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Biochem Quiz 4 Winter > Hepatic Function Questions > Flashcards

Hepatic Function Questions Flashcards

1
Q

What are 4 hepatic roles in glucose metabolism?

A

1: storage of glycogen
2: release of glucose to maintain blood glucose
3: conversion of other sugars to glucose
4: gluconeogenesis from other C sources

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2
Q

What causes fasting hypoglycemia?

A

due to failure to maintain blood glucose between meals

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3
Q

Why is the liver a so good at the storage of glycogen?
Is LV uptake of glucose governed by Insulin?
What is the significance of glucokinase as opposed to hexokinase?

A

hepatic cells can store more glycogen than any other cells
can do so because of high concentration of glucose - gets the glucose before anywhere else
uptake of glucose not regulated by insulin - have glut 2 and glut 3
insulin-dependent glut 4 everywhere else
glucokinase increases activity in response to high levels of glucose

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4
Q

adipose cells and glycogen

A

need a little bit to hydrolyze FA?

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5
Q

What is glycogenosis type I (von gierke’s disease)?
What is the cause?
What are the symptoms?
What is the treatment?

A

lack of glucose-6-phosphatase
get large liver (can store glycogen, but can’t break down liver)
fasting hypoglycemia, ketosis, hyperuricemia, hyperlipemia
give glucose between meals or raw starch which is digested slowly

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6
Q

What does galactose-1-phosphate uridyl transferase deficiency cause?
What are the symptoms?
What is the treatment?

A 
Classical Galactosemia
lactose not converted to glucose
large liver
failure to thrive
jaundice
don't consume milk
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7
Q

What enzymes are required for the epimerization of galactose to glucose?

A 
conversion of D-glucose to D-galactose
need galactokinase (galactose-1-phosphate) and galctose-1P uridyl transferase
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8
Q

What enzymes are needed for the epimerization of fructose?

A

need fructokinase and fru-1-P aldolase

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9
Q

What is the trouble with high amounts of fructose? What transporter is used in the intestines?
Why are high amounts of fructose toxic to the LV?

A

1: can give diarrhea because absorption of fructose through glut5 transporter not very effective
2: don’t want to inject IV fructose - toxic to liver - fructokinase very active - so turns all of it to fructose 1 phosphate - eventually run out of phosphate
Frutose 1-P aldolase is much slower than fructokinase, so F1P builds up causing fatty liver

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10
Q 
carnivorous meal causes what to happen?
Glucose levels?
Insulin levels?
glucagon levels?
cAMP levels?
Gluconeogenesis? Glycogen synthesis?
A

AA to glucose-6-phosphate to glycogen
and glucose
increase in insulin
increase in glucagon
+/- cAMPlarge increase in large supply in AA
can drive both gluconeogenesis and glycogen synthesis

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11
Q 
alcohol...
What effects on NAD/NADH?
hypo or hyperglycemia?
What is the enzyme that metabolizes alcohol?
Why?
A

hepatic oxidation of ethanol results in depletion of cytosolic NAD+
most common reason for hypoglycemia
liver oxidizes EtOH by alcohol dehydrogenase - uses NAD+
- gluconeogenesis from pyruvate requires NAD+, as does conversion of lactate to pyruvate

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12
Q

liver in nitrogen metabolism name six functions.

Slide 34 in hepatic 1

A

1: synthesis of urea
2: catabolism of excess dietary AA
3: conversion of extrahepatic AA carbons to glucose
4: N shuffling after a meal
5: oxidation of xanthine to hypoxanthine to uric acid
6: fine-tuned regulation of AA pools between meals

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13
Q

n- shuffling

A

after meal, n from excessive dietary AA used to make less excessive AA

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14
Q

ketogenic diets

A

can reduce seizures in children
don’t have to be starving to produce ketones
lipid-rich, carbohydrate deprived diests
rich in coconut oil (has medium-chain FA)

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15
Q

short and medium-chain FA

A

go directly to liver through portal vein
very efficient
mitochondria can pick up and bypass carnitine system

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16
Q

FA in hepatocytes

A

used as fuel
those not used esterified to TG and transfered through lumen to VLDLs and exported from liver
Come from adipocytes between meals
liver picks up 1/3 of FA and repackages as VLDL
converts to TG or ketone bodies because FA are detergents, so need to be in different form after meals lipogenesis liver can’t utilize TG

17
Q

where is lipoprotein lipase mostly found?

A

mostly in muscle, endothelial cells, and lactating mammary gland

18
Q 
control of lipogenesis
insulin?
glucagon?
low cAMP
long term regulation?
A

increased by insulin
decreased by glucagon
after carb-rich meal, excess glucose converted to FA by liver
in short term, low cAMP permits activation of glycolysis and AcCOA carboxylase
longer term regulation involves induction of synthesis of lipogenic enzymes by SREBP1c and glucose (CHREBP)

19
Q

ketogenesis in liver
Can the liver use ketones as fuel?
What compound is necessary to make ketones?

A

only hepatocytes can make ketones
but they can’t use them
need acetylacetate from glucose

20
Q

liver in desaturation of FA

A

double bonds are introduced in liver by desaturase

but liver can’t make essential FA (double bonds in the last 7C) - these must be obtained in diet

21
Q

role of liver in lipoprotein metabolism

A

synthesis of VLDL
degradation of Ch(mu) remnants
synthesis of apoA1 to nascent HDL
uptake of cholesterol from HDL2 (SR-B1) receptor
fatty liver may result from decreased VLDL export or excessive TG synthesis

22
Q

liver in de novo synthesis and degradation of choline

A

through VLDL, liver provides extrahepatic tissues not only cholesterol but also P-choline

23
Q

liver in de novo synthesis of cholesterol
What induces?
What decreases?

A

induced by SREBP-2

decreased by cholesterol uptake in ch(mu) remnants and by reuptake of LDL

24
Q

liver in biliary elimination of cholesterol and bile acids

A

much of cholesterol is eliminated (only way to get rid of it) most bile salts reabsorbed and reutilized

25
Q

what can be the causes of accumulation of TG in the liver?

A

1: increased supply of FA (from adipocytes, diet, or lipogenesis or decreased mitochondrial oxidation)
2: defective assembly of VLDL (liver intoxication, choline deficiency, severe protein deficiency in infants - kwashiorkor)

26
Q

What are substrates for gluconeogenesis during meals?

What are substrates during starvation?

A 
Meals: amino acids, glycerol, fructose, galactose
Starvation:
lactate from RBCs and muscle
glycerol from adipocytes
amino acids from skeletal muscle
27
Q

What is the most important regulatory step in glycolosis and gluconeogenesis?
What is the major regulator in the liver?

A

The interconversion of Frc-6-P and Frc-1,6-bP is the most important regulatory target in glycolysis/gluconegenesis.
In liver Frc 2,6-bP, a product of PFKII, is its major regulator.

28
Q

High F2,6BP leads to the conversion of…

Low F 2,6 BP leads to the conversion of…

A

High: F6P to F1,6P to glycolosis
Low: F1,6P to F6P to gluconeogenesis

29
Q

In the LV cAMP causes what to F2,6BP?

In the muscle, cAMP-dependent phosphorylation of PFK2 leads to what F 2,6BP?

A

decrease of F 2,6 BP and stimulation of gluconeogenesis

Increase of F 2,6 BP and stimulation of glycolosis

30
Q 
What are the effects of a carniverous meal on...
Insulin
Glucagon
cAMP
Amino Acids
A

All increase

cAMP goes both up and down

31
Q

Ketogenesis…
stimulated or inhibited by…
Insulin?
Glucagon?

A

inhibited by insulin

stimulated by glucagon

32
Q

What is the LV’s role in detoxification of hydrophobic compounds?

A

The liver expresses multiple conjugation enzyme systems that covalently attach undesirable fat-soluble substances (bilirubin, drugs, toxins, etc.) to water-soluble molecules (amino acids, glutathione, modified sugars, sulfate). The resulting conjugate is usually eliminated in the bile.

33
Q

Describe plasma bilirubin and fecal pigments in the case of jaundice…

1) Hemolytic
2) Hepatic
3) Hepatocellular
4) Obstructive

A 
1) indirect plasma bilirubin and increased fecal pigments
2 - 4) decreased fecal pigments
2) indirect plasma bilirubin
3) direct and indirect plasma bilirubin
4) direct plasma bilirubin.
34
Q

What are the causes of these jaundices…

1) Hemolytic
2) Hepatic
3) Hepatocellular
4) Obstructive

A

1 Intravascular hemolysis and/or excessive clearance of red cells by speen macrophages.
2 Inability of hepatocytes to take up or conjugate bilirubin.
3 Hepatocyte injury by virus or toxins results, in addition, to disruption of liver architecture or clogging of canaliculi.
4 Obstruction of bile flow may result from a biliary stone or pancreatic cancer.

35
Q

what is the LV role in SYNTHESIS AND DEGRADATION OF MOST CIRCULATING PLASMA PROTEINS.

A

Hepatocytes synthesize serum albumin, most globulins and the elements of the blood coagulation cascade
(Some plasma proteins however, originate elsewhere, notably immunoglobulins, protein hormones)
Hepatocytes are also the site of endocytosis and degradation of most plasma proteins (except albumin which is degraded in other tissues as well)

Biochem Quiz 4 Winter (6 decks)

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