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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
Q

primary substrate for cholesterol synthesis and 3 key intermediates

A

● 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
Q
  1. Identify the major regulated enzyme in the cholesterol biosynthetic pathway
A

● HMG-CoA Reductase

27
Q
  1. List four processes that influence cholesterol balance in tissues and describe the central role of the liver in maintaining cholesterol balance
A

● 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
Q
  1. Explain why a genetic deficiency of cell surface receptors for apolipoprotein B results in hypercholesterolemia
A

● 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
Q

what does lcat do

A

● 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
Q

what does acat do

A

● 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
Q
  1. Explain the rationale for treating hypercholesterolemia with statins
A

● 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
Q
  1. Explain the rationale for treating hypercholesterolemia with cholestyramine
A

● 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
Q
  1. Name the enzyme that catalyzes the rate-limiting step in bile acid synthesis
A

● Cholesterol-7-α-hydroxylase

34
Q

why is citrate important in fat synthesis

A

● 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
Q

enzyme that catalyzes the rate limiting step in FA synthesis, describe three different mechanisms for regulation of this enzyme

A

● Acetyl-CoA carboxylase, requires biotin, deactivated by phosphorylation, inhibition by palmitoyl coA, activation by citrate

36
Q
  1. Describe the role of citrate synthase, citrate lyase, malate DH, malic enzyme and the pentose phosphate pathway in FA synthesis
A

generate citrate and NADPH

37
Q

how is malonyl coA made

A

from carboxylation of acetyl-CoA by acetyl-CoA carboxylase

38
Q

the four core reactions catalyzed by FAS

A

condensation -> reduction -> dehydration -> reduction

39
Q
  1. Describe the role of acyl carrier protein (ACP) in FA synthesis, and name the cofactor for ACP
A

● 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
Q

significance of mammary fatty acids

A

10 carbon fatty acid can diffuse into portal blood, standard palmitic acid cannot

41
Q

two proteins with high affinity for fatty acids

A

albumin in blood, fatty acid binding protein in cell

42
Q

why is carnitine important

A

beta oxidation occurs in mito matrix, carnitine shuttles it in by transferring on activated acyl fatty acids

43
Q

ATP generated from oxidation of palmitic acid

A

129

44
Q
  1. Describe the consequences of a deficiency in either carnitine or a genetic deficiency in carnitine acyltransferase-I
A

leads to decrease in ability to oxidize FA; characterized by nonketonic hypoglycemia

45
Q
  1. Explain why administration of some drugs can induce a carnitine deficiency
A

● 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
Q
  1. Describe the role of peroxisomes in FA oxidation and indicate how β-oxidation in peroxisomes differs from β-oxidation in mitochondria
A

● 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
Q

Refsums disease

A

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
Q

● Zellweger syndrome

A

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
Q

Where does ketosis occur

A

mitochondria liver and kidney

50
Q

where does ketooxidation occur

A

mitochondria of extrahepatic tissue

51
Q

most prevalent lysosomal storage disorder and identify the most effective treatment

A

● 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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