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Fuel Metabolism 2016 > fat > Flashcards

fat Flashcards

1
Q

insulin increases ___ of lipids 2

A

synthesis and storage

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2
Q

glucagon increases ____ of lipids 3

A

mobilization, oxidation, making ketones

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3
Q

what is emulsification

A

breaking something into smaller particles to increase surface area

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4
Q

major enzyme in lipolysis and its cofactor

A

pancreatic lipase and colipase

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5
Q

two secondary lipolytic enzymes

A

cholesterol esterase, phospholipase A2

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6
Q
  1. Provide an explanation of why a diet enriched in TG containing medium chain FA would be beneficial to a patient suffering from a lipid malabsorption syndrome
A

● Medium chain FA can diffuse straight through the intestinal cell into the portal vein and then the liver, so it would bypass most places where a deficiency might occur

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7
Q
  1. Explain why a person with lipid malabsorption might have any of the following conditions: night blindness, a bleeding disorder, osteoporosis, inability to maintain weight
A

● Lipid malabsorption leads to a deficiency in fat soluble vitamins (ADEK)
● Vitamin A deficiency = night blindness
● Vitamin D deficiency = osteoporosis
● Vitamin E deficiency = anemia
● Vitamin K deficiency = defective blood clotting
● Inability to maintain weight is due to lost calories from dietary fat

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8
Q

effect of a deficiency in bile salts

A

fat would not be emulsified, resulting in less breakdown and less diffusing across the membrane into intestinal cells (more in feces, feces will be chalky/clay-colored)

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9
Q

effect of a deficiency in pancreatic lipase

A

TG and DG not broken down completely, less diffuse across membrane into intestinal cells (more in feces, may lose weight)

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10
Q

effect of a deficiency in colipase

A

similar to pancreatic lipase, but less drastic decrease in activity

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11
Q

effect of a deficiency in apoprotein B-48

A

less chylomicrons (lack outer shell component), resulting in build up of fats in intestinal cells and liver, low circulating levels of chylomicrons and lipoproteins

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12
Q

effect of a deficiency in fatty acyl CoA synthetase

A

fatty acids can’t be activated; less reformation of TG, potential backup of monoglyceride and FA in intestinal cells

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13
Q

how are fatty acids transported in blood

A

mostly bound to albumin

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14
Q

how do chylomicrons get to target tissue

A

lymph to blood system, too big for capillaries

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15
Q

source and function of chylomicrons

A

intestine, transport dietary triglyceride to peripheral tissue

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16
Q

source and function of VLDL

A

liver, triglyceride transport

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17
Q

source and function of IDL

A

plasma vldl, precursor to LDL

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18
Q

source and function of LDL

A

plasma idl, transport cholesterol to peripheral tissue

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19
Q

source and function of HDL

A

liver and intestine, reservoir of apoproteins, reverse transport of cholesterol to liver

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20
Q
  1. Name two apoproteins that serve as ligands for cell surface receptors
A

Apo B (LDL receptors) and Apo E (Remnant receptors)

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21
Q

name two apoproteins that are activators of enzymes involved in lipoprotein metabolism

A

Apo C (lipoprotein lipase) and Apo A (reverse cholesterol transport)

22
Q
  1. Describe two metabolic fates of IDLs
A

● Conversion to LDLs by hepatic lipase

● Taken up by liver (via apo E  remnant receptors or apo B  LDL receptors)

23
Q
  1. Describe the metabolic role of the ABCA1 protein; name the disorder that results from a defect or deficiency in this protein
A

● ABCA1 mediates the rate-controlling step in reverse cholesterol transport (transfer of unesterified cholesterol and phospholipids from the cell to HDL)
● Tangier’s disease results from a deficiency in ABCA1 which causes the characteristic deficiency in HDL; serum profile shows decreased Apo A-1, decreased cholesterol, and elevated TG; presents in kids with large yellow-orange tonsils filled with foam cells

24
Q

molecular defect underlying familial hypercholesterolemia

A

inherited defect in LDL receptor, and is the most common disease of lipid metabolism – type II hyperlipoproteinemia (DEADLY!)

25
primary substrate for cholesterol synthesis and 3 key intermediates
● Acetyl-CoA is the source of all carbons in synthesized cholesterol ● HMG-CoA – 6 carbons; formed from 3 acetyl-CoA ● 5-C Isoprene units: ● Geranyl Pyrophosphate (C10), Farnesyl Pyrophosphate (C15), Squalene (C30) ● Lanosterol – first intermediate with a typical 4-ring closed structure
26
3. Identify the major regulated enzyme in the cholesterol biosynthetic pathway
● HMG-CoA Reductase
27
4. List four processes that influence cholesterol balance in tissues and describe the central role of the liver in maintaining cholesterol balance
● Absorption/uptake of dietary cholesterol  chylomicron remnant  liver ● De novo synthesis of cholesterol in the liver ● Extrahepatic de novo synthesis  HDL  liver ● Secretion of HDL and VLDL from the liver ● Free cholesterol secreted in the bile ● Conversion of cholesterol to bile acids and salts in the liver ● The liver is responsible for collecting all dietary cholesterol and synthesizing new cholesterol, as well as packaging it for transport to other tissues and for excretion (“gatekeeper”)
28
5. Explain why a genetic deficiency of cell surface receptors for apolipoprotein B results in hypercholesterolemia
● LDL binds to LDL-receptors on all cells via apoB-100 ● If there is a deficiency, then there is more cholesterol in plasma because it cannot get into tissue ● In addition to hypercholesterolemia, can lead to accelerated atherosclerosis and tendon xanthomas as well as a predisposition to coronary artery disease ● Treatment options include statins, cholestyramine, liver transplant, or LDL aphresis (dialysis)
29
what does lcat do
● LDL binds to LDL-receptors on all cells via apoB-100 ● If there is a deficiency, then there is more cholesterol in plasma because it cannot get into tissue ● In addition to hypercholesterolemia, can lead to accelerated atherosclerosis and tendon xanthomas as well as a predisposition to coronary artery disease ● Treatment options include statins, cholestyramine, liver transplant, or LDL aphresis (dialysis)
30
what does acat do
● ACAT is involved with intracellular storage of cholesterol as cholesterol esters (mostly steroid synthesizing organs: adrenals, gonads, liver); fatty acyl donor is fatty acyl-CoA
31
7. Explain the rationale for treating hypercholesterolemia with statins
● Statins inhibit HMG-CoA Reductase, limiting the synthesis of cholesterol from acetyl-CoA and reducing the back-up in the blood caused by a lack of LDL receptors
32
7. Explain the rationale for treating hypercholesterolemia with cholestyramine
● Cholestyramine works in the intestine and decreases absorption of cholesterol from the diet by binding bile salts; more excretion = less cholesterol storage in the body!
33
9. Name the enzyme that catalyzes the rate-limiting step in bile acid synthesis
● Cholesterol-7-α-hydroxylase
34
why is citrate important in fat synthesis
● Acetyl-CoA is formed in the mito matrix, while FA synthesis occurs in the cytosol. IMM impermeable to acetyl-CoA, so it is translocated as citrate (TCA cycle intermediate) ● The citrate shuttle is used to get Acetyl-CoA (and OAA) from the mitochondrion to the cytosol
35
enzyme that catalyzes the rate limiting step in FA synthesis, describe three different mechanisms for regulation of this enzyme
● Acetyl-CoA carboxylase, requires biotin, deactivated by phosphorylation, inhibition by palmitoyl coA, activation by citrate
36
5. Describe the role of citrate synthase, citrate lyase, malate DH, malic enzyme and the pentose phosphate pathway in FA synthesis
generate citrate and NADPH
37
how is malonyl coA made
from carboxylation of acetyl-CoA by acetyl-CoA carboxylase
38
the four core reactions catalyzed by FAS
condensation -> reduction -> dehydration -> reduction
39
7. Describe the role of acyl carrier protein (ACP) in FA synthesis, and name the cofactor for ACP
● ACP is an anchor for the growing FA chain during synthesis ● Cofactor is covalently attached phophopantetheine ● At the end of a cycle, the acyl group is transferred to the condensing enzyme and the ACP that is released is primed with a new malonyl group so that the cycle can continue
40
significance of mammary fatty acids
10 carbon fatty acid can diffuse into portal blood, standard palmitic acid cannot
41
two proteins with high affinity for fatty acids
albumin in blood, fatty acid binding protein in cell
42
why is carnitine important
beta oxidation occurs in mito matrix, carnitine shuttles it in by transferring on activated acyl fatty acids
43
ATP generated from oxidation of palmitic acid
129
44
6. Describe the consequences of a deficiency in either carnitine or a genetic deficiency in carnitine acyltransferase-I
leads to decrease in ability to oxidize FA; characterized by nonketonic hypoglycemia
45
7. Explain why administration of some drugs can induce a carnitine deficiency
● Low MW organic acids (such as valproic acid) can form acyl-carnitines that are excreted, resulting in less carnitine available for the carnitine shuttle
46
8. Describe the role of peroxisomes in FA oxidation and indicate how β-oxidation in peroxisomes differs from β-oxidation in mitochondria
● Peroxisomes are important for oxidation of very long chain FA (VLCFA; C26+) and branched chain FA (BCFAS); analogous to β-oxidation in mitochondria but with different isozymes ● Energy yield is less: FADH2 formed in the first step of each cycle cannot lead to ATP synthesis because it is regenerated by O2 to form H2O2
47
Refsums disease
a genetic deficiency in α-hydroxylase (which starts BCFA α-oxidation); symptoms include retinis pigmentosa, neuropathy, hearing loss, ataxia; treatment is elimination of phytanic acid (a BCFA), including dairy, beef, lamb, and some veggies
48
● Zellweger syndrome
absence of peroxisomes, which results in accumulation of VLCFAs and BCFAs (both oxidized in peroxizomes) and the inability to synthesize plasmalogens; extensive brain, kidney and liver damage leading to death by around 6 months of age; no treatment
49
Where does ketosis occur
mitochondria liver and kidney
50
where does ketooxidation occur
mitochondria of extrahepatic tissue
51
most prevalent lysosomal storage disorder and identify the most effective treatment
● Gaucher’s disease is an autosomal recessive disease common in Ashkenazi Jews, ● Treatment is enzyme replacement therapy using a recombinant glucocerebrosidase

Fuel Metabolism 2016 (6 decks)

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