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BIOCHEMISTRY 2 > Lipids 1-3 > Flashcards

Lipids 1-3 Flashcards

1
Q

What are the functions of lipids?

A

1) E-storage
2) biological membranes
3) messenger molecules
4) building blocks for hormones
5) covalent modification on protiens

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2
Q

What are the classes of lipids?

A

1) FAs
2) Neutral glycerides
3) phospholipids
4) sphingolipids
5) cholesterol & derivatives

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3
Q

What is the structure of FAs in humans?

A
  • Even numbered
  • 12-24 carbons long
  • all DBs are cis, DBs separated by exactly 1 methylene group, unbranched
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4
Q

What is the naming/numbering of lipid’s carbons?

A
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5
Q

What is the importance of the cis-double bond?

A

It prevents stacking, so fatty acids have lower melting temperature. More double bonds, the most likely a FA is in liquid state at room temperature.

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6
Q

What are essential FAs?

A
  • FAs that we cannot synthesize; those with omega 3 bonds
  • Ex. Linoleic acid & a-Linolenic acid
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7
Q

Which fats are healthier?

A
  • Unstaurated fats
  • Less packed
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8
Q

What are the differences beween mediterranean. wester, and low-fat diet?

A
  • Mediterranean diet: 38% fat (mainly monosaturated) , 42% carbs, 20& protien
  • Western diet: 38% fat (mainly saturated)
  • Low-fat diet: 20% fat, 65% carbs, 15% protein
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9
Q

What are neutral glycerides?

A
  • Glycerol, mono-di-tri-glycerides
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10
Q

What is the structure of phospholipids?

A
  • The alcohol can be: serine, ethanolamine, choline, inositol, glycerol
  • Name: Phosphatidyl serine
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11
Q

What is cardiolipin?

A
  • Its is phospholipid in mitochondrial inner membrane
  • Also named Diphosphatidyl glycerol
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12
Q

What are sphingolipids?

A
  • Lipids containing a backbone of sphingoid bases, a set of aliphatic amino alcohols that includes sphingosine.
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13
Q

What is the structure of Sphingomyelin?

A
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14
Q

What is the structure of Glycosphingolipids?

A
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15
Q

What is the importance of cholesterol?

A
  1. Membrane component
  2. Bile salts
  3. Steroid hormones (progesterone, estrogen, aldosterone, cortisol, androgens)
  4. Vitamin D

*Chylomicrons release contents in cell surface

*Dietary cholesterol has little influence on plasma cholesterol in healthy people

*HMGcoA reductase is always active in patients with high cholesterol. It synthesizes cholesterol always.

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16
Q

What are lipoproteins?

A

–>Assembly of proteins & lipids, which allow fats to move through the water inside and outside cells. Proteins serve to emulsify fat molecules.

–> Ex) chylomicron, LDL(β;-lipoprotein), VLDL (Pre β-lipoprotein), HDL (α-lipoprotein)

–> LDL

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17
Q

What apoprotein in LDL is related to heart disease?

A

B100

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18
Q

What generates the main lipoproteins?

A

1) HDL is generated by liver & intestine, (lowest TAG, high cholesterol)
2) LDL is generated by VLDL, (LDL has low TAG and highest cholesterol)
3) VLDL is generated by liver, (high TAG, low cholesterol)
4) Chylomicrons are generated by the intestines, (highest TAG, lowest cholesterol)

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19
Q

What are the functions of the main lipoproteins?

A
  • HDL: deliver cholesterol from peripheral tissues to the liver for elimination or for ssteroid synthesis
  • LDL: deliver cholesterol to the peripheral tissues and to the liver
  • VLDL: deliver endogenous TAG to peripheral tissues
  • Chylomicrons: deliver dietary TAG to peripheral tissues (adipose tissue, muscle, lung)
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20
Q

How are lipids broken down in the body?

A
  • Lipids degradation primarily occurs in the small intestine, where bile salts emulsify & pancreatic enzymes degrade these 3 releasing FAs:

CE–cholesterol esterase–> cholesterol + FA

PL –Lipases–> Glyceryl-P-ryl-choline + 2FAs

TAG – pancreatic lipase–> 2-monoacyl-glycerol + 2FAs

  • In the form of chylomicrons, lipids are taken to the lymph & then to the blood
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21
Q

What are some characteristics of bile salts?

A
  • Needed in small intestine to emulsify fats
  • The bile duct connects the liver to the intestines
  • Made in the liver
  • ~25g used during digestion/day
  • Most bile salts are re-absorbed in the intestines
  • Made out of cholesterol (0.5/day) to replace bile salts that were excreted
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22
Q

What are the types of gallstones?

A

1) Cholesterol stones: light yellow to dark green or brown, 80% cholesterol by weight
2) Pigment stones: small and dark. Bilirubin and calcium salts found in bile. >20% cholesterol
3) Mixed stones: 20-80% cholesterol. Calcium carbonate, palmitate phosphate, bilirubin, & other bile pigments

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23
Q

What is PTL?

A

Pancreatic triglyceride lipase: from pancreas, only cleaves at position 1 and 3

–> In the intestinal lumen, with bile salts, it converts:

   TAG --\> two  FAs + one 2-monoacylglycerol

–> Become mixed miscelles

–>Transported through FATP4 to i_ntestinal mucosa_

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24
Q

What happens with fats at the intestinal mucosa (enterocytes)?

A

1) Reform triglycerides: 2 FAs+ 1 2-MAG —> TAG
2) P-lipids & apoB-48/C/E make TAGs into chylomicrons (only carry fat from diet)
3) Chylomicrons also contain: phospholipids, fat-soluble vitamins, apolipoprotein B-48 from AAs, & cholesteryl ester
4) Chylomicrons go into the lymphatic system and then the blood stream

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25
Q

What is steatorrhea?

A
  • Excess lipid in feces (very tinky, floats)
  • Can occur because:
  1. There is o_bstruction of bile duct_
  2. Pancreatic juice duct obstruction (or lack of pancreatic juice?)
  3. Defective intestinal mucosal cells
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26
Q

What are some disorders affecting chylomicrons?

A

1) Abetalipoproteinamia: apo B-100 defect (no VLDL /chylomicrons/LDL, so no long chain FA absorption; GI symptoms, cognitive problems)

2) LPL deficiency: high blood levels of chylomicrons

3) Apo C-II deficiency: on surface of chylomicrons & VLDL, & is normally required for LPL activation. Mutation prevents clearance of chylomicrons from blood

4) Low LPL activity: extreme plasma chylomicron & TAG levels; liver & pancreas problems. Fat-restricted diet.

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27
Q

What is our total energy expenditure?

A

* Adaptive thermogenesis: variable, regulated by brain. Responds to temperature and diet. Brown adipose tissue.

*Physical activity: variable

*Obligatory energy expenditure: resting metaboic rate ~1300 kcal/day

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28
Q

What are olestra and orlistat?

A
  • Olestra: “fake fats,” cannot be digested. 6-8 FA on sucrose
  • Orlistat: lipase inhibitor. Do not figest TAGs from diet. Can cause GI problems.
29
Q

What is LPL?

A
  • Lipoprotein Lipase

Triglycerides ——-> glycerol + 3 FAs

30
Q

What are some characteristics of FA catabolism?

A
  • TAGs are the preferred storage form
  • FA degradation is a cylcic process (β-oxidation)
  • β-oxidation: in inner mitochondrial matrix
  • The brain cannot break down FAs
  • More reduced ->more energy content
31
Q

How do we go from triacyl glycerol to Acetyl-CoA?

A

In adipose tissue:

1) triacyl glycerol —lipases—-> FA + glycerol

2) glycerol– deihydroxyacetone phosphate—> glucose + acetyl-CoA

32
Q

What are the B-oxidation steps?

A

1) FA + ATP –> Acyl adenylate
2) Acyl adenylate + HS-CoA –> AcylCoA
3) AcylCoA + FAD —> trans-Δ2-EnoylCoA + FADH2
4) trans-Δ2-Enoyl CoA + H2O —> L-3-Hydroxyacyl CoA
5) L-3-Hydroxyacyl CoA + NAD+—> 3-Ketoacyl CoA + NADH
6) 3-Ketoacyl CoA + HS-CoA —thiolysis–> Acyl CoA + Acetyl CoA

33
Q

What are some cofactors required for B-oxidation of odd # chain FAs?

A
  • Biotin
  • Vitamin B12
  • Mn & Co
34
Q

How are FAs transported into the mitochondria?

A

-Carnitine Pamitoyl Shuttle

  1. FA –> FattyAcyl-CoA
  2. Into mito-intermembrane space
  3. C.P. Transferase I converts FattyAcyl-CoA into Acyl-Carnitine
  4. Acyl-Carntine goes through inner membrane
  5. CP. Transferase II converts it back to FattyAcyl-CoA
35
Q

How much ATP is obtained from B-oxidation?

A

12:0

5 FADH2 (x2) –> 10

5 NADH (x3) –> 15

6 AcetylCoA (x12) –> 72

1 AcylCoA synthesis –> -2

__________________________

95 ATPs (2.5 more than glucose per unit weight)

36
Q

What is Zellweger syndrome?

A
  • No functional peroxisomes
  • Defect in degradation of FAs 26+ & α-oxidation
  • Affects CNS and other organs
  • No treatment, do nt survive beyond 1 year
37
Q

What is Refsum syndrome?

A
  • Defect in degradation of 3-methyl-branched FA (phytanic acid)
  • Neurological disease caused by accumulation of phytanic acid
  • Treatment: phytanic acid restricted diet (fat-containing products from ruminant animals & high-fat fish)
38
Q

When does physiological ketosis take place?

A
  • Late pregnancy
  • Neonatal period
  • High fat diet
  • Starvation
  • Extreme exercise
39
Q

What occurs in pathological ketosis?

A
  • Refers to diabetic & alcoholic ketoacidosis
  • Cells cannot absorb glucose, liver does gluconeogenesis
  • Oxaloacetate decreases (no TCA), and B-oxidation increases
  • Ketone bodies increase causing acidosis & loss of fliud & minerals. Can lead to comma id pH is too low
40
Q

What is Hypoketotic hyploglycemia?

A
  • Symptom of starvation due to inefficient use of FAs as 1ry E-source
  • Muscle weakness, sleepiness, mood changes
  • Treatment: dietary modification, frequent intake of low-fat, high-carb food, (to keep adequate glucose levels to prevent body from moving fat to the liver for energy)
41
Q

What are the energy sources under starvation or very low-carb diet?

A
  • Glucose from gluconeogenesis
  • 3-Hydroxy-butyrate/ketone bodies (from acetyl-CoA from FAs)
  • Acetoacetate (ketone body)
  • Amino acids
42
Q

What is the preferred energy source in the brain?

A
  • glucose preferred fuel
  • no ß-oxidation
  • starvation ketone bodies
43
Q

What is the preferred energy source in muscle?

A
  • Glucose, FA, ketone bodies
  • Large glycogen storage (1200 kcal)
  • ß-oxidation in resting muscle
  • little citric acid cycle when glucose is used (–> Cori cycle)
44
Q

What is the preferred energy source in the heart?

A
  • FA, ketone bodies
  • has no glycogen
  • almost exclusively aerobic
45
Q

What is the preferred energy source in adipose tissue?

A
  • glucose, FA
  • needs glucose to make glycerol
  • TG storage (135.000 kcal)
46
Q

What is the preferred energy source of kidneys?

A
  • glucose, FA, ketone bodies
  • uses about 10% of total oxygen
  • very important for gluconeogenesis
47
Q

What is the preferred energy source of the liver?

A
  • glycogen storage (400 kcal)
  • glycolysis to get building blocks for biosynthesis
  • does not use glucose, FA or ketone bodies
  • makes glucose from ala, lactate, pyruvate
  • energy from alpha-keto acids (aa degradation)
  • under starvation cond. ß-oxidation
48
Q

How does FA synthesis occur?

A
  • Liver and adipose tissue (humans: almost exclusively in liver)
  • Synthesis from acetyl-CoA & malonyl-CoA
  • In cytosol
  • Acyl units are carried by Acyl Carrier Protein (ACP)
  • Glucose or AA –> acetylCoA

8 acetyl CoA + 14 NADPH + 14 H+ + 7 ATP ——–> palmitic acid (16:0)

49
Q

How does alcohol trigger FA synthesis?

A
  • Alcohol increases liver NADH levels. This will inhibit isocitrate dehydrogenase in mito
  • Accumulation of citrate, & so it goes to cytosol through a shuttle
  • In the cytosol, citrate releases acetylCoA when coverted to oxaloacetate
50
Q

What are the basic types of regulation of FA metabolism?

A
  • Short-term: RAPID: allosteric covalent modification
  • Long term: SLOW: rate of synthesis (ex. after a few days of diet)
51
Q

What is long-term regulation of FA metabolism?

A

Lipogenic enzymes:

  • Acetyl CoA Corboxylase
  • FA Synthase
  • Citrate Lyase
  • Malic enzyme
  • DH of Pentose Phosphate Pathway

–> are upregulated by: high CH diet, high insulin levels

–>downregulated by: high fat/low carb diet & fasting

52
Q

What are some examples of short term regulation of FA synthesis?

A

Isocitrate DH: allosteric inhibition by ATP

CPT1 (Cartnitine-Palmitoyl-Translocase):
allosteric inhibition by malonyl CoA (prevents ß-oxidation)

Acetyl CoA carboxylase: inhibited by phosphorylation (AMPK), activated by citrate, inhibited by palmitoyl CoA

Insulin: activates
Glucagon and epinephrine: inactivate

53
Q

What are the functions of adipose tissue?

A
  • Energy storage
  • Protection of organs
  • Insulation
  • Storage fat soluble vitamins
  • Synthesis of adipokines
54
Q

What happens to adipocytes when a person gains weight?

A
  • Modest weight gain: in a non-obese person, adipocytes get bigger
  • Big weigth gain: if adipocytes reach their maximum size, there is recruitment and proliferation of new pre-adipocytes
  • Weight loss: decrease in fat cel size
55
Q

What are leptin and ghrelin?

A

LEPTIN

  • produced by adipocytes
  • decreases appetite
  • increases caloric expenditure (inc. metabolic rate)
  • long term effects

GHRELIN

  • produced by stomach
  • increases appetite
  • short and long term effects
  • injection into the bloodstream dramatically increases appetite
56
Q

What is the importance of cholic acid?

A
  • Cholic acid (a bile acid) increases energy expenditure
  • In mice, high fat diet + cholic acid had weight similar to a mice in regular diet
  • By increasing activity of brown adipose tissue, which prevents diet-induced obesity & insulin-dependent diabetes <in></in>
57
Q

What is the function of brown fat cells?

A

–>Store fat in muscle. They use a lot of energy in producing heat (instead of aTP) in the mitochondria.

58
Q

Where do phospholipases cleave phospholipids?

A
  • Between FAs and glycerol
  • Between phosphate and alcohol
  • Between glycerol and phosphat_e (Phospholipase C)_
59
Q

What is Tay-Sachs disease?

A
  • Enzyme deficiency in lysosomes that is in charge of cleaving a sugar in gangliosides
  • Fatal neurodegeneration, blindness, macula, muscle weakness, seizures
  • Recessive
60
Q

What is Goucher disease?

A
  • Accumulation of cerebrosides
  • Hepatosplenomegaly, osteoporosis, may have CNS involvement
  • Recessive
61
Q

What are the steps of endocytosis?

A
  1. Receptors in cell membrane bind ligands (glu, AAs, G-6-P) and cluster
  2. Early endosome forms
  3. Late endosome undergoes pH drop bc of proton pump
  4. Receptors & ligands dissociate. Some receptors (like LDL) are recycled
62
Q

What are the steps of iron endocytosis?

A
  1. Diferric transferin (Apo-transferrin + Fe) bind the transferrin receptor
  2. This trigger endocytosis
  3. Endosome fusion and pH drop (ions are free and exit endosome)
  4. pH increases, and receptors are recycled
63
Q

What is congenital adrenal hyperplasia?

A
  • A series of defects in steroid hormone synthesis
  • Ex. hydroxylase deficiency -> no cortisol, no sex hormones
64
Q

Where do we get cholesterol from?

A
  • 0.5g/day from diet taken from LDL
  • 0.5g/day from cytoplasmic synthesis (from acetyl CoA)
  • no degradation pathway, excreted as bile salts
65
Q

What is Familial Hypercholesterolemia, FH?

A

-High LDL-cholesterol plasma levels:

-Heterozygous: 1/500. Blood cholesterol: >300 mg/dl. LDL: >220. Untreated: 85% myocardial infarction bx 60
Treatment: statins (Lipitor, Crestor)

-Homocygous: frequency 10-6
Blood cholesterol: 500-1200 mg/dl
Untreated: myocardial infarction before age of 30
Treatment: LDL apheresis (physical removal of LDL)

66
Q

What are the possible causes of Familial Hypercholesterolemia, FH?

A

(1) no LDLR made (gene deletion)
(2) LDL_R not localized_ properly (mutant)
(3) LDLR has _low affinity for apo B-10_0
(4) LDLR does not accumulate in coated pits
(5) _LDLR does not release LD_L in late endosomes, so LDL receptor is degraded in lysosome

67
Q

What are the normal levels of lipoproteins?

A

LDL chol: 160 or less,

HDL chol: less than 45,

TG: less than 150. Mg/dL

68
Q

How are foam cells?

A
  • Oxidized LDL+B100 get taken up by macrophages
  • Macrophages can take up more oxidized LDL from blood, and they can get very big and make foam cells
  • Foam cells can attach to epithelial layer of vessels, which can cause inflammation and plaques that block flow
  • Only oxidizes if LDLRs are in the bloodstream too long (stimulated by NO, O2-, H2O2. Inhibited by vitE)

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