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Biochemistry > lipid metabolism II > Flashcards

lipid metabolism II Flashcards

1
Q

what lipases are involved in the breakdown of TAGs

A

ATGL - adipose triglyceride lipase

hormone sensitive lipase (HSL)

lipoprotin lipase (LPL)

monoacylglycerol lipase (MAG Lipase)

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2
Q

transport of Fatty Acids:

short chain fatty acids ____

long chain complexed with ____ for transport

A

soluble

albumin

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3
Q

breakdown of TAGs

fat cell:

TAG → ____ and ____ ____

liver cell:

glycerol → ____ → ____

glycerol → ____ → ____

other tissue:

fatty acids → ____ ____ ____ → ____ ____ → TCA cycle

A

fat cell:

glycerol and fatty acids

liver cell:

glycolysis → pyruvate

gluconeogenesis → glucose

other tissues:

fatty acid oxidation → acetyl CoA

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4
Q

activation of HSL is modulated by ____

A

phosphorylation

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5
Q

____ and ____ are 2 major signals that promote mobilization of TAGs

A

hunger and exercise

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6
Q

major controllers of HSL signaling in hunger and exercise:

____ (secreted in response to hunger)

____ (secreted in resopnse to exercise)

both of these phosphorylate HSL (activate it) and promote ____ in ____

A

glucagon

epinephrine

lipolysis in adipocytes

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7
Q

mechanisms of regulation of HSL:

____ status signal inhibits mobilization of TAGs

____ (secreted in resopnse to high carb meal)

____ HSL (via activation of protein phosphatase I) to inhibit lipolysis

A

fed

insulin

dephosphorylates

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8
Q

perilipin:

  1. family of proteins that coat ____ ____ in ____ and muscle cells
  2. regulate ____ by controlling physical access to ____ (lipid breakdown enzyme)
  3. perilipins regulated by ____ (phosphorylation allows association with HSL) which promotes lipolysis
  4. overexpression of Perilipin I ____ lipolysis
  5. target of ____ treatment
A
  1. lipid droplets adipocytes
  2. lipolysis HSL
  3. PKA
  4. inhibits
  5. obesity
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9
Q

fatty acid breakdownA: an overview:

phase I:

phase II:

A

phase I: activation and transport to mitochondiral matrix

phase II: beta oxidation

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10
Q

TAGs → diacylglycerol (via ____ ) → monoacylglycerol (via ____ ) → glycerol (via ____ )

A

HSL

lipoprotein lipase

MAG

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11
Q

activators of HSL:

inhibitors of HSL:

A

glucagon, epinephrine, norepinephrine,

insulin

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12
Q

mobilization of FAs from Adipocytes: hunger and exercise

  1. glucagon and/or epinephrine bind to ____
  2. ____ is formed
  3. cAMP activates ____
  4. PKA phosphorylates ____ and ___
  5. glucagon and epinephrine also release another activator that activates ____
A
  1. GPCR
  2. cAMP
  3. PKA
  4. perilipin and HSL
  5. ATGL
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13
Q

mobilization of FAs from Adipocytes: Fed

  1. ____ binds to RTK (receptor tyrosin kinase)
  2. RTK activates ____
  3. protein phosphatase 1 (PP1) dephosphorylates and inactivates ____
A
  1. insulin
  2. protein phosphatase 1
  3. HSL
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14
Q

phase I FA breakdown:

  1. as long-chain FA-albumin complex crosses the plasma membrane, it loses ____
  2. outer mitochondrial membrnae is not permeable to ____ FAs
    1. must first be combined with ____ to make fatty acyl CoA in cytosol
  3. fatty acyl CoA has now crossed the outer mitochondrial membrane and is present in the ____ space
  4. fatty acyl CoA cannot cross ____ mitochondrial membrane
    1. ____ must be added which replaces CoA
  5. ____ is now permeable across the inner mitochondrial membrane
  6. once in the mitochondrial matrix, ____ is replaced with ____ to form fatty acyl CoA
  7. fatty acyl CoA becomes substrate for ____
A
  1. albumin
  2. free
    1. CoA
  3. intermembrane
  4. inner
    1. carnitine
  5. fatty acyl carnitine
  6. carnatine CoA
  7. beta-oxidation
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15
Q

translocation to mitochondrial matrix:

  1. carnitine → acyl carnitine via ____ ____ ____
  2. acylecarnitine translocates across inner mitochondrial membrane via ____
  3. acyl carnitine → carnitine via ____ ____ ____
A
  1. carnitine acyltransferase I
  2. translocase
  3. carnitine acyltransferase II
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16
Q

carnitine acyltransferase I is the rate limiting enzyme of

carnitine acyltransferase I is inhibitied by

A

fatty acid degradation

malonyl CoA

17
Q

enzymes in phase I:

  • fatty acyl CoA synthetase:
    • located on the ____ ____ ____
    • activates long chain FAs using ____
    • forms a ____ bond between FAs and CoA to form fatty acid CoA
  • carnitine palmityltransferase I (CPT-1) (also - carnitine acyltransferase)
    • located in ____ ____
    • transfers fatty acyl from fatty acid CoA to ____
    • forms FA - ____
    • rate-limiting enzyme in ____ ____
    • inhibited by ____
  • carnitine-acylcarnitine translocase
    • antiporter: ____ (in) ⇔ ____ (out)
  • carnitine palmitoyltransferase II
    • transfers Fatty acyl from FA-carnitine to ____
    • forms FA - ____
    • fatty acid CoA is now in the ____
A
  • fatty acyl CoA synthetase
    • outer mitochondrial membrane
    • ATP
    • thioester
  • carnitine palmityltransferase I (CPT-1)
    • intermembrane space
    • carnitine
    • carnitine
    • FA degradation
    • malonyl CoA
  • carnitine-acylcarnitine translocase
    • FA-carnitine carnitine
  • carnitine palmitoyltransferase II
    • CoA
    • CoA
    • mitochondrial matrix
18
Q

4 steps phase II: beta-oxidation:

      1. 4.
A
  1. oxidation: acyl CoA Dehydrogenase (ACAD)
    1. FADH2 which enters ETC to form 2 ATP
  2. hydration:
  3. oxidation:
    1. NADH which enters ETC to form 3 ATP
  4. thiolysis:
    1. releases Acytl CoA that enters into TCA cycle
19
Q

four main steps of beta-oxidation generate:

A

FADH2 (via acyl CoA dehydrogenase - ACAD) (1st oxidation step)

NADH (via 2nd oxidation step)

Acetyl CoA (via thiolysis) enters TCA cycle

20
Q

calculation of ATP released from beta-oxidation of palmitic acid:

FADH2 :

NADH :

Acetyle CoA:

Total:

ATP used:

Net ATP:

A

FADH2: 7 x 2 = 14 ATP

NADH: 7 x 3 = 21 ATP

Acetyl CoA: 8 x 12 = 96 ATP

Total: 131 ATP

ATP used: 2

Net ATP: 129 ATP

21
Q

ketone bodies are ____ - soluble and ____ compounds

A

water

acidic

22
Q

3 types of ketone bodies

A

acetoacetate

beta-hydroxybutyrate

acetone

23
Q

ketone bodies:

are produced only in ____

provide energy for ____ tissues and ____ during fasting and starvation

A

liver

peripheral

brain

24
Q

formation of ketone bodies:

  1. 2 molecules of ____ combine to make ____
  2. a third molecule of ____ is added to acetoacetyl CoA to form ____
  3. 3-hydroxy-3-methyl-glutaryl CoA breaks down and releases CoA to form ____ which then goes on to form other ketone bodies
A
  1. acetyl CoA acetoacetyl CoA
  2. acetyla CoA 3-hydroxy-3-methyl-glutaryl CoA
  3. acetoacetate
25
Q

utilization of Acetoacetate:

  1. other ketone bodies can break down to form ____
  2. acetoacetate → acetoacetyl CoA (via ____ )
  3. acetoacetyl CoA → 2 Acetyl CoA (via ____ ) which can enter TCA cycle
A
  1. acetoacetate
  2. CoA transferase
  3. thiolase
26
Q

what conditions favor production of ketone bodies

A

fasting and starvation

(no glucose, not undergoing glycolysis) (relying on FA degradation)

27
Q

first few hours of fasting:

A

energy source is blood glucose, followed by glycogen stored in muscle and liver

next gluconeogenesis in liver (synthesis of new glucose)

28
Q

after 1 day of fasting:

A

energy source is TAGs stored in adipose tissue

TAGs broken down to release FFA which undergo Beta oxidation

29
Q

after 3 days of fasting:

A

ketone bodies are made in liver and proteins in muscles are broken down

glycerol from TAGs and glucogenic amino acids from proteins enter gluconeogenesis

supply energy to brain and RBCs

30
Q

after 1-2 weeks of starvation:

A

brain switches to ketone bodies as major energy source

31
Q

after 2-3 months of starvation:

A

TAGs are depleted, proteins are main source

coma and death

32
Q

diabetic ketoacidosis (DKA):

  1. glucose cannot enter ____ or ____ cells
  2. when glucose is not being utilized, the ____ is shut down
  3. free fatty acids are released and broken down via beta-oxidation to ____
  4. excess acetyl CoA leads to production of ____ ____
  5. since ketone bodies are acidic, blood pH ____
  6. ____ and ____ can result
A
  1. fat or liver
  2. TCA
  3. acetyl CoA
  4. ketone bodies
  5. drops
  6. coma and death
33
Q

physiological ketosis

A

mild to moderate increase in ketone bodies

occurs in fasting, during pregenancy, after prolonged exercise and ketogenic diet

34
Q

pathological ketoacidosis:

A
  • occurs when glucagon/insulin ratio is increased, favoring FA breakdown
  • increased aceyl CoA in hepatic mitochondria
  • increased gluconeogenesis - reduced oxaloacetate
  • increased ketone bodies
  • acetone exhaled via breath, friuty odor in individuals with uncontrolled diabetes

Biochemistry (32 decks)

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