Liver + Gallbladder Flashcards
what is the sinusoid in a hepatic lobule and how does the blood move here
A single portal venule will drain into an area where terminal branch of hepatic arteriole divides and joings into a SINUSOID CAPILLARY BED (MIXING OF PORTAL + ARTERIAL BED blood) theres lots of kupferr cells (monocyte derived immune cells) blood then drains into central vein, then into the hepatic veins which drain into inferior vena cava..
where is bile made and by which cells
in the liver by CHOLANGIOCYTES (bile secreting cells)
what monomers are these made up of
1) sucrose
2) lactose
1) Sucrose = Fructose + Glucose
2) Lactose = Galactose + Glucose
simple definition of glycolysis
glycolysis= break down of glucose
simple definition of glycogenolysis
glycogenolysis= break down of glycogen
simple definition of gluconeogenesis
gluconeogenesis= creation of glucose
simple definition of glycogenesis
glycogenesis= creation of glycogen
what is the effect of insulin on the liver?
Effect of insulin on the liver
* Signals the fed state
* Promotes glycogen synthesis
* Suppresses gluconeogenesis
* Accelerates glycolysis
○ increase fatty acid synthesis
Counteracted by glucagon
difference between saturated and unsaturated fat/ fatty acid
Saturated fatty acids have hydrocarbon chains connected by single bonds only.
Unsaturated fatty acids have one or more double bonds.
Where are free fatty acids (FFA) made, also not all FFA made in liver– where else do we get fats from and where are they absorbed
The free fatty acids made in liver (FFA) made denovo in liver when theres lots of glucose. They form triglycerides and then can go out into the body in v low density lipoprotein (VLDL) particles. Often these particles have cholesterol in them- they’re a good way of delivering fat to rest of body where needed. Not all FFA made in the liver i.e. when we eat a fatty meal (in diet) fat will be abosrbed in spherical bodies called CHYLOMICRONS {Chylomicrons are large triglyceride-rich lipoproteins produced in enterocytes from dietary lipids—namely, fatty acids, and cholesterol}. These chylomicrons will come into the liver and spill out there content and go into liver’s FFA pool
explain insulin resistance (e.g. in type 2 diabetes)
→ Insulin resistance is when we have insulin but the liver, doesn’t listen to it. Whatever reasons (e.g. signalling pathways don’t work that well, receptors not phosphorylated as they should be) not correct response to insulin even tho u have lots of it. In type 2 u are not responding to insulin as if u are in the fed state. Because u are not able to manage glucose, this activates transcription factors which means u start making new lipids. Inappropriately, u are making new glucose and u are not making glycogen, u also are not suppressing lypolysis. You are getting more fat in liver= fatty liver aka STEATOTIC LIVER DISEASE
- Increased glucose (activates ChREBP)
- De novo lipogenesis (SREBP1)
- Activates PKCe (inhibits IR tyrosine kinase)
- Inappropriate gluconeogenesis
- FOXO1-mediated
- Impaired glycogen synthesis (muscle and liver)
- Akt2-mediated
- Impaired suppression of lipolysis in adipocytes
Glycerol and FFA
Fructose has been proven to have a role in steatotic (fatty) liver disease. Fructose is found in high fructose corn syrup. Explain how fructose leads to steatotic liver disease with reference to enyzme involved
Most enzymatic reactions, the product inhibits the enzyme. In FRUCTOKINASE enzyme the product does not turn it off i.e. it is a non limiting reaction, so no matter how much fructose u consume u don’t turn of fructokinase and therefore don’t turn off new lipid production which leads to fatty acid production in liver which leads to steatotic liver disease. Fructose also doesn’t turn off ur satiety centre like glucose does.
explain ketogenesis
Ketogenesis
→ is a metabolic pathway that produces ketone bodies, which provide an alternative form of energy for the body. The body is constantly producing small amounts of ketone bodies that can make 22 ATP each in normal circumstances, and it is regulated mainly by insulin
→ In absence of glucose (starvation)
* Switched off by insulin
→ Breakdown of lipids and proteins
→ Use of Acetyl CoA to produce ketone bodies
* Acetoacetate, D-β-Hydroxybutyrate
Turned back into Acetyl CoA in brain
so u can get energy without glucose intermediate
What happens if insulin is missing, how does this lead to ketoacidosis
What happens if insulin is missing?
=hyperglycaemia, u wont be able to turn off the break down of fats in adipose tissue (lypolisis) when lipids are broken down u get lots of acetyl CoA= ketones are made. If these ketones aren’t taken up by the brain and turned into acetyl CoA again these ketones can accumulate and form ketoacids and patients can develop KETOACIDOSIS
how many amino acids are there in the body. What do we mean by essential, non-essential and conditionally non-essential amino acids
20 amino acids in body
(9) essential amino acids are aa’s that humans cannot synthesize from metabolic intermediates
(4) non-essential amino acids are aa’s that humans can synthesize from metabolic intermediates
(7) conditionally essential amino acids are aa’s that are usually not essential, except in times of illness and stress
