Lipid Flashcards
Block 1 - New notes (112 cards)
1
Q
How are body lipids compartmentalized
A
membrane associated, trialglycerol in adipocytes, transported in plasma with proteins
2
Q
Non-polar lipids are
A
hydrophobic/lipophilic (water fearing)
2
Q
Functions of lipids
A
energy source, structure, barrier, cushing action, metabolic regulators, thermal/electrical insulators, main components of prostaglandins
2
Q
Polar lipids are
A
hydrophilic/lipophobic ( water loving)
3
Q
What are amphopathic lipids
A
both water loving and fearing
3
Q
Complex lipids
A
phospholipids, glycolipids, lipoproteins
3
Q
Simples lipids
A
SFA + UFA, MAG, DAG, TAG, neutral fats, cholesterol
4
Q
derived lipids
A
From simple or complex, steroids, ketone bodies, eicosanoids, fat-soluble vit (A,D,E,K)
5
Q
What are eicosanoids
A
prostaglandins, thromboxanes, leukotrients
6
Q
what are fatty acids
A
building blocks that are free as fatty acyl esters, provide energy during fasting, released from adipose and bound to plasma albumin
7
Q
B-oxidation
A
energy production in most tissues
7
Q
Fatty acid structure
A
have hydrocarbon chain with carboxyl group, has anionic groups
8
Q
LCFA are
A
associated with protein in blood plasma, highly water insoluble
9
Q
What are saturated fatty acids
A
no double bonds, nice and straight
9
Q
are longer fatty acids chsin more soluble, insoluble, or amphipathic
A
longer are more insoluble, shorter are more amphipathic, more insoluble need to attach to albumin + lipoproteins
10
Q
what are unsaturated fatty acids
A
one or more double bonds, Cis DB change direction, always at 3-carbon intervals, more CDB lower melting temp
11
Q
Arachidonic acid
A
omega 6 fatty acids, first DB is 6 from end
12
Q
length of SCFA
A
2-5
13
Q
length of MCFA
A
6-12
14
Q
length of LCFA
A
13-21
15
Q
length of VLCFA
A
22 + ( found mainly in brain)
16
Q
Essential FAs
A
essential for metabolism and cannot be synthesized, Linoleic acid (w-6), Linolenic acid (w-3)
17
Q
sources of essential FA
A
nuts, seeds, vegatable oil, algae, fish oils
18
Q
Linoleic Acids
A
precursor of arachidonic acid
19
Alpha-linolenic Acid
needed for growth and development, also ricosanoid synthesis
20
Eicosanoids
derived from essential fatty acids, signaling molecules ; extremely potent, are local hormones with extremely short half-lives
21
Physiological eicosanoids
inflammatory
22
Pathologic eicosanoids
hypersensitivity
23
What is Archidonic acid a precursor for
Prostaglandin, thromboxanes, leukotrienes
23
What are Leukotrienes
synthesized in eukocytes, not inhibited by NSAIDs, mediators of allergic response + inflammation
24
what are Prostaglandins
pain + fever response, action on repro + GI track, action on brochopulmary tone, regulate hormones, Ca movement, inflammation
25
What are thrombocanes
synthesized on platelets, promote platelet homeostasis
26
Phospholipids are
a polar phosphate head + 2 non-polar FA tails with glycerol backbones
26
Leukocytes
WBCs : marcrophages, neutrophils, eosinophils, and mast cells
26
A polar head is
hydrophilic : phosphate group + polar head (can change mlecules)
27
A non-polar tails is
hydrophobic : FA or FA-derived hydrocarbons
28
General structure of phospholipids
2 FA tails + Glycerol + phosphate + Alchol (polar group)
29
where are phodpholipids
in membranes, intracellular messenger, important components of surfactant and detergent-like molecules
30
Glycerophospholipids
glycerol backbone, majority of phospholipids and prevalent in membranes
31
Shingophospholipids
have sphingosine backbone, derived from serine + palmitate, attached to LCFA hydrocarbon tail, Important in brain tissue, mainly LCFA or VLCFA
32
Phosphatidic acid
precursor of glycerophospholipids
33
Sphingomyelin
main sphingophospholipid
34
Cardiolipin
componet of inner mitochondrial membrane, maintains ETC complexes
35
Platelet-Activating factor
activates inflammatory cells, platelets aggregation, in hypersensitivity (anaphylactic)
36
Cell cytosolic precursors
FA CoA (FA + CoA) + glycerol-3-phosphate
36
Erythrocytes
Cannot synthesize phospholipids
36
Glyerophospholipids
synthesized from cell cytosolic precursors
36
where are glycerophospholipids synthesized
in sER membranes
37
where are lipid modifications occur
golgi apparatus
38
fate of glycerophospholipids
compostition of membranes or secreted in vesicles
39
what is FA CoA
2 FA linked to coenzyme A joined with a glycerol-3-phosphate to yield phosphatidic acid, different polar head groups results in different diacylglycerol, enzyme converts phosphatidic acid to diacylglycerol
40
Phospholipases
breaks down phospholipids, found in toxins + venoms, also pathogenic bacteria produce this (spreads infection)
41
Glycolipids do
maintain cell membrane stability for cellular recognition, made of carb+lipid
42
Glycosphingolipids
subclass of glycolipids, has no phosphate, Ceramide back bone, part of membranes, high concentration in nerves
43
Cholestrol
very hydrophobic, 4 hydrocarbon rings, can be synthesized as well as ingested, made of acetyl-coa
44
Functions of cholesterol
structural component of cell membranes + lipoproteins, precursors of bile acid, steroid hormone + Vitamin D
45
what controls cholesterol homeostasis
the liver
46
cholestrol ester
even more hydrophobic, plasma cholesterol with FA, not found in membranes, present in low levels associated with lipoprotiens
47
Steroid hormones are
precursed by cholecterol, glucocorticoids, mineralocorticoids, sex hormones, transported in blood (hydrophobic)
48
Lipoproteins types
VLDL - very low density, LDL - low density, HDL - high density
49
Functions of lipoproteins
keep lipids soluble for transport
50
Lipid digestion
starts in mouth + stomach, completed in SI, detergent action is needed for emulsification
51
enzymatic Lipid digestion
in stomach (Lingual lipase + gastric lipase are acid stable)
52
Steps in lipid digestion
1. emulsification
2. hydrolysis
3. micelle formation
4. absorption
53
what is the pancrease for
main organ of lipase synthesis + secreation
54
Emulsification
starts in stomach goes to duodenum, increases surface area of hydrophobic droplets
54
2 components of emulsification
mechanical mixing by peristalsis and use of detergent of conjugated bile salts
55
Bile salts
synthesized in liver, stored in gallbladder, amphipathic derivatives
56
Bile
bile salts + free cholesterol
56
Pancreatic enzymes for lipid digestion
triacylglycerol, cholesteryl ester, phopholipase
57
Triacylglycerol
to large for intestinal cells, hydrolyzed by pancreatic lipase + co-lipase, end product 1 MAG + 2 FFA
58
Cholesteryl ester
hydrolyzed by cholesterol esterase (incrased by bile salts) end products - cholesterol + FFA
58
Phopholipase
pancreatic juice is rich in this, increased by bile salts end product lysophosphlipid + FFA
59
when is pancreatic enzymes enter
in luminal phase
60
what are mixed micelles
end product mixed with bile salts, transport lipids from gut lumen to microvilli, form a collidal suspension
61
End products of enterocytes absorption
FFA, free cholesterol, lysophospolipids and monoglycerides
62
What happens in enterocyte absorption
short +medium chains are taken directly by enterocyte membrane, combines with bile salts and lipid-soluble vitamins to form mixed micelles
62
Lipid soluble vitamins
A, D, E, K
62
Re-esterification
once absorbed is moved to see (put back together)
62
where does chylomicron mature
Golgi apparatus
63
Short + medium CFA
will no re-esterified, directly absorbed into hepatic portal to bind to albumin and carried to liver
64
what is Chylomicron
made up of re-esterified lipids, cholesterol and proteins, spherical structures, highly hydrophobic, released from enterocytes via exocytosis
65
What happens to the TAG from chylomicron
degraded to FFA + glycerol by lipoprtein lipase in peripheral tissue
66
peripheral tissue examples
Skeletal muscle, adipose, heart, lung, kidney, liver
67
Free fatty acids from chylomicron will enter
muscle or organ for energy, adipocytes for storage, or remain in blood
68
Glycerol from chylomicron will enter
liver to synthesis glycerol-3-phosphate (glycolysis or gluconeogensis)
69
chylomicron remnants will
go to liver and hydrolyze into components and recycled
70
Panceratic lipases
cholecyoskinin, secretin
71
Choleytodkinin (CCK)
produced by I cells of duodenum, stimulates bile and secretionof digestion enzymes, decreased gastric motility
72
Secretin
produced by S cells of duodenum, released in response to low pH of chyme, stimulates biocarbonate secrection, neutralize pH
73
Steatorrhea
loss of lots of fat in stool, chatacteristic of pancreatic exocrine insufficiency, inflammatory bowl disease, intestinal lymphatic obstruction, defective chylomicron synthesis, bile salt deficiency, maldigestion/malabsorption can reslut in Vit deficiencies
74
Fatty acids are
synthesized from and oxidized to acetyl-Coa, oxidized in mitochondrial, synthesized in cytoplasm, conditions that promote synthesis inhibits oxidation (vice-versa)
75
De Novo fatty acid synthesis
occurs in cytosol of livers cells, mammory gland, adipose tissue, others- small amount in kidney, brain, lung
76
Substrates for De Novo
excess carbs + proteins (acetyl coenzyme A from mitochondria)
77
De Novo products
palmitate (palmitic acids), can be elongated in sER
78
smooth endoplasmic reticulum
enzymes present cause denaturation of LCFA by adding CDB, polyunsatutated FA are produced by desatutation and elongation
78
Acetyl CoA caroxylase
activated by citrate, inactivated by palmitoyl Coa, regulated by insulin
79
Steps of De Novo
1. Cytosolic acetyl coa production
2. ACoA carboxylation to Malonyl CoA
3. Synthesis of Palmitate 16:0
80
Cytosolic acetyl coa production
move acetate from mitochondrial acetyl coa to cytosol (from m matrix), produced by oxidation of pyruvate, cannot cross membrane, incorporated into citrate for transport, citrate is produced by condensation of AcoA with OAA, then is cleaved to OAA + ACoA by ATP citrate layse
81
ACoA carboxylation to Malonyl CoA
catalyzed by acetyl CoA Carboxylase (ACC), biotin + ATP required, rate-limiting step + regulated step in FA synthesis
82
Synthesis of Palmitate 16:0
driven by FA synthesis, addistion of 2 carbons to carboxyl end of acyl acceptors, NADPH is required, results in production of palmitate, carbon provided by ACoA
83
lipogenesis
stored as triacylglycerol, stored as lipid droplets in adipocytes, 3 FA in TAG can vary
84
Lipolysis
mobilization of fat releasing from TAG form, helps with hormone-sensitive-lipase (HSL)
85
B-Oxidation
pathway for FA catabolism in mitochondria, LCFA must form FACoA before oxidizing, carnitine shuttle is required for FACoA to get into mitochondria, each cycle is catalyzed by enzyme with chain length specificity and produces 1 A CoA + 1 NADH + 1 FADH2
86
Carnitine
synthesized from lysine + methionine in liver + kidney, also can be absorbed, deficiencies cause decrease ability for LCFA as fuel for tissues
87
First cycle of B-oxidation
sequence of 4 reactions involving b-carbon that shortens FA by 2 carbons
88
4 reactions of first cycle
1. reducition-produces FADH2
2. hydration
3. second reduction - produces NADH
4. CoA dependent frees 1 acetyl CoA
89
1 palmitoyl Cox produces
8 ACoA, 7 NADH, 7 FADH2 (129 ATP total)
90
Ketone bodies are
alternative fuel, important energy for peripheral tissues, hydrophilic, can cross blood brain barrier + placental barrier, used in proportion to concentrate by extraphepatic tissue, lipolysis of TAG stimulates production, save glucose during fasting, high amount of NADH makes ACoA go into ketogenesis
91
Acetoacetate + b-hydroxybuterate
free soluble lipids, transported in plasma oto peripheral tissue, once in peripheral, converted back to Acetyl CoA, negative feedback on HSL activity in adipocytes
92
Ketolysis
creating ketones in peripheral tissus, 3-hydroxybutyrate is oxidized to acetoacetate, acetoacetate + CoA molecule = acetacetyl CoA, acetacetyl CoA -> 2 acetyl CoA
93
RBC
cannot use ketone bodies as energy source due to lack of mitochondria
