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Biochemistry Block 1 > B-oxidation (oxidative metabolism of lipids in liver and muscle) > Flashcards

B-oxidation (oxidative metabolism of lipids in liver and muscle) Flashcards

1
Q

what is the major source of energy in liver and muscle ,and in other tissues with the exception of bran and red cells

A

FATS

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2
Q

The fatty acids oxidation proceeds in both the________and the _________?

A

peroxisomes and mitochondrion

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3
Q

what are the major end products of b oxidation?

A

acetyl coa and reduced forms of FADH2 and NADH

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4
Q

in the liver acetyl coa is converted into?

A

to ketone bodies (ketogenesis)

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5
Q

lipolysis is regulated by hormonal mechanisms involving?

A

gucagon, epinephrine and cortisol

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6
Q

fatty acids are activated by ?

A

formation of a high energy thiester bond with coenzyme A

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7
Q

in blood fatty acids are bound to which molecule?

A

albumin

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8
Q

the length of the fatty acid dictates?

A

where it is activated to coA

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9
Q

what kind of fatty acids can pass the membrane via passive diffusion?

A

short and medium chain fatty acids

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10
Q

what is the function of the carnitine shuttle?

A

bypasses the impermeability of the mitochondrial membrane to coenzyme A

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11
Q

CPT1( carnitine palmitoyl transferase 1 is located in which side of the membrane?

A

outer side of mitochondrial membrane

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12
Q

an acyl carnitine transporte or TRANSLOCASE in the inner membrane mediates?

A

the tranfer of acyl-carnitine in to the mitochodrion

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13
Q

what is the function of CPTII

A

Regenerates the acyl coa

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14
Q

the carnitine shuttle operates in which mechanism?

A

antiport mechanism

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15
Q

what inhibits the carnitine shuttle ?

A

MALONYL-COA

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16
Q

The common intermediate in the oxidation of carbohydrates and lipids is ?

A

ACETYL-COA

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17
Q

The caloric value of fats is about ????

A

twice that of sugars

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18
Q

on b oxidation, for each cycle was formed?

A
  1. acetyl coa
  2. FADH2
  3. NADH
  4. FATTY ACYL-COA with two fewer atoms
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19
Q

oxidation of the B carbon(c-3) facilitates what?

A

sequential cleavage of acetyl units from the carboxyl end of fatty acids

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20
Q

peroxisomes are involved in the oxidation of?

A

number of substrates, including urate, and long-,very-long and branched chain fatty acids

21
Q

peroxisomes is the principal site of production of?

A

hydrogen peroxide and account for 20% of oxygen consumption in hepatocytes

22
Q

in peroxisomes b oxidation their acyl-coa dehydrogenase is an?

A

oxidase rather than a dehydrogenase

23
Q

what is zellweger syndrome?

A

defect in import of enzymes into peroxisomes , severe multiorgan disorder leading to death usually at about 6 moths of age

24
Q

what are fibrates?

A

class of hypolipidemic drugs that act by inducing peroxisomal proliferation in liver

25
Q

which type of fatty acids yields to less FADH2 when they are oxidized?

A

unsaturated - since they are already partially oxidized

26
Q

odd chain fatty acids produce ?

A

succinyl coa from propionyl coa

27
Q

propionyl coa is converted to succinyl coa by?

A

multistep process involving three enzymes and the vitamins biotin and cobalamin

28
Q

what kind of oxidation initiates oxidation of branched chain fatty acids to acetyl coa and propionyl coa ?

A

alfa-oxidation

29
Q

what are phytanic acids?

A

branched chain polyisoprenoid lipids found in plan chlorophylls

30
Q

what is the first and essential step in catabolism of phyanic acids?

A

alfa oxidation to a pristanic acid , releasing the alfa carbon as carbon dioxide

31
Q

what is refsums disease?

A

rare neurological disorder , characterized by accumulation of phytanic acid deposits in nerve tissues as a result of a genetic defect in alfa oxidation.

32
Q

whats considered an autosomal recessive disease characterized by hypoketotic hypoglycemia , present in infancy and characterized by high concentrations of medium chain carboxylic acids, acyl carnitines and acyl glycines in plasma urine . hyperammonemia may also be present as a reuslt of liver damage

A

MCDA (medium chain fatty acyl coa dehydrogenase deficiency )

33
Q

MCAD deficiency is treated with?

A

frequent feeding, avoidance of fasting and carnitine supplementation

34
Q

defects in methylmalonyl coa mutase or deficincies in vitamin b12 lead to??

A

methylmalonic aciduria

35
Q

what is ketogenesis?

A

pathway for regenerating coa from excess acetyl coa

36
Q

in the liver the accumulation of acetyl-coa with concomitant depletion of coa, eventually limits?

A

b-oxidation

37
Q

what happens when b-oxidation of fatty acids is impaired?

A

fatty acids are oxidized, one carbon at a time , by alfa-oxidation or from the omega carbon by microsomal cytochrome P450 -dependent hydroxylases and dehydrogenases.

38
Q

during gluconeogenesis what is the primary source of ATP?

A

free coa is required to initiate and continue the cycle of b-oxidation

39
Q

in gluconeogenesis free coa is regenrated and the acetate group appears in blood in form of ?

A

3 water soluble lipid derived products: acetoacetate, b-hydroxybutyrate and acetone

40
Q

ketone bodies involves the synthesis and decomposistion of ?

A

hydroxymethylglutaryl (HMG)-CoA

41
Q

The enzymes HMG-COA synthase and lyase are unique to________?

A

hepatocytes

42
Q

the appearance of ketone bodies in the urine is an indicator of ?

A

active fat metabolism and gluconeogenesis

43
Q

ketogenesis is a result of ?

A

deficiency in carnitine metabolism

44
Q

what controls the direct rate of glycogen and glucose metabolism in liver?

A

insulin, glucagon, epinephrine and cortisol

45
Q

the process know as lipolysis is controlled by the adipocyte enzyme?

A

HORMONE SENSITIVE LIPASE

46
Q

In what kind of disease there are high blood concentrations of cortisol , hyperglycemia, muscle wastage and redistribution of fat from glucagon sensitive adipose depots to atypical sites such as the cheeks, upper back and trunk?

A

CUSHIING’S SYNDROME

47
Q

episodes of nonketotic hypoglycemia, development of fulminant heaptic failure, crdiomyopathy, rhabdomyolysis and ocassinally neuropathy and retinopathy are symptoms of ?

A

long chain l-3 hydroxyacyl coa dehydrogenase (LCAD) deficiency.

48
Q

in long chain l-3 hydroxyacyl coa dehydrogenase (LCAD) deficiency the most striking feature is ?

A

association with maternal HELLP(hemolysis,elevated liver enzymes and low platelets) and AFLP( acute fatty liver of pregnancy)

Biochemistry Block 1 (6 decks)

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