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BECOM II Exam 4 > GI & Liver metabolism I&II > Flashcards

GI & Liver metabolism I&II Flashcards

1
Q

xenobiotics

A

taking things in from the outside that are not part of your everyday routine
-ex. drugs, poisons

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2
Q

how does acetyl CoA get into the cytosol?

A

binds to OAA –> convert to citrate –> enter cytosol and broken down by citrate lyase to OAA and acetyl CoA –> start making FAs

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3
Q

Acetyl CoA

A

2C units

contains CoA - made from vit. B5 (pantothenic acid)

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4
Q

ACC (acetyl CoA carboxylase)

A

rate limiting

  • starts FA synthesis
  • activated by energy and citrate –> adds CO2 to acetyl CoA to make malonyl CoA
  • deactivated by long chain FAs
  • AMP-kinase (low energy) turns off through phosphorylation
  • also short term regulation of TAG synthesis
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5
Q

biotin (vit. B7)

A

needed for most carboxylase enzymes

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6
Q

FA synthesis

A
  • add 2C additions (acetyl groups) with fatty acid synthase –> 16C product
  • anabolic process - requires reducing equivalents –> NADPH in cytosol
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7
Q

beta oxidation

A
  • FAs enter mitochondria through carnitine shuttle

- inhibit CPT1 with malonyl CoA –> prevent FAs from entering mitochondria

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8
Q

how do you make TAGs?

A

FAs are esterified to glycerol

  • liver - make glycerol3P from glycerol kinase or DHAP
  • adipocytes - make glycerol3P if it is well fed and running glycolysis; NO glycerol kinase
  • dehydration synthesis rxn
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9
Q

ChREBP (carbohydrate response element binding protein)

A

long term regulation of TAG synthesis

  • activated by carbs to transcribe genes that make FAs (ex. FA synthase or ACC)
  • inhibited by AMP & PKA
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10
Q

hormone sensitive lipase

A

breaks down (hydrolyzes) TAGs into free FAs and glycerol

  • free FAs transported in blood to tissue by albumin
  • glycerol goes to liver for gluconeogensis
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11
Q

how do you form ketone bodies?

A

2C acetyl groups –> 4C acetoacetate –> broken down into acetone or 3-hydroxybutyrate

  • increased in fasting, carb restrict diets, or starvation
  • production spares glucose
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12
Q

what happens if ketone body production is greater than use?

A

ketonuria or ketonemia

-can cause diabetic ketoacidosis –> pH can decrease

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13
Q

function of lipoproteins

A

transport fat throughout body

  • chylomicrons - least dense
  • HDL - most dense
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14
Q

how are most of the TAGs broken down?

A

pancreatic lipases

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15
Q

formation of bile salts

A

cholesterol –> 7alpha hydroxylase –> 7 hydroxycholesterol –> chenodeoxycholic acid or cholic acid

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16
Q

function of bile salts

A
  • interact with FAs to form micelles
  • emulsifying agents
  • increase water solubility through conjugation of glycine or taurine in liver
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17
Q

mutation in 7 alpha hydroxylase enzyme

A

bile acid/salt disorder

  • no bile salts –> no micelles –> poor fat absorption –> fatty stool
  • cannot form bile salts –> build up cholesterol –> gallstones
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18
Q

role of CCK

A
  • slow motility of stomach
  • increase pancreatic enzymes
  • GB contraction to release bile
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19
Q

role of secretin

A

-pancreatic release of bicarb to neutralize stomach acidity

20
Q

bile salt deficiency disorder

A

making cholesterol faster than being converted into bile salts
-take oral bile salts (chenodeoxycholic acid) for treatment

21
Q

what is needed for chylomicrons

A

ApoB48

  • cholesterol on the inside, PLs on the outside
  • TAG loading requires MTP to dock with ApoB48 or 100
  • deficient MTP –> abetalipoproteniemia
22
Q

role of lipoprotein lipase

A

found in the tissues

  • activated by ApoCII to release FAs from chylomicrons
  • FAs enter tissue
  • glycerol goes back to liver
23
Q

phase 1 liver detox rxn

A

fat soluble toxins

  • cytochrome p450 enzymes
  • try to make more water soluble
  • substrate for phase 2
24
Q

phase 2 liver detox rxn

A

water soluble toxins

  • conjugation pathway –> sulfation, glucoronidation, GSH
  • excreted as waste
25
Q

acetominophin toxicity

A

metabolized by CYTp450 enzymes –> glucoronidation and sulfation

  • detoxed by GSH
  • alcohol –> reduces GSH leading to toxicity
  • treat with n-acetylcystein (NAC) to boost GSH
26
Q

function of cholesterol

A
  • membrane fluidity
  • forms bile salts and vitamin D
  • precursor for steroids
  • come from diet or synthesis in liver –> synthesized in cytosol w/ a lot of reducing equivalents
  • 1/3 free in blood, 2/3 bound to lipoproteins (linoleic acid)
27
Q

cholesterol absorption

A
  • absorbed by intestinal micelles –> Niemann Pick C1
  • inhibited by ezetimibe to lower cholesterol
  • plant sterols excrete cholesterol in enterocytes
28
Q

where do all Carbons come from during cholesterol synthesis?

A

acetyl CoA

-HMG-CoA –> mevalonate by HMG-CoA reductase (rate limiting step)

29
Q

regulation of cholesterol synthesis

A

regulated by phosphorylation

  • AMP, glucagon, sterols –> inactivate HMG-CoA reductase
  • insulin, thyroid hormone, high ATP –> activate HMG-CoA reductase
30
Q

what is the 5C unit of cholesterol?

A

dimethylallyl pyrophosphate

-formed from mevalonate

31
Q

squalene synthase

A

catalyzes rxn from farnesyl pyrophosphate to squalene

-uses a lot of NADPH

32
Q

function of statins

A

mimic HMG-CoA substrate for HMG-CoA reductase enzyme –> competitive inhibitor
-transition state analog

33
Q

cholesterol and bile acids

A
  • cholesterol –> primary bile acids (more water soluble through hydroxylation) - emulsification
  • bacteria deconjugate primary to secondary
  • liver conjugates bile acids with glycine or taurine –> more water soluble and ionized
34
Q

ingested cholesterol transport from enterocyte

A

-taken up by chylomicrons (use ApoB48) –> lymphatics, thoracic duct, left subclavian

35
Q

cholesterol transport from liver

A

-taken up by VLDL and LDL (use Apo100)

36
Q

ApoB gene

A

makes ApoB48 and ApoB100

-deficiency –> abetalipoproteinemia

37
Q

nonalcoholic fatty liver disease (hepatic steatosis)

A

imbalance b/w hepatic TAG synthesis and VLDL secretion

38
Q

what shuttles cholesterol to liver or to peripheral tissues?

A

LDL

39
Q

role of cholesterol ester transfer protein (CETP)

A

takes TAG from VLDL to put on HDL with the exchange of cholesterol

  • VLDL forms LDL
  • do this bc HDL removes cholesterol from periphery (lowering risk for atherosclerosis)
40
Q

function of HDL

A

uses ApoA1 along with ApoC and ApoE

-reverse cholesterol transport –> take cholesterol from tissues back to liver

41
Q

LCAT

A

used to add ester to cholesterol to put it into chylomicron core - make more room on outside for more cholesterol binding
-activated by ApoA1 on HDL

42
Q

ABCA1 protein

A

used to help add cholesterol to HDL in the tissues

43
Q

function of bile salts and fiber on cholesterol

A

lowers absorption of cholesterol by binding to and excreting it

44
Q

phosphorylation

A

anabolic pathways –> turns off

catabolic pathways –> turns on

45
Q

how is cholesterol regulated

A

long term by sterol response element (SRE) and sterol response element binding protein (SREP) –> controls expression of HMG CoA reductase expression

BECOM II Exam 4 (10 decks)

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