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73 Cards in this Set

  • Front
  • Back
What are the main roles of a liver?
maintenance of blood glucose
biosynthesis/degradation of AA
production of urea (elimination of ammonia)
biosynthesis of blood plasma proteins
formation of bile acids from cholestrol
degradation of purines and pyrimidines
conjugation of bilirubin
storage of iron and BitB12
detoxification/inactivation of drugs, poisons, etc.
Which of these is not an liver function?

production of urea
storage of bilirubin
storage of iron and vitB12
maintenance of blood glucose
storage of bilirubin
What is the only form of energy for RBCs
What does the brain use for energy during fasting?
ketone bodies
What is the liver a master at?
regulating blood glucose levels
What energy sources can the brain not use?
long-chain fatty acids

Limited capacity to oxidize AA
How does glucose enter the portal system during the well fed state?
through absorption in the small intestines
During the well fed state, where does most of the glucose go?
it cirrculates to other tissues in the body (but some goes to the liver)
Glucose that goes to the liver during the well fed state is transformed into what?
pyruvate, CO2 and H20
used in the pentose phosphate pathway to produce NADPH (for biosynthesis of long-chain fatty acids for storage)
Where does the liver obtain most of its energy from during the well fed state?
oxidation of fatty acids (especially 10-12 carbons or less) and oxidation of excess AA
What is the by-product of the AA and fatty acids chains oxidations and what is the by-product used for?
ATP is the by-product

ATP is used to produce endogenous proteins for secretion and hepatic function
During the well fed state, what controls liver function?
During the well fed state, what process is inhibited and what is stimulated?
gluconeogensis is inhibited

Glycolysis is stimulated
What does glycolysis generate?
Produce cholesterol and fatty acid synthesis
After eating, what different process are occuring?
protein biosynthesis
What is considered early fasting state?
3-4hrs after eating
During the early fasting state, what is the concentration of glucose?
Is glucagon a catabolic or anabolic hormone?
What is the main source of blood glucose during early fasting?
hepatic glycogen
What are the two main storages for glycogen?
What is glycogen storages used for?
endogenous muscle metabolism
What is glycogenolysis?
releasing glycogen from liver and muscles
What is gluconeogensis?
making glucose from:
glycerol (from TGA) proprionate from beta-oxidation of fatty acids with odd number of Carbons
What are the AA that are used to make glucose?
What is the Cori Cycle?
Lactate from the muscles and RBC is converted into pyruvate----which is converted into glucose
What is the glucose alanine cycle?
In a transamination process an AA loses an amine group which allows it to be transported from the muscles to the liver---there it is converted back to pyruvate (to be used to make glucose)
Glycogen stores are depleted by 85% after how long?
1 day
In the later fasting state, what is the main source of glucose?
hepatic gluconeogensis
What is important about ketogenesis?
spares glucose for the brain (which can't use long chain FA)
Why can ketones be used by the brain, but FA can't?
Ketones are water soluble and can cross the BBB
Where are ketone bodies produced?
During early and late fasting, what are the processes that are occuring?
During the well fed state, is the liver lipogenic or lipolytic?
Can ketone bodies be formed from lipids?
How does a normal person store their chemical energy?
usually stored in fat rather than glycogen (150X as much)
During the early fasting state what process are occuring?
glycogen depletion
What process is curtailed during the later fasting state?
glycogenolysis (due to glycogen depletion)
Is the dependence of gluconeogenesis diminished with later fasting states?
it is somewhat diminished, but not eliminated.
What is Acetyl-CoA used to produce?
water-soluble ketones
Can the liver oxidize ketone bodies to use them?

Ketone bodies are used extrahepatically
Are lipids used in later fasting states?
lipolytic use of fats are more pronounced during later fasting states
Is liver protein biosynthetic?
What are the carbon skeletons from AA oxidation used for?
Where is alanine produced and where is it sent?
Alanine is produced in the muscles and transported into the liver
What is alanine transaminated with?
What is great about Ketogenesis?
it is glucose and protein sparing
Is acetyl-CoA gluconeogenic?
In relation to cholesterol, how does the liver react in a well fed state?
cholesterogenic (50% of cholesterol--the rest is formed in the gut or skin)
What is the immediate precursor to Cholesterol?
If ATP/ADP ratio is high, what will the citrate levels be like?
If there are high Citrate levels--what happens?
Citrate is transported to the cytosol and cleaved to acetyl-CoA and OAA
What is the enzyme that cleaves citrate?
ATP-citrate lyase
Where are primary bile acids formed?
liver and stored in the gallbladder
How do cholate and chenodeoxycholate differ from Cholesterol?
1.shortened side chain
2.additional OH group
3.Fully saturated (fused ring structure)
What do cholate and chenodeoxycholate do?
Acting as detergents, they convert cholesterol to be more polar.
How does cholate and chenodeoxycholate make cholesterol more polar?
solubilize cholesterol w/in the bladder

solubilize lipids to be degraded more efficiently by intestinal lipase
What happens if there is an deficiency in bile acid production?
decrease in bile acid causes an increase in cholesterol----results in gallstones and steatorrhea
How much bile acid is lost through feces/day?
0.5 grams
In Diabetes mellitus, Type I, what state is the body in?
catabolic state--even with elevated glucose
What will exacerbate the hyperglycemia?
1.hepatic gluconeogensis from lactate, AA and glycerol
2.hepatic conversion of glucose and AA to fat storage is depressed
3.insulin dependent glucose uptake is depressed
In Type I diabetes, does the body mobilize fat and if so, what does that result in?

Results in elevated ketone bodies which could lead to coma or death
Why is a pt with type I diabetes more likely to develop hypertriglyceridemia?
All the fat mobilizations can't all be converted to ketone bodies, so the excess FA is converted into TAGs and secreted by the liver as VLDLs

Insulin may induce LPL
Why is DM Type I more of a pan metabolic disorder?
because of its effects on fat and protein metabolism
Compared to Type I, what is the metabolic derangement of Type II DM?
It is not as severe as it is in the case of Type I
In Type II DM is there a lot of ketogenesis?
No, because the FA are not as extensively mobilized from adipocytes
Why would a pt with Type II DM develop hypertriglyceridemia
it is the result of increased FA biosynthesis and TAG formation
What does increased resistance to insulin also result in?
diminished biosynthesis of Lipoprotein lipase--which exacerbates hypertriglyceridemia
Type II DM frequently is due to what two conditions?
high insulin levels
pancreatic B-cell failure
What process is evident usually in obesity?
What are some problems with the liver and metabolism when dealing with an alcoholic?
TOO much NADH (not enough NAD+ to carry out other processes)
What processes in the liver require NAD+
1.lactate oxidation to pyruvate
2.gluconeogenesis from lactate
3. fatty acid B-oxidation
What conditions could result from too much alcohol?
1.fasting serum hypoglycemia
2.accumulation of hepatic TAGs (fatty liver)
3. lactic acidosis
What does aerobic exercise do?
1.switches to FA utilization when liver glycogen stores become depleted is like the fasting state, but ketone bodies do not increase as much.
3. hepatic gluconeogensis increases as glycogen decrease