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NUTR 301 - nutritional BIOCH and Metabolism > Lipids > Flashcards

Lipids Flashcards

1
Q

What are the primary functions of lipids in the body?

A

Energy storage, cell membrane structure, insulation, precursor to hormones

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2
Q

How are glycerolipids structured, and what are their primary functions?

A

Glycerolipids have a glycerol backbone to which one, two, or three fatty acids are attached via ester bonds, forming mono-, di-, or triacylglycerols. Their primary functions include energy storage and serving as components of cell membranes

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3
Q

What distinguishes glycerophospholipids from other lipids, and where are they found in the body?

A

Glycerophospholipids have a glycerol backbone with two fatty acids and a phosphate group
- structural components of cell membranes

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4
Q

Describe the structure of free fatty acids (FFAs)

A

FFAs have a carboxylic acid head and a hydrocarbon tail. In plasma, most are bound to albumin, especially during fat catabolism

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5
Q

How are fatty acids classified by chain length?

A

Fatty acids are classified as short-chain (≤6 carbons), medium-chain (8-14 carbons), or long-chain (>14 carbons)

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6
Q

Explain fatty acid nomenclature using the example 18:2n-6

A

18 is the number of carbons, 2 is the number of double bonds, and n-6 indicates the position of the first double bond from the methyl end

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7
Q

what is the formula for palmitic acid? what is another name for it?

A

16:0
-hexadecanoic acid

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8
Q

how does the miller and omega notation differ?

A

Miller: specifies positions of where the loast db starts from the carboxyl (acid) end
-For example, 18:2n-6 indicates a fatty acid with 18 carbons and the last double bond at carbons 12 (n = 18 ; 18-6 =12)

Omega: specifies position of the first double bond from the methyl (omega) end
-For example, 18:3n-3 denotes a fatty acid with 18 carbons and the first double bond located three carbons from the omega (methyl) end

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9
Q

How does hydrogenation affect fatty acids?

A

Hydrogenation adds hydrogen to unsaturated fats, altering their properties by changing double bonds and creating trans fats as a by-product, which can raise LDL cholesterol

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10
Q

how does saturation affect structure of fats in different T? why is this?

A

saturated fats are solid at room T whild unsaturated fats are typically liquid
-the unsaturation causes kinks in the structure and prevents the fat from fully packing into a solid, increasing fluidity

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11
Q

what kind of fat is palmitoleic acid? where is it found?

A

MUFA, omega 7
-marine animal oils, plant and animal oils

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12
Q

what kind of fat is oleic acid? where is it found?

A

MUFA, omega 9
-plant / animal fats
-* most common in humans

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13
Q

what kind of fat is linoleic acid? where is it found?

A

PUFA, omega 6
-plant oils (soybean, corn, safflower, canola, nuts/ seeds)

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14
Q

what kind of fat is alpha-linoleic acid? where is it found?

A

PUFA, omega 3
-seed oils

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15
Q

what kind of fat is arachidonic acid? where is it found?

A

PUFA, omega 6
-animal fats

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16
Q

what kind of fat is ecosapentaenoic (EPA) / docosahexanoic acid (DHA)? where is it found?

A

both omega 3 PUFA
-fatty fish / seafood

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17
Q

what kind of fat is myristic acid? where is it found?

A

saturated fat
-coconut oil, animal / plant oils

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18
Q

what kind of fat is palmitic acid? where is it found?

A

saturated fat
-animal / plant fats

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19
Q

what kind of fat is stearic acid? where is it found?

A

saturated fat
-animal fat, some plants

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20
Q

what kind of fat is arachidic acid? where is it found?

A

saturated fat
-peanut oil

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21
Q

what kind of fat is lignoceric acid? where is it found?

A

saturated fat
-natural fats and peanut oil

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22
Q

What are triacylglycerols (TAGs), and where are they stored?

A

TAGs, composed of glycerol and three fatty acids, are the main form of fat storage found in adipose tissue

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23
Q

what are common sources of saturated vs trans fat?

A

saturated: butter, bacon, lard, cream cheese
Trans: fried foods, margarine, baked goods

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24
Q

what reaction creates TAGs? what does it produce?

A

condensation reaction of glycerol + 3FA makes TAG + 3H2O

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25
Q

what types of TAGs are there?

A

Simple- 3 FA are the same
complex- atleast one FA differs

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26
Q

How does chain length and saturation affect lipid properties?

A

Shorter chains and more double bonds increase fluidity, while longer chains and fewer double bonds enhance stability and firmness

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27
Q

what type of fat is most susceptible to oxidation?

A

PUFA

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28
Q

what is expected of the structure of Sn-1 glycerophospholipids vs Sn-2?

A

Sn-1 typically saturated FA
Sn-2 typically unsaturated FA

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29
Q

what are the 5 majot classes of glycerophospholipids?

A

Phosphatidyl:
1) chlorine
2) ethanolamine
3) serine
4) inositol
5) glycerol

CLESING

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30
Q

What is the function of phospholipids (PPLs)?

A

cell membrane structure, intracellular messengers, emulsifiers in food processing

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31
Q

Describe the structure and function of cholesterol in the body

A

Cholesterol, found as free or esterified forms, modulates membrane properties and serves as a precursor for steroid hormones and bile acids

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32
Q

what is phytosterol?

A

plant source of sterol, similar to cholesterol

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33
Q

Name the five classes of steroid hormones derived from cholesterol

A

Androgens, estrogens, progestins, mineralocorticoids, and glucocorticoids

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34
Q

What role do bile acids play in fat digestion?

A

Bile acids, derived from cholesterol, emulsify dietary fats, aiding in their digestion and absorption in the intestine

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35
Q

How efficient is lipid digestion, and what form do most dietary lipids take?

A

Lipid digestion is highly efficient, with >90% of ingested fats as TAGs and only ~4% escaping in feces. Long-chain fatty acids are the most abundant in food

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36
Q

What roles do gastric lipase and lingual lipase play in lipid digestion?

A

These enzymes are crucial for triglyceride digestion in infants, as they have low pancreatic lipase activity. They hydrolyze fats at specific positions on glycerol

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37
Q

what is the major enzyme involved in TAG digestion? where is it activated?

A

pancreatic lipase
-intestinal lumen
-works on Sn1/Sn3

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38
Q

where and how does fat digestion occur?

A

begins in the mouth (lingual lipase) and stomach (gastric lipase) through chemical digestion

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39
Q

What is the role of cholecystokinin (CCK) in lipid digestion?

A

CCK is released in response to chyme, slowing gastric emptying and stimulating the gallbladder to release bile acids

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40
Q

How does emulsification facilitate lipid digestion?

A

Emulsification breaks large fat globules into smaller droplets, increasing the surface area for enzyme activity, primarily by bile saltse

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41
Q

what do TAGs breakdown into from digestion by pancreatic lipase?

A

Monoglyceride +2 FFA

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42
Q

what do TAGs breakdown into from digestion by gastric lipase? what does it efficiently hydrolyse? why is this important?

A

attacks Sn3 to make 1,2-diacylglycerols + FFA
-hydrolyzes milk fat efficiently because infants lack pancreatic lipase

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43
Q

what drug inhibits gastric and pancreatic lipases?

A

orlistat

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44
Q

explain digestion of TAGs from the mouth to small intestine

A

1) Mouth: Initial Digestion by Lingual Lipase (Sn3)
-Breaks down to FFA and diglycerides

2) Stomach: Gastric Lipase Action (Sn3)
-Breaks down to FFA and diglycerides

3) Small Intestine: Main Site of Digestion
Phase 1: bile emulsification
-CCK stimulates bile secretion to emulsify fats increasing accessibility to enzymes
Phase 2: pancreatic lipase activity (Sn1/Sn3)
-pancreatic lipase binds to bile salts to breakdown TAGs and diglycerols into monoglycerides and FFA

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45
Q

What is the function of pancreatic phospholipase A2?

A

It hydrolyzes fatty acids at the sn-2 position of phosphatidylcholine(most abundant phospholipid) , producing lysophosphatidylcholine and a free fatty acid

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46
Q

How are cholesterol esters digested? Can they be absorbed intact? what is produced?

A

Pancreatic cholesterol esterase hydrolyzes cholesterol esters, converting them into free cholesterol + FFA
-cholesertol must be in the free form to be absorbed

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47
Q

Describe the absorption of lipids by enterocytes.

A

Lipids must cross the unstirred water layer via mixed micelles containing bile salts and lipids, facilitating their absorption by enterocytes

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48
Q

What are the 2 mechanisms of lipid uptake into enterocytes? what types of lipid do they transport?

A

1) passive diffusion
-glycerol and short/medium chain FA
2) Carrier mediated transport
-long chain FA, monoacylglycerols, cholesterol

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49
Q

What is the role of Niemann-Pick C1-like 1 (NPC1L1) protein?

A

NPC1L1 is a major sterol transporter involved in the uptake of cholesterol or phtosterols into enterocytes

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50
Q

What are phytosterols, and how do they impact cholesterol absorption? what are sources of them?

A

Phytosterols are plant-based compounds similar to cholesterol. They reduce cholesterol absorption by competing for incorporation into micelles and promoting cholesterol export
-found in vegetable oils, nuts and added to mayonaise and other spreads

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51
Q

what is the function of ABCG5 and ABCG8 in phytosterol action?

A

they are transporters responsible for export of plant sterols out of the intestinal lumen

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52
Q

how does the presence of plant sterols impact cholesterol absorption? what impact does this have on health?

A

In the intestine, they compete with dietary and biliary cholesterol for incorporation into micelles. By reducing the amount of cholesterol that gets incorporated into these micelles, plant sterols decrease the absorption of cholesterol into the bloodstream

-Cholesterol that is not absorbed is excreted in the feces
-plant sterols can lead to lower levels of LDL (“bad”) cholesterol in the blood

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53
Q

Explain the enterohepatic circulation of bile acids

A

Bile acids are stored in the gallbladder between meals and are relased into the intestine and recycled to the liver via the hepatic portal vein once no longer needed, reducing the need for new bile acid synthesis

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54
Q

How are lipids packaged in enterocytes?

A

Lipids are re-esterified and packaged into chylomicrons for transport into the lymphatic system and eventually circulation
This is done in 2 pathways:
1) monoacylglycerol pathway
2) glycerol-3-phosphate pathway

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55
Q

Describe the monoacylglycerol pathway in enterocytes, where are the enzymes for this pathway found?

A

re-esterification of monoacylglycerols into diacylglycerols using MGAT and then into triglycerides using DGAT
-these enzymes are found in the membrane of the ER

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56
Q

Describe the glycerol 3-phosphate pathway in enterocytes, how does it differ from the monoacylglycerol pathway?

A

glycerol 3-phosphate is converted to disacylglycerol using GPAT then into TGs using DGAT
-this is a slower (minor) pathway and only occurs when monoacylglycerol (Sn2) is lacking

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57
Q

What happens to cholesterol in enterocytes?

A

Cholesterol is re-esterified by cholesterol acyltransferase (ACAT) to form cholesterol esters for incorporation into chylomicrons

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58
Q

How are phospholipids re-formed in enterocytes?

A

Lysophospholipids are reacylated to form complete phospholipids, contributing to cellular and chylomicron membranes

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59
Q

Summarize the transport of lipids from the enterocyte

A

Glycerol, short- and medium-chain fatty acids (soluble and can go directly to the liver) enter the hepatic portal vein, while triglycerides,

cholesterol esters, and phospholipids are packaged into chylomicrons and transported via the lymphatic system

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60
Q

What are the main classes of lipoproteins?

A

chylomicrons, very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL)

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61
Q

Describe the major functions of chylomicrons, where are they formed? what major apolipoprotein do they contain?

A

they transport dietary lipids from the intestine to circulation and eventually to the liver
-made in the intestine, contain B48

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62
Q

What is the primary function of VLDL? what is it converted into? where is it made? what is its major apolipoprotein?

A

a) VLDL transports endogenous triglycerides and cholesterol from the liver to peripheral tissues
b)it is converted to IDL and then to LDL through lipoprotein lipase (LPL) activity
c) made in the liver
d) B100 is its major apolipoprotein

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63
Q

How is LDL formed, and what is its main function?

A

LDL is formed from the conversion of VLDL to IDL and then to LDL. Its main function is to deliver cholesterol to tissues

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64
Q

What is the primary role of HDL? where is it made? what is its major apolipoprotein?

A

transports cholesterol from peripheral tissues back to the liver for excretion or recycling
-made in the live / intestine
-major lipopoprotein is AI

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65
Q

What are apolipoproteins, and why are they important?

A

proteins that bind lipids to form lipoproteins. They serve structural functions, facilitate lipid transport to receptors, and act as ligands for cell surface interactions

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66
Q

What is the function of lipoprotein lipase (LPL)? what activates it and what inhibits it?

A

LPL hydrolyzes triglycerides in chylomicrons and VLDL into free fatty acids and glycerol for uptake by tissues
-ApoCII activates , while ApoCIII inhibits

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67
Q

What are the main steps of lipoprotein metabolism?

A

1) Chylomicrons: Formed in the intestine, they transport dietary triglycerides and cholesterol to tissues. Lipoprotein lipase (LPL) breaks down their triglycerides, forming chylomicron remnants taken up by the liver.

2) VLDL (Very-Low-Density Lipoproteins): Produced by the liver, VLDL transports endogenous triglycerides and cholesterol. LPL converts VLDL to IDL (Intermediate-Density Lipoprotein) and then to LDL.

3) LDL (Low-Density Lipoproteins): Delivers cholesterol to tissues. Excess LDL can lead to plaque formation in arteries if not cleared effectively by LDL receptors.

4)HDL (High-Density Lipoproteins): HDL removes excess cholesterol from tissues and transports it back to the liver for excretion or recycling through reverse cholesterol transport.

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68
Q

Describe hepatic triglyceride lipase (HTGL), what is its purpose?

A

processes apoE-containing lipoproteins, hydrolyzing triglycerides in HDL and IDL
-it aids in clearance of lipoprotein remnants (creates cholesterol rich lipoproteins)
-converts IDL to LDL
-creates smaller HDL particles to recycle excess cholesterol to the liver

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69
Q

What is the role of lecithin-cholesterol acyltransferase (LCAT)? what cofactor is involved? why is it important?

A

LCAT catalyzes the esterification of free cholesterol in HDL to cholesteryl esters
-ApoA1 is the cofactor
-this is essential for maturation of HDL

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70
Q

what do you expect the cholesterol fractions in plasma to look like during fasting? explain why this makes sense

A

plasma cholesterol fractions consist primarily of LDL, followed by HDL, VLDL and the least in chylomicrons

Chylomicrons and VLDL levels are expected to be low because they are primarily involved in the transport of dietary lipids and endogenous triglycerides, which are not actively produced or absorbed during a fasting state

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71
Q

Why is cholesterol highest in LDL during fasting?

A

During fasting, the liver releases VLDL for energy needs. As VLDL loses triglycerides, it is converted into LDL, concentrating cholesterol in LDL particles. With reduced dietary intake, cholesterol transport shifts primarily to LDL, making it the main carrier of cholesterol during fasting

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72
Q

How are lipoproteins cleared from plasma by receptor-mediated pathways?

A

Approximately 90% of lipoproteins are cleared by hepatic LDL receptors, which recognize apoB100 and apoE on LDL and chylomicron remnants

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73
Q

How does the body regulate cholesterol synthesis? what regulates this?

A

through HMG CoA reductase, the rate-limiting enzyme in cholesterol production
- High levels of cholesterol inhibit this enzyme
- Low levels of cholesterol stimulate the enzyme

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74
Q

What role do LDL receptors play in cholesterol homeostasis?

A

it binds and internalizes LDL particles, reducing circulating cholesterol. The number of LDL receptors is regulated by cellular cholesterol levels

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75
Q

How do dietary intake and endogenous synthesis affect cholesterol balance?

A

Increased dietary cholesterol intake suppresses endogenous synthesis by downregulating HMG CoA reductase, while reduced dietary intake can increase synthesis to maintain sufficient cholesterol levels

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76
Q

What is the impact of statin drugs on cholesterol homeostasis?

A

Statins inhibit HMG CoA reductase, reducing cholesterol synthesis. This decreases intracellular cholesterol levels, leading to increased LDL receptor expression and greater clearance of LDL from the bloodstream

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77
Q

What role does HDL play in cholesterol homeostasis? how is cholesterol excreted?

A

HDL facilitates reverse cholesterol transport by collecting excess cholesterol from peripheral tissues and transporting it back to the liver for excretion
-Excess cholesterol is excreted through bile, where some are lost through feces

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78
Q

where does cholesterol synthesis take place?

A

cytosol, close to ER

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79
Q

what is the typical ratio of endogenous vs exogenous cholesterol in the body?

A

endogenous: de novo synthesis 800-1500mg / day
exogenous: dietary 100-300mg /day

tightly regulation so changes in either of these will down / upregulate the other

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80
Q

What is hypercholesterolemia, and why is it significant?

A

elevated blood cholesterol levels, often due to increased intake of total fat
-raises the risk of cardiovascular disease and atherosclerosis

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81
Q

Explain the reverse cholesterol transport process involving HDL

A

HDL transports cholesterol from peripheral tissues to the liver for excretion, helping to reduce cholesterol accumulation and providing protective effects against cardiovascular disease

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82
Q

How does bile contribute to cholesterol homeostasis?

A

Bile, derived from cholesterol, helps emulsify dietary fats for digestion and absorption.

Excess cholesterol is excreted through bile, which can be reabsorbed or lost in feces, aiding in cholesterol regulation

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83
Q

What is the ratio of synthesis vs excretion of biliary / dietary cholesterol?

A

they are made and excreted in almost equal quantities of ~1.2g/day

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84
Q

What are the key steps in lipoprotein metabolism?

A

1) Chylomicrons: Formed in the intestine to transport dietary triglycerides and cholesterol. They deliver triglycerides to tissues via lipoprotein lipase and become chylomicron remnants, taken up by the liver.

2) VLDL (Very-Low-Density Lipoproteins): Produced by the liver to transport endogenous triglycerides and cholesterol. They are converted to IDL and then LDL after triglyceride removal.

3) LDL (Low-Density Lipoproteins): Delivers cholesterol to peripheral tissues. High levels can lead to cholesterol buildup in arteries.

4) HDL (High-Density Lipoproteins): Collects excess cholesterol from tissues and returns it to the liver for excretion or recycling through reverse cholesterol transport.

85
Q

how are long chain FA made? what determines the rate of this synthesis? what is the normal rate of de novo synthesis?

A

de novo lipogenesis
-determined by genetics, diet, and if we are in fed / fatsing state (higher synthesis with insulin resistance and fed state)
-most ppl have a low rate (<5% of FA )

86
Q

what is the major organ of FA synthesis? where else does it occur?

A

liver

87
Q

What is the first committed step in fatty acid synthesis?

A

The conversion of acetyl-CoA to malonyl-CoA by acetyl-CoA carboxylase (ACC)
-rate limiting step

88
Q

What are the 2 sources of acetyl-CoA used for fatty acid synthesis? which state would each be most active?

A

1) PDH rxn- fed state
2) FA oxidation -non-fed state

89
Q

How does malonyl-CoA regulate fatty acid oxidation?

A

inhibits carnitine palmitoyltransferase-1 (CPT-1), preventing the transport of fatty acids into mitochondria for oxidation
-ensures reciprocal regulation of synthesis in the cytosol and oxidation in the mitochondria

90
Q

Where in a cell does fatty acid synthesis occur, and what is its main product?

A

Fatty acid synthesis occurs in the cytosol, and its main product is palmitate (16:0)

91
Q

What role does citrate play in fatty acid synthesis regulation?

A

Citrate acts as a ‘feed-forward’ activator of acetyl-coA carboxylase
-indicates fed state, promoting FA synthesis

92
Q

What is the role of fatty acid synthase (FAS)?

A

Fatty acid synthase catalyzes the multi-step elongation of fatty acids, adding two-carbon units to a growing acyl chain
-it is the 2nd final committed step

93
Q

How is fatty acid synthase regulated? what factors will increase / decrease FAS?

A

primarily at the transcriptional and translational levels by factors like SREBP-1c (drives elongation) and ChREBP

increased FAS: fed state, CHO (upregulates SREBP & ChREBP)
decreased FAS: fasted state, PUFAs

94
Q

Describe the elongation and desaturation processes of fatty acids

A

Elongation adds two carbons at a time, usually occurring in the smooth endoplasmic reticulum.
Desaturation introduces double bonds, with certain desturases catalyzing the formation of various unsaturated FA

95
Q

What are the 3 sources of fatty acids composition in adipose tissue? what is majority of adipose FA?

A

1) dietary sources (exogenous)
2) dietary FA that have been elongated / desaturated
3) de novo synthesis

-1/2 of adipose FA is oleate and 1/4 is palmitate

96
Q

What are the primary sources of fatty acids used by the cell for triglyceride synthesis?

A

1) de novo synthesis
2) FAs taken up form circluation as FFA
-that were released by lipolysis of adipose tissue
-that were generated locally from circulating lipoproteins by lipoprotein lipase

97
Q

How are fatty acids taken up by cells?

A

1) Passive diffusion
2) FA transporters
- FA translocase (FAT)
- FA transporter proteins (FATPs)
- plasma membrane FA binding protein (FABPpm)

98
Q

how are FA transported within the cell?

A

bound to FA binding proteins (FABPs)

99
Q

Where does triglyceride re-esterification occur in cells? what enzyme catalyzes this?

A

on the surface of the endoplasmic reticulum
-acyltransferase catalyzes this

100
Q

What are the two pathways for triglyceride biosynthesis?

A

1) monoacylglycerol (major in entoerocytes)
2) Glycerol 3-phosphate (enterocytes and other tissues)

101
Q

where does TG synthesis occur?

A

in all tissues that store TG

102
Q

why is fructose lipogenic?

A

it bypasses the PFK-1 regulatory step in glycolysis and is converted to intermediates that promote de novo lipogenesis such as glyceraldehyde and DHAP

103
Q

What does “anhydrous fat storage” mean, and why is it important?

A

“Anhydrous fat storage” refers to the storage of triglycerides in adipose tissue without water

Unlike glycogen, which binds water, fats are stored in a nearly water-free state, making them a highly efficient energy reserve. This allows fats to store more energy per gram and occupy less space, providing a dense source of long-term energy for the body (2x more energy/g)

104
Q

Why are triglycerides (TG) a major form of energy storage in the body?

A

they are calorically dense (9 kcal/g) and stored in an anhydrous form

105
Q

What is the importance of stored fuel, such as TGs, in the body?

A

1) provide energy between meals / exercise
2) protect lean body mass from catabolism
3) extend survival during calorie deficit

106
Q

explain the postprandial fat curve and how insulin resistance would impact it

A

Normal State: Postprandial triglycerides peak and gradually decline due to efficient breakdown and uptake

Insulin Resistance: Elevated and prolonged triglyceride levels due to impaired LPL activity, increased VLDL production, and continued lipolysis

107
Q

How are fats transported in the body?

A

1) non-esterfied or FFA bound to albumin
2) Triglycerides in lipoproteins
- requires hydrolysis (lipoprotein lipase)

108
Q

in what state would you expect to see higher levels of FFA? why?

A

in the fasted state
-during the fasted state when insulin levels are low glucagon and epinephrine promote lipolysis in adipose tissue, leading to the release of FFAs from triglyceride stores

109
Q

What is the role of lipoprotein lipase (LPL)? what is its role in regards to the postprandial curve slope?

A

hydrolyzes triglycerides in lipoproteins, releasing free fatty acids and glycerol
-it defines the initial post porandial curve slope

110
Q

what processes occur during the initial rise in the post prandial curve? which of these processes are seen in the highest amount? when does this change?

A

absorption, secretion/repackaging from intestinal enterocytes, secretion of chylomicrons / appearance in blood stream, initial hydrolysis of chylomicron and disposal of FFA from TAG and clearance

the absorption outweighs the other processes initially, until absorption slows down and hydrolysis/clearance will outweigh absorption, showing a decline in the curve

all processes are active but to different extents due to fed vs fasted state

111
Q

how does the postprandial curve of a carb vs fat differ in the initial graph? why?

A

postprandial curve for a fat will have a slower peak due to the time it takes to metabolize the triglycerides to FFA by lipoprotein lipase

glucose shows a spike within minutes due to quicker metabolism

112
Q

where is lipoprotein lipase made? where is it secreted from?

A

made and secreted by the adipocytes

113
Q

explain regulation of lipoprotein lipase during fasted vs fed state?

A

FED STATE:
-increases in adipocytes, increasing fat storage
-lower in muscle cells since energy needs are met by glucose

FASTED STATE:
-decreases in adipose, reducing FA storage
-increases in muscle cells during fasting to oxidize FA for energy

114
Q

How do muscle triglycerides differ from adipose tissue TG storage?

A

Muscle TGs are used as an energy source during fasting and prolonged exercise but are not released into circulation

115
Q

How is fatty acid release from adipose tissue regulated?

A

FFAs are released through hydrolysis of TGs stored in adipocytes. This process is mediated by enzymes such as adipose triacylglycerol lipase (ATGL) and hormone-sensitive lipase (HSL)

116
Q

Where can Glycerol 3-phosphate come from for TG synthesis in the liver vs adipose tissue?

A

Liver: Glycerol 3-phosphate comes from glucose, pyruvate or phosphorylated glycerol

Adipose: Glycerol 3-phosphate only comes from glucose or pyruvate
-lacks glycerol kinase

117
Q

what are the substrates for TG synthesis?

A

Fatty acyl coA (activated FA) + Glycerol 3-phosphate (backbone)

118
Q

what are FFA bound to during circulation? why?

A

bound to albumin to increase solubility

119
Q

how are chylomicrons a source of FFA?

A

the liver takes up chylomicron remnants and the remaining TGs present in these particles are sources of FFA

120
Q

What are triacylglycerol hydrolases? what do they do? what are 3 common types of these hydrolases?

A

Triacylglycerol hydrolases catalyze the hydrolysis of stored trglycerides into FFAs + monoglycerols

1) ATGL is a hydrolase that specifically targets triglycerides, initiating their breakdown by hydrolyzing the first fatty acid, leading to the production of diacylglycerol and free fatty acid

2)TGH functions more broadly in triglyceride hydrolysis within tissues like the liver and contributes to lipid metabolism, including VLDL secretion

3) Hormone sensitive lipase (HSL) hydrolyzes diacylglycerols into monoacylglycerols and FFAs. It is regulated by glucagon, epinephrine (activators) and insulin (inhibitor)

121
Q

How is hormone-sensitive lipase (HSL) regulated?

A

-phosphorylated by protein kinase A (activates HSL) from glucagon release
-dephosphorylated by insulin (inactivates HSL activity)

122
Q

what affect does monoacylglycerol lipase have on mobilization of stored TG?

A

it will liberate FA in Sn2 position if in high enough [ ]

123
Q

What is the function of perilipin, and why is it important?

A

Perilipin coats lipid droplets in adipocytes, restricting access to lipases
-it helps regulate the mobilization and breakdown of fat to control lipolysis

124
Q

how does perilipin act when it is phosphorylated vs unphosphorylated? what signals phosphorylation?

A

Unphosphorylated Perilipin: Coats and protects lipid droplets, preventing unnecessary or excessive triglyceride breakdown
-insulin
Phosphorylated Perilipin: Undergoes a conformational change that facilitates the recruitment and activation of lipases, allowing for controlled lipolysis
-glucagon / epinephrine

125
Q

In which tissues is HSL most active, and why?

A

1) adipose tissue
-mobilizes stored triglycerides during fasting or stress,
2)muscle
-lipid metabolism and energy production

126
Q

What happens to HSL activity during fasting?

A

activity increases due to the release of hormones like glucagon and epinephrine
-enhanced lipolysis and mobilization of FFA for energy

127
Q

What happens to plasma fatty acids during fasting?

A

concentrations increase during fasting and decrease after meals, reflecting mobilization and utilization of stored fats

128
Q

What enzymes catalyze the hydrolysis of triglycerides?

A

adipose triacylglycerol lipase (ATGL), hormone-sensitive lipase (HSL), and monoacylglycerol lipase, each acting on specific parts of the TG molecule

129
Q

what is the randle cycle? why is it important?

A

It is the glucose-fatty acid cycle
- It demonstrates how increases in exogenous or breakdown of endogenous lipids will block the utilization og glucose because lipids are being used as fuel

130
Q

explain what you would expect in terms of the % of energy expenditure of glycogen, TG, plasma FFA and plasma glucose in muscle cells during exercise over time:

A

1) TG will initially increase as they are mobilized to muscle, then be used around 1hr
2) FFA will increase over time
3) glycogen will decrease
4) glucose will stay relatively the same

131
Q

explain what you would expect in terms of the rate of oxidation of CHO, ketones and protein over time during fasting:

A

1) inital spike in oxidation of CHO; with delpletion of stores around 24 hr
2) fat + ketone oxidation beginning ~24hr with a peak ~5 days
3) minimal protein oxidation, peak ~24hr then plateu once fat + ketones begin to be oxidized

132
Q

What initiates fatty acid oxidation? where does this occur?

A

activated into fatty acyl-CoA in the cytosol and transported into mitochondria for oxidation

133
Q

what role does malonyl-coA play in FA oxidation? how do you expect its levels to change during fasting?

A

it is an inhibitor of CPT-1 (transporter of activated FA into mitochondria)
-its levels will drop during fasting which promotes FA oxidation

134
Q

how is malonyl coa produced?

A

-ACC complex converts Acetyl coA to malonyl-coA

135
Q

What enzyme activates fatty acids?

A

Fatty acyl-CoA synthase (thiokinase) activates fatty acids in the cytosol

136
Q

What are the four reactions in beta-oxidation?

A

Oxidation (FAD), hydration, oxidation (NAD+), and thiolysis release acetyl-CoA

137
Q

what enzyme is needed in the first rxn of FA oxidation? what is the cofactor involved?

A

acyl coA dehydrogenase
-FAD to make FADH2

138
Q

what enzym is needed for the 2nd rxn of FA oxidation? what other reactant is involved?

A

enoyl coA hydratase
-H2O

139
Q

what enzyme catalyzes the 3rd rxn in FA oxidation? what cofactor is involved?

A

beta-hydroxyacly coA dehydrogenase
-NAD+ to make NADH

140
Q

what enzyme catalyzes the 4th rxn in FA oxidation? what cofactor is involved?

A

thiolase
-CoA-SH

141
Q

what is produced after 1 round of OHOT rxn in FA oxidation?

A

1 Acetyl coA and an acyl coA that is 2C shorter

142
Q

how does FA oxidatoin differ for odd-chain FA? how does this affect metabolism of this kind of fat?

A

the final end products are Acetyl-coA and Propionyl-coA
-Propionyl coA can be converted into succinyl coA and taken through the TCA then gluconeogenesis to make glucose

143
Q

how does FA oxidation differ for medium chain FA?

A

diffusion into the mitochondria is passive and does not require CPT1

144
Q

how does oxidation of unsaturated FA differ? how does this impact energy from the oxidation of unsaturated FA?

A

the initial dehydrogenase rxn is not required due to the FA already having a db
- this results in less energy production from unsaturated fats due to loss of FADH2 production from the initial dehydrogenase reaction (1.5 less ATP per db )

145
Q

Where are ketone bodies synthesized, and what are the primary types?

A

Synthesized in the liver, the primary ketone bodies are acetoacetate and beta-hydroxybutyrate

146
Q

why does ketolysis not occur in the liver?

A

the enzyme that activates ketone bodies is not present (SCOT)
-can make ketones but not use them for energy

147
Q

what is ketogenesis coupled to?

A

FA oxidation

148
Q

when is acetone made during ketogenesis? what conditions?

A

when ketone levels are very high
-starvation and diabetic keto acidosis
-acetone smell on breath

149
Q

where does ketolysis occur?

A

in the cytosol

150
Q

what is the rate limiting step in ketolysis?

A

SCOT
-transfer of CoA to acetoacetate

151
Q

what are the steps in ketogenesis?

A

1) 2 acetyl coA liked and one coA removed to form acetoacetyl coA
2) formation of HMG-coA using Acetyl coA
3) Acetyl coA removed to form acetoacetate
-acetoacetate can be converted into beta-hydoxybutyrate or acetone

152
Q

what enzyme removes a coA from the joinng 2 Acetyl coA groups in the first step of ketogenesis?

A

a thiolase

153
Q

what enzyme generates HMG-CoA in ketogenesis? what cofactors are involved?

A

HMG-CoA synthase
-Acetyl coA + H2O

154
Q

what enzyme removes Acetyl coA from HMG-CoA in ketogenesis? what is formed?

A

HMG-CoA lyase
-acetoacetate

155
Q

how do you expect [FFA] to change as a result of prolonged fasting? what does this do to beta-hydroxybutryate levels?

A

[FFA] levels dont change much past 1.5mmol, however, beta hydroxybutryate levels will continue to increase

156
Q

provide an example of clinical significance of ketogenesis:

A

Type 1 diabetes can cause diabtees ketoacidosis
decreasded insulin -> increased FA oxidation -> increased Acetyl coA -> increased ketone production -> decreased blood pH -> decreased binding of O2 to Hb

157
Q

What are the major biological roles of EFAs in lipids?

A

structural integrity (skin ceramides), cell signaling (eicosanoids), and membrane function

158
Q

how does the structure of PUFA’s increase signaling?

A

kinks in the structure increase fluidity allowing for more efficient signaling

159
Q

what FA are considered essential? why?

A

Linoleic (LA) and alpha-linolenic (ALA)
- Humans lack enzymes to add double bonds beyond the delta-9 position

160
Q

what FA is 18:2n-6?

A

Linoleic acid

161
Q

what FA is 18:3n-3

A

alpha-linolenic acid

162
Q

which FA are conditionally essesntial? why are they not essesntial?

A

EPA, DHA and AA
-body can make in limited quantities

163
Q

what are common sources of omega-3 PUFAs?

A

marine animals

164
Q

what are common sources of ALA? what type of FA is this?

A

canola oil, chia, hemp, flaxseed oil
-omega 3 PUFA

165
Q

what are common sources of EPA / DHA? what FA are these?

A

oily fish (salmon, anchovy, herring)
-omega 3 PUFA

166
Q

what are common sources of LA? what type of FA is this?

A

veg oil
-omega 6 PUFA

167
Q

what are common sources of AA? what type of FA is this?

A

animal fat, liver, fish
-omega 6 PUFA

168
Q

what are common sources of DPA? what type of FA is this?

A

animal tissues
-omega 6 version of DHA

169
Q

explain the significance of LC-PUFA synthesis and metabolism?

A

these are distinct pathways that share the same enzymes, however, they cannot cross over
-depending on what is consumed in the diet will dictate what metabolite is made as a result

170
Q

How are long-chain PUFAs like EPA and DHA synthesized?

A

Through elongation and desaturation of ALA and LA, regulated by enzymes like FADS1 and FADS2

171
Q

what enzyme catalyzes the production of AA and EPA?

A

FADS1

172
Q

what is retroconversion in FA production? what can this produce?

A

long-chain fatty acid (LCFA) is shortened by removing two carbon atoms at a time
-can produce EPA from DHA

173
Q

how does conversion of ALA to EPA and DHA differ between women and men?

A

it is higher in women with ~20% converted to EPA and ~10% converted to DHA
-compared to 8% and 4% in men

174
Q

which FA are used to make eicosanoids?

A

EPA and AA

175
Q

provide an example of what eicosanoids derived from EPA / AA make?

A

prostaglandins and thromboxanes

176
Q

what are major causes of EFA deficiency?

A

1) dietary LA deficiency (<3g/day)
2) infants fed low fat diets
3) patients who are unable to eat

177
Q

name 3 symptoms of EFA deficiency?

A

1) decreased growth in children
2) decreased immune function
3) impaired reproduction / organ function

178
Q

what is a symptom of n-3 deficiency?

A

decreased visual acuity

179
Q

True or False: n-6’s and n-9’s can compensate for n-3 deficiencies

A

FALSE
only n-6’s can compensate for n-3 deficiency

180
Q

what FA will be increased when ALA is deficient?

A

omega 6 FA such as LA and AA

181
Q

what FA pathways will be upregulated when both n-3 and n-6 FA are deficient?

A

n-9 synthesis will be upregulated

182
Q

what nutrient source is vital post natal? why?

A

breast milk
-it contains DHA

183
Q

why are pre-term infants at risk for deficiency?

A

in the last trimester DHA accumulates in neural tissues at a high rate, pre term infants may not have a significant amount of [DHA]

184
Q

what EFA is highest in brain tissue?

A

DHA&raquo_space;»EPA

185
Q

what are common functional needs for DHA?

A

cerebrum, myelin sheath and retinal photoreceptors

186
Q

what does the variation in breast milk depend on?

A

mothers diet, genetics, lactation stage, maternal and infant health status

187
Q

what are 4 major functions of n-6’s?

A

1) eicosanoid formation
2) signal transduction
3) gene expression
4) skin water barrier

188
Q

what are the 3 major transcription factors do PUFAs impact?

A

1) PPARs
2) LXR
3) SREBP

189
Q

what effect do DHA / EPA have on inflammation?

A

decrease it by decreasing pro-inflammatory cytokines

190
Q

what is the major n-3 used for eicosanois synthesis?

A

EPA

191
Q

what effect do high levels of EPA have on the body?

A

-decreased production and increased clearance of TG from blood (when fasted)
-increased beta oxidation
-decreased lipolysis from adipocytes
-decreased plasma FFA
-decreased CM production (fed state)

192
Q

how does the change in increased EFA consumption differ between membrane composition vs adipose tissue?

A

it changes membrane composition to a certain extent where adipose tissue has no limit

193
Q

what phospholipase is important for eicosanoid synthesis? why?

A

Phospholipase A2 which hydrolyzes at sn-2 position
-EFA are incorporated into PL at the the sn-2 position

194
Q

what are the main pathways for ecosanoid synthesis? what types of eicosanoids are produced?

A

cyclic pathway- cyclooxygenase (COX)
-produced prostaglandins and thromboxanes

linear pathwaysl lipoxygenase (LOX)
-leukotrienes

Cytochrome P450 (CYP)
-makes hydroxylated products

195
Q

provide 3 examples of EFA biomarkers? are they short or long term?

A

1) adipose tissue (long term)
2) cheek cell phospholipids (long term)
3) plasma lipids (short term-reflect diet)

196
Q

where do eicosanoids act on?

A

released into extracellular fluid and act on local / adhacent cells (autcrines and paracrines)

197
Q

provide 5 examples of physiological affects of eicosanoids?

A

1) inflammatory response
2) reproductive function
3) smooth muscle contraction / relaxation
4) get health / integrety
5) regulation of blood pressure

198
Q

What 2 pathways are involed in the COX pathway?

A

COX1 - constitutive (causes problems if blocked)
COX2- inducible

199
Q

how does the eicosanoid synthesis from AA vs EPA differ? what types of prostaglandins vs leukotrienes are made? how does this impoct their function?

A

AA makes 2-series PGs and 4-series LTs (pro-inflammatory)

EPA makes 3-series PGs and 5-series LTs (less biologically active and inflammatory which can decrease inflammation)
-EPA / DHA is less potent and competes w AA for eicosanoid synthesis

200
Q

how does the competition of EPA /DHA with AA for eicosanoid synthesis impact what is synthesized?

A

The balance of dietary intake determines how much ARA or EPA is synthesized
-Western diets are typically higher in omega-6 PUFAs which can reduce the amount of EPA produced since they compete for elongation and desaturation

201
Q

What is the role of arachidonic acid derivatives in inflammation?

A

Prostaglandins: Vasodilation, pain, fever.
Leukotrienes: Vascular permeability, immune cell recruitment.

202
Q

What distinguishes chronic , acute amd pathalogical inflammation?

A

acute: protective response to injury

pathalogical: sustained duration, insufficient regulation, peripheral tissue damage (extreme condition)

chronic: low and sustained inflammation (lower than during infection or trauma)
-common in healthy population
-can induce insulin resistance

203
Q

How do EPA and DHA influence inflammation?

A

1) produce less inflammatory eicosanoids
2) reduce inflammation mediators
3) produce pro-repsolving mediators (resolvins, protectins, maresins)

204
Q

How do EPA and DHA improve health outcomes?

A

1) Reduce inflammation in autoimmune diseases and Alzheimer’s
2)Improve cardiovascular and metabolic health (e.g., lower MI/stroke risk, hypertension)
3)Mitigate cancer cachexia by reducing inflammation and preserving lean tissue

205
Q

why is there no AI for MUFAs or SFAs?

A

they are not essential and can be made in the diet

206
Q

what age group has an AI for fat? what is it?

A

infants
-31-30g/day for babies 0-12 months

207
Q

what is the recommended intake for n-6 and n-3? what is the n-6:n-3 ratio?

A

n-6: 12-17g/day
n-3: 1.1-1.6g/day

5:1

208
Q

What are the best dietary sources of EPA and DHA?

A

Fish: Mackerel (2500 mg/100g), Herring (1700 mg/100g), Salmon (1200 mg/100g)

Supplements: Fish oil capsules and liquids (300-1250 mg)

Enriched products: Omega-3 eggs, fortified juices

209
Q

what are plant based sources of n-6 and n-3 fats?

A

n-3: canola oil, chia, hemp hearts, flax seeds

n-6: soybean oil, corn oil, walnuts, hemp hearts, soybeans, tofu

NUTR 301 - nutritional BIOCH and Metabolism (5 decks)

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