggregation ( the clumping of blood cells together)
- Increase of Blood pressure
The role of eicosanoids n-3
- Decrease of blood clotting
- Decrease of platelet aggregation
- Decrease in blood pressure
How does consumption of EPA and DHA influences our body?
Lower cholesterol,LDL-chol,TGs
Higher HDL-chol
As a result 10 times lower incidence of heart attacks and strokes
What is RDA for omega 3
1 g/day( 9 calories)
What drug can you buy in the drugstore by prescription as a source of omega 3?
LOVAZA-Omega 3 fatty acid ethyl esters
How can you change the type of fat consumed and leaving total fat the same?
Replacing the steak with the grilled salmon
Butter for olive oil
Cheese for avocado and sunflower seeds
In what form we can usually find phospholipids ?
phosphatidyl choline=lecithin
How lecithin is used in food industry and in what products it is found?
To stabilize emulsion. Because it is an amphipathic molecule, It can held together fat and water. Eggs and mustard
What molecule does vitamin D resemble?
Cholesterol, that is why fat soluble vitamin
Name hormones that are derived from cholesterol?
Sex hormones: progesterone, testosterone, estradiol
Bile acid: cholic acid
Why cholic acid is a bile acid, the role in the emulsification of the fats
Usually water and fat in the stomach are separated. As the , cholic acid is like phospholipids( have both polar and unpolar parts) , it can bring fat into water. So, the bile separates a big drop of fat into little droplets(micelles), making it more available for the enzymes
Describe the digestion of lipids
- In mouth salivary lipase, which is activated in the stomach. Emulsification in the stomach mostly due to peristalsis
When chyme gets into duodenum, CCK( a hormone) is activated by fat presence.
CCK stimulates gallbladder contraction->bile acids->emulsification
Secretin stimulates pancreas contraction->enzymes(pancreotic lipase, pancreotic phospholipase)
Final digestion on the brushborder
Do people with cholecystectomy eat food with fat?
Yes, they do not have the gallbladder, the bile is delivered to the duodenum in equal portions, so when a really fatty meal is consumed, they cannot digest it
How does lipase work?
The lipase breaks down 1 and 3 ester bonds in TGs, leaving a monoglyceride and 2 fatty acids.
What happens on the brushborder after the TGs have been broken?
Short, medium-chain fatty acids and glycerol are water soluble, so they are absorbed directly into the bloodstream. Long fatty acids and monoglycerides are transferred through the brushborder and reassembled into new triglycerides. Within the intestinal cells, the newly made triglycerides and other lipids (cholesterol, phospholipids, and fat-soluble vitamins) are packed with protein into lipoprotein transport vehicles known as chylomicrons. The intestinal cells then release the chylomicrons (via a process called pinocytosis) into the lymphatic system.
What happens to fat in large intestine?
Cholesterol and fat bonded to fibre leave the body with the feces
What is chylomicron?
The chylomicrons are the largest and least dense of the lipoproteins. They transport diet-derived lipids (mostly triglycerides) from the small intestine (via the lymph system). Typical chylomicrons have tryglycerides, cholesterol, fat soluble vitamins surrounded by phospholipids( the hydrophobic molecules on the inside and the hydrophylic parts in the outside allow the chylomicrons to travel in the blood). Also it has several apolipoproteins that guides the chylomicron through the body.
Where do chylomicrons are made?
In the intestinal epithelial cell
Different types of body lipoprotein and their differences
- Chylomicron - the least dense, a it is mostly triglycerides.
- VLDL( very low density lipoprotein)- half triglycerides, 1/6 cholesterol, 1/6 phospholipid and little protein
- LDL(low density lipoprotein)- mostly cholesterol
- HDL( high density lipoprotein)- the most dense. Mostly protein
Describe the scheme how chylomicrons travel
Chylomicrons->lymph->the thoracic duct->blood
How does blood sample differ when you are fating and when you are fed?
When fasting, plasma is clean and yellowish
When fed-cloudy,whitish. The chylomicrons are so big that we can see them in plasma
Blood content
55% plasma
less than 1% leukocytes
45% red blood cells(erythrocytes)
Lipid transport in the body
1) When chylomicrons are absorbed in the lymph and brought back to the bloodstream near the thoracic duct, where is big blood flow, in order to dilute them.
2) As chylomicrons are travelling around the body, they are giving away TGs for cells.(14 hours in average)
3) Special protein receptors on the membranes of the liver cells recognize and remove these chylomicron
remnants from the blood.
4)The liver rearranges chilomicron molecule and mix it with the non-dietary fat. (in the liver cells are making cholesterol, fatty acids, and other lipid compounds.) Packaged with proteins as VLDL (very-low-density lipoproteins) and shipped to other parts of the body.
5)As the VLDL travel through the body, cells remove triglycerides, causing the VLDL to shrink. As VLDL lose triglycerides, the proportion of lipids shifts. Cholesterol becomes the predominant lipid, and the lipoprotein
density increases. The VLDL becomes an LDL (low-density lipoprotein).
6)The LDL (“bad cholesterol”) circulate
throughout the body, making their contents available to the cells of all tissues—muscles (including the heart muscle), fat stores, the mammary glands, and others.
The cells take triglycerides, cholesterol, and phospholipids to build new membranes,
make hormones or other compounds, or store for later use. Special LDL receptors on the liver cells play a crucial role in the control of blood cholesterol
concentrations by removing LDL from circulation.
PARALLEL to VLDL production
HDL is secreted by the liver. As HDL circulates in the body , it takes up the cholesterol from tissues and LDL( with the special enzyme). At some point it is taken by the liver, mediated by another receptor. So HDL teakes the cholesterol from the body and brings it back to the liver.
What does low HDL mean?
One of the criteria of having metabolic syndrome
Why it is important to take LDL particles as soon as possible from the bloodstream?
Because they can cause damage (atherosclerosis)
What is familial hypercholesterolemia?
A genetic disorder, which makes the body unable to remove LDL cholesterol from the blood. This results in a high level of LDL in the blood. Usually people died in their teens from the heart attack, cholesterol accumulated in their skin ,eyes
Where do lipids go after the intestine?
There are two ways: 1) directly to the liver
2) blood as chylomicrons
Why decreasing intake of cholesterol can decrease the risk of heart attack?
The liver monitors the level of cholesterol. When it thinks that the level is low, it makes more receptors on its surface in order to absorb more LDL particles-> low LDL cholesterol level
What are the protective and the damaging circuit in the lipid transport?
LDL is the damaging circuit and HDL is the protective
How can we make the liver think that it needs more cholesterol?
By consuming more MUFAs and PUFAs
What cells are most likely to absorb TGs?
First and foremost, the triglycerides—either from
food or from the body’s fat stores—provide the cells with energy.
Unlike the liver’s glycogen stores, the body’s fat stores have virtually unlimited capacity, thanks to the special cells of the adipose tissue. Unlike most body cells, which can store only limited amounts of fat, the fat cells of the adipose tissue readily take up and store triglycerides.
What happens in the body when we are fasting?
This state is called, catabolic state and it is driven by glycagon. Hormone(glucagon) sensitive lipase( the enzyme) hydrolyses TGs to fatty acids and glycerols, because TGs cannot cross the membrane. Fatty acids and glycerol get directly into the blood. As FA cannot travel on themselves n the blood(toxic), they are carried by albumin.Energy-hungry cells anywhere in the body can then capture these compounds(FA+albumin) and take them through a series of chemical reactions(through acetyl CoA) to yield energy, carbon dioxide, and water.
Although fat provides energy during a fast, it can provide very little glucose to give energy to the brain and nerves.( TG has 51 carbons and only 3 can be converted to glucose)
Do we have chylomicrons when we are fasting?
No
What proteins are involved in the fasting state?
Albumin- it has a high affinity to FA, minerals and waste products.
NO lipoproteins are involved during fasting state
What happens in the fed state?
Anabolic state, regulated by insulin.
Lipogenesis is happening in the liver form the excess of glucose. Chylomicrons are travelling through the body and giving away TGs. Adipose cells store fat after meals when a heavy traffic of chylomicrons
and VLDL loaded with triglycerides passes by. An enzyme—lipoprotein lipase (LPL)—hydrolyzes triglycerides from lipoproteins, releasing fatty acids that enter the adipose cells. Inside the cells, other enzymes reassemble these lipids into triglycerides again for storage. Triglycerides fill the adipose cells, storing a lot of energy in a relatively small space.
Contrast transport of lipids in fed and fasting state
In fed( anabolic state) 1) insulin increases
2) Chylomicrons number increases
3) Fat synthesis increases( lipogenesis in the liver from glucose and amino acids)
4) VLDL released. Lipoprotein lipase on adipose cells captures circulating TGs for storage
In fasting state( catabolic)
1) NO chylomicrons
2) insulin decreases, glucagon increases
3) Hormone sensitive lipase in adipose cells hydrolyses TGs( lypolysis) and releases FAs and glycerol
4) Albumin carries FAs to the cells , where FAs are oxidized to acetyl CoA by B-oxidation
What is Lypolysis and lipogenesis
Lypolysys happens in adipose cells when fasting. TGs are hydrolyzed to FAs and glycerol
Lipogenesis- in the liver, from glucose and AAs during anabolic state(fed)
Hypercholesterolemia, what is it, levels of choleterol to diagnose
Hypercholesterolemia is a condition characterized by very high levels of cholesterol in the blood.
equal or more than 5mmol/L
By lowering the serum cholesterol level by 1 %…
You are lowering the risk of heart attack by 2 %
Is there a cause and effect between cholesterol level and early death?
No, there is only a correlation between them.
Steps in atherosclerosis
1) Infiltration of LDL particles in the junction of epithelial layer and the lining of the artery. LDL accumulates in the wall of the artery.
2) Immune cells (monocytes, or macrophages) come to LDL, because they are not meant to be there.
3) Macrophages absorb cholesterol from LDL, turining into foam cells and causing more inflammation.
4) Accumulation of inflamed foam cells leads to fibrotic artery wall that attracts collagen.
5) The wall increases in bulk, the blood has more difficulties to go through the artery.
6) As the artery becomes more rigid, it becomes more hard for it to expand and to be elastic( higher blood pressure)
7) Calcium also can get in the inflamed part and make it more hard
8) The erosion of the lining
9) Smaller lumen and rough surface promote clot formation and thrombus
10) A blood clot , can cut off the blood flow, causing heart attack or inclusive stroke
What does aspirin do?
It makes the blood more liquid, can help a little with the thrombus
Three major steps of atherosclerosis
1) Fatty streak
2) fibrous plaque
3) complicated lesion
How can fish consumption help with atherosclerosis?
Omega 3 makes the platelets less sticky and prolongs the clotting time
What does pain in the chest during exercise mean?
A blood clot in the coronary artery, a stent or a by-pass may be needed
Simple description of atherosclerosis
Accumulation of cholesterol-> immune response->calcification->becomes hard and rigid
What happens to atherosclerosis with the healthy lifestyle?
The process slows down, HDL can remove some of the cholesterol, decrease severity
How does non-enzymatic addition of glucose to the apolipoprotein affect?
LDL becomes damaged, they are more likely to invade artery walls.
When the ligand is damaged, less LDL is taken from the blood stream, LDL circulates longer, More damage to LDL
Examples of vulnerable groups for damaged LDL?
Smokers( oxidation of AA and FA) , T2DM(glycation of AA and FA)
Small lumen of arteries results in
Heart-attack
Stroke
High blood pressure
Myocardial infarction
Why the test for total cholesterol is not effective? What should we do instead?
Because it measures both LDL cholesterol and HDL cholesterol and they do different things.
LDL has only one apolipoprotein ( apolipoprotein B-100). Measure for this protein
Cholesterol. What is made from
Water,acetylCoA, NADPH
What is HMGCoA reductase?
The enzyme that reduces HMGCoA. A rate controling agent for cholesterol production
Statins, what is it
A class of drugs that inhibits HMGCoA reductase and as a result decrease LDL( for example, Lipitor). Have series of side effects
Risk factors of atherosclerosis (3 non-modifiable and modifiable)
-Age
-Postmenopausal women( N1 killer is atherosclerosis)
-Genetics
Modifiable:
1)Stress
2)Sedentary
3)Obesity-visceral(inflammation, insulin resistance)
4)Hypertension ( positive feedback-arteries became looser)
5)High LDL/low HDL
6)Homocysteine ( inflammatory, can cUSE AN OXIDATIVE STRESS)
7)Glucose intolerance (glycation, damage to LDL)
8)Chronic inflammation( gum disease increase inflammation)
What lipoprotein is synthesized when exercising?
HDL
High risk for atherosclerosis from diet
1) High energy intake-> obesity
2) High fat( saturated fat)
3) High alcohol
4) High GI CHOs
5) Low dietary fiber
6) low(high) vitamins/minerals
Health effects of lipids
1) saturated fats(animal fats),plam oil,cocunut oil increases LDL
2) Trans fat(hydrogenation) increase LDL
3) Monos decrease LDL
4) Omega 3 decrease LDL,blood pressure,blood clotting
5) High fat is concentrated energy promotes obesity
6) Very low fat/high CHOs diets-excess CHO is synthesized into saturated FAs which increase LDL
Describe the cholesterol flow in the body
Free cholesterol in the stomach
In the blood- lipoproteins
We absorb cholesterol( cholesterol in the diet+from the bile acids) from the gut, but we also produce cholesterol in the liver, from which we make bile.
LDL receptors take LDL fromt he blood( with the cholesterol)
How influence cholesterol production
Increasing by saturated fat
Decreasing by MUFAs and PUFAs
How do bile acids get back to the liver
With the help of the special enzymes they are reabsorbed
Ways to decrease cholesterol(drugs,phytosterols)
Phytosterols( we do not absorb them ,but it competes wit animal cholesterol for absorption, so less cholesterol is absorbed) - effective to some extent
-Lovaza( omega 3 ethyl ester) Raises HDL,lowers tryglycerides
- Statins( HMGCoA reductase inhibitors. Lipitor, Crestor(super-statin)
- Ezetimibe(cholosterol absorption inhibitor)+statin(less production of cholesterol in the liver)
- Repatha( increases LDL receptors)
- Soluble fiber binds bile acids that stimulates cholesterol production in the liver and increases LDL receptors
Approaches to decreases CVD
1) PUFA,MUFA vs Sat
2) omega 3 vs omega 6
3) weight loss
4) exercise
5) moderate alcohol if anything
6) B vitamins to reduce homocysteine
7) Soluble Fibre to bind chol, and for glycemic control
8) Complex CHOs with low glycemic index
9) Plant sterols
10) Cholesterol binding drugs( alike soluble fiber)
11) Chol transport-inhibiting drugs
12) Chol synthesis- inhibiting drugs
Recommendations for fat
No AI and UL( no sufficient data)
- 20-35% of energy adults (40% for 1-3 years)
- Saturated fat - as low as possible, max 10% of cals
- No trans fat
- N-6 PUFA - 5-10% of energy ( 12-17g) RDA
- N-3 PUFA -0.6-1.2% of energy( 1.1g-1.6g) RDA
- ratio 8:1( the reality 15:1)
