MCP u6 images Flashcards

1
Q
A

glycerophospholipid

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2
Q

what is this?

A

ether glyercophospholipids

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3
Q

?

A

sphingomyelin

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4
Q
A

galactocerebroside

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5
Q

what does phospholipids include?

what do they all have in common?

A
  1. glycerophosphopid
  2. ether glycerololipids
  3. sphinogophospholipids

POLAR HEAD GROUPS which are linked by a a PHOSPHODIESTER bond to CARBON 3 of the glycerol or sphingosine backbone.

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6
Q

sphingolipids include?

A
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7
Q

what is this?

A

phosphotidylcholine

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8
Q
A

phosphatidylserine

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9
Q

what is this?

A

cerebroside

glycosphingolipids with one galactose or glucose attached

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10
Q
A

acetoacetate

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11
Q

what is this?

A

b-hydroxybutarate

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12
Q

what is this?

A

cholestoerl

)eight)carbon) hydrocarbon)attached)to)carbon) 17,)of)the)D)ring;

)hydroxyl group attached to carbon 3 of the A ring

and a double bond between carbon 5 and 6 of the B ring.

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13
Q

what is in primary bile acid? secondary?

A
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14
Q

where do all the phoshpolipases cleave?

A
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15
Q

what is this? how is it changed from cholesterol?

A

cholesteorl ester

esterfied at carbon 3 to have a fatty acid (instead of OH)

more hypdrophobic

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16
Q

what is this? what is ti used in?

A

fatty acid synthase

Phosphopantetheine is’ linked’to’a’serine’ within’the’acyl carrier’ protein’(ACP)’portion’ of’FAS.

SH’group’reacts’with’ malonyl CoA to’form’a’ thioester bond.

17
Q

describe how what is needed for fatty acid synthesis is generated from pryuvate?

A
18
Q

how is NADPH needed for fatty acid syntheiss generated?

A
19
Q

describe the regulation of acetyl coa carboxylase

A

activation:

citrate polymerization

insulin stimulates the phopshatase to activate it

caloric intake/ACC transcription levels

inactivated by: glucagon/epinpehrine stimulates the phosphorylation of it

palmitoyl coa levels

amp

20
Q
A

steroid

21
Q

where do different places of alcohol degradation take place?

A

in cytosol of liver

  1. oxidation of ethanaol to acetaldehyde by alcohol dehydrogenase

in mitochondria

2. oxidation of a by acetylalhyde to acetate by acetaldhye dehydrogenase (both have 12 letters)

in muscle

  1. acetate converted to acetyl coa by acetyl coa synthase

for MEOS, alcohol is oxidaized to acetylaldehyde occurs in the ER

22
Q

what eznymes occur here?

A
23
Q

pathway of amino acids in the FED state?

A
  1. can bypass the liver, become proteins in other tissues
    LIVER
  2. make proteins, and nitrogen contianing compounds
  3. make glucose to be converted to glycogen in the liver
  4. excess can be made into triacylglycerols -> VDL
24
Q

what metabolic processes are decreased during STARVATION

A
  1. gluconeogenesis
  2. protein degradation
    * *3. production of urea**
  3. muscles using KB (goes to brain)
25
Q

metabolic changes during STARVATION
___ levels go up

A

ketone body, lactate

26
Q

describe nitrogen excretion levels from 12 hours after eating, and then over time in prolonged starvation

A

12 hours after you stop eating
nitrogenous products/urea goes way
up

but then DECREASES after a period of time (DAYS/WEEKS) it

27
Q

metaoblic effects of epinephrine

A

Epinephrine (Epi) stimulates glycogen breakdown in muscle and liver, gluconeogenesis in liver, and lipolysis in adipose tissue.

28
Q

metabolic effects of glucocorticoids

A

Glucocorticoids stimulate lipolysis in adipose tissue and the release of amino acids from muscle protein. In liver, glucocorticoids stimulate gluconeogenesis and (opposite to the effect of epinephrine) stimulate the synthesis of glycogen.

29
Q

metabolic changes in untreated type 1 diabetes?

A
  • Zero circulating insulin
  • Uninhibited, maximal (‘runaway’)

lipolysis in fat cells
• Maximal production of KB by liver
• KB production overwhelms KB removal

  • metabolism in extrahepatic tissues - excretion by kidneys
  • exhalation of acetone

• ↑ KB in blood, causing metabolic acidosis

30
Q

effects of insulin resistance on adipocytes?

A

dec

  1. RELEASE OF LIPOPROTEIN LIPASE (less TG storage)
  2. TG STORAGE
  3. GLUCOSE UPTAKE via glut4 transporters

inc

  1. lipolysis from fat stores
  2. cytokine release
31
Q

what causes DAG accumulation in obese pts? what does this cause?

A
  1. excessive caloric intake (increased lipid synthesis)
  2. defects in adipocyte metabolism
  3. defects in mitocondria function
  4. gene variation in APO c3
  5. reduced AMPK signaling

CAUSES:

  1. translocation of GLUT4 -> inhibiting insulin stimulated uptake of glucose
  2. glycogen synthase *