Hepatic Function Questions Flashcards
What are 4 hepatic roles in glucose metabolism?
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
What causes fasting hypoglycemia?
due to failure to maintain blood glucose between meals
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?
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
adipose cells and glycogen
need a little bit to hydrolyze FA?
What is glycogenosis type I (von gierke’s disease)?
What is the cause?
What are the symptoms?
What is the treatment?
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
What does galactose-1-phosphate uridyl transferase deficiency cause?
What are the symptoms?
What is the treatment?
Classical Galactosemia lactose not converted to glucose large liver failure to thrive jaundice don't consume milk
What enzymes are required for the epimerization of galactose to glucose?
conversion of D-glucose to D-galactose need galactokinase (galactose-1-phosphate) and galctose-1P uridyl transferase
What enzymes are needed for the epimerization of fructose?
need fructokinase and fru-1-P aldolase
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?
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
carnivorous meal causes what to happen? Glucose levels? Insulin levels? glucagon levels? cAMP levels? Gluconeogenesis? Glycogen synthesis?
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
alcohol... What effects on NAD/NADH? hypo or hyperglycemia? What is the enzyme that metabolizes alcohol? Why?
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
liver in nitrogen metabolism name six functions.
Slide 34 in hepatic 1
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
n- shuffling
after meal, n from excessive dietary AA used to make less excessive AA
ketogenic diets
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)
short and medium-chain FA
go directly to liver through portal vein
very efficient
mitochondria can pick up and bypass carnitine system
FA in hepatocytes
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
where is lipoprotein lipase mostly found?
mostly in muscle, endothelial cells, and lactating mammary gland
control of lipogenesis insulin? glucagon? low cAMP long term regulation?
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)
ketogenesis in liver
Can the liver use ketones as fuel?
What compound is necessary to make ketones?
only hepatocytes can make ketones
but they can’t use them
need acetylacetate from glucose
liver in desaturation of FA
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
role of liver in lipoprotein metabolism
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
liver in de novo synthesis and degradation of choline
through VLDL, liver provides extrahepatic tissues not only cholesterol but also P-choline
liver in de novo synthesis of cholesterol
What induces?
What decreases?
induced by SREBP-2
decreased by cholesterol uptake in ch(mu) remnants and by reuptake of LDL
liver in biliary elimination of cholesterol and bile acids
much of cholesterol is eliminated (only way to get rid of it) most bile salts reabsorbed and reutilized
