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Flashcards in hepatic function 1 and 2 Deck (25)
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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


fasting hypoglycemia

due to failure to maintain blood glucose between meals


storage of glycogen

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
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?


glycogenosis type I (von gierke's disease)

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


galactose-1-phosphate uridyl transferase deficiency

lactose not reabsorbed
large liver
failure to thrive
don't consume milk


epimerization of galactose

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


epimerization of fructose

need fructokinase and fru-1-P aldolase



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

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



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

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

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


ketogenesis in liver

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

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


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

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)