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Why is the structure of a biological membrane often described in the fluid mosaic model? Which components of the membranes can be used to modulate the fluidity of the membranes?

The fluid mosaic describes that phospholipids generate the membrane and that phospholipids and the embedded proteins can move laterally in the phospholipid bilayer.

The fatty acid composition of membrane lipids determines in general the fluidity of the membrane. In the plasma membrane, the fluidity is in addition regulated by cholesterol.

[cholesterol is mainly found in the plasma membrane, the fluidity of the other intracellular membranes is mainly regulated by fatty acid composition.]


What is a glycocalyx? Is it outside or inside of the plasma membrane?

The glycocalyx consists of sugar residues found in glycolipids and in glycoproteins. It is outside of the plasma membrane and provides a network-shield and can also be involved with cell-cell recognition.


Describe in general the lipid composition in the plasma membrane of the liver! Is the plasma membrane different regarding the outer leaflet and the inner leaflet?

The plasma membrane contains mainly the glycerophospholipids PC and PE.
The outer leaflet contains mainly PC and spingomyelin.
The inner leaflet contains mainly PE and some PS and PI.
Cholesterol is found in both leaflets.


Compare in particular the amounts of cholesterol, sphingomyelin and cardiolipin in different membranes to each other!

The plasma membrane contains cholesterol and sphingomyelin, which are mostly
absent in mitochondria.
The inner mitochondrial membrane contains cardiolipin, which is not found in
remarkable amounts in the plasma membrane in humans.


How does cholesterol affect the fluidity of the plasma membrane? Does cholesterol increase the fluidity close to the polar head groups of the phospholipids plasma membrane? Explain!

Cholesterol decreases the fluidity close to the polar head groups of
the phospholipids plasma membrane due to its steroid ring system.

But cholesterol increases the fluidity of the bilayer in the middle of the plama membrane inside, where the fatty acids determine the fluidity and cholesterol contains its hydrocarbon tail.

Cholesterol achieves to increase the fluidity in that part of the bilayer, due to the fact at it separates the phospholipids and leads to more space between the fatty acyl-groups.


How does cholesterol stabilize the membrane at changing temperatures? How do fatty acids change at different temperatures?

Changed temperatures affect mainly the fluidity of the fatty acids in the plasma membrane as the melting points of fatty acids has a large variety. Cholesterol in the membrane has a buffering effect in order to keep the fluidity in the necessary range.

The fatty acid composition of the plasma membrane is carefully arranged and even allows areas with different parts with different fluidity.

You don’t want large membrane fluidity changes due to abnormal temperature changes which can happen for example during fever or extreme cold temperatures.

At increasing temperatures, the fatty acid residues get more fluid. In this case,
cholesterol can reduce the fluidity and stabilize the membrane.

At decreasing temperatures, the fatty acid residues get more rigid. In this case, cholesterol can increase the fluidity and stabilize the membrane.


Which polyunsaturated fatty acid is more fluid, linoleic acid or arachidonic acid?

Linoleic acid has 18 carbons and two double bonds.
Arachidonic acid has 20 carbons and four double bonds.

Increase of carbon number increases the melting point and double bonds
decrease the melting point.

Even at more carbons with 20 carbons, arachidonic acid is more fluid than linoleic
acid due to its four double bonds.

[Just a reminder, humans can form arachidonic acid from linoleic acid. A fatty acid can be elongated at the carboxyl end and double bonds can be introduced forming 9 or they can be formed between 9 and the carboxyl end.]


The transport through the phospholipid membrane can be described as passive transport or active transport. Related to passive transport, does simple diffusion or does facilitated diffusion involve a transport protein? How is the direction of facilitated diffusion determined?

Simple diffusion does not involve a transport protein, it just needs a concentration gradient that allows certain molecules to move through membranes with the gradient.

Facilitated diffusion needs a specific transport protein. The movement is saturable
and one can measure the maximal transport and the concentration of the
transported molecule at half maximal transport [for enzyme kinetics, maximal
product formation was measured]

The direction of facilitated diffusion depends on the concentration of the
transported molecule. The specific transporter protein allows transport into the
cell or transport to the outside of the cell.


The facilitated transport of glucose uses different transporters (GLUT).
Which GLUTs transport efficiently glucose at normal blood glucose levels? Which of the GLUTs can transport large quantities of glucose?

GLUT-1 and GLUT-3 are efficient glucose transporters at normal blood glucose levels, and they are found for example in RBC and brain, and in neurons, respectively.

GLUT-2 in the intestinal mucosal cell towards the portal vein, can transport large quantities of glucose and it transports also galactose and fructose.

GLUT-2 is also found in the hepatocyte membrane.

GLUT-2 is also found in the kidney for reuptake of glucose.
It is also found in the -cells of pancreas in order to “measure” the glucose concentration in the blood.


Describe the concept of facilitated transport using the glucose transporter GLUT-2 in the liver as example. What role has the concentration of glucose?

Facilitated transport using a GLUT uses the concept that the glucose transfers a membrane using a specific transport protein in facilitated transport but can only flow with the concentration gradient from the higher
glucose concentration to a lower glucose concentration.

GLUT-2 has a high maximal transport with low affinity for glucose, and it can transport large quantities of glucose.
The concentration of glucose is very important, and at high glucose concentration in the blood, the glucose will enter the liver cell facilitated by GLUT-2.

On the other hand, under conditions of low blood glucose levels, the liver performs the pathways of gluconeogenesis and glycogen degradation and generates free glucose is in high concentration inside the hepatocyte. The generated glucose can now leave the cell via the same transporter GLUT-2 into the blood.


Compare GLUT-1, GLUT-2, GLUT-3, GLUT-4 and GLUT-5 to each other. Which are high affinity transporters and which are low affinity transporters? Which GLUT is insulin-dependent, which one transports mainly fructose?

The high affinity GLUT transporters are GLUT-1, GLUT-3 and GLUT-4.
The low affinity GLUT transporters are GLTU-2 and GLUT-5.

The insulin-dependent GLUT is GLUT-4. This transporter is normally stored
inside of in fat cell and muscle cells, and insulin leads to the recruitment and
positioning of GLUT-4 into the plasma membrane of responding cells.
In diabetic patients that can be a problem.

The GLUT that transports mainly fructose is GLUT-5. This transporter is found to the outside of the intestinal mucosal cells in order to transport dietary fructose.

GLUT-5 is also found in testes in seminal vesicle cells and facilitate the release of fructose into the seminal fluid.

[Sperm cells use fructose as major sugar energy source. Seminal vesicle cells use blood glucose to synthesize eventually fructose. Dietary fructose is mainly metabolized in the liver and is normally not much available in blood.]


After discussing passive transport, let’s continue with active transport. How can one describe the primary active transport performed by Na+/K+-ATPase? What is actively pumped out of the cell and what is pumped into the cell? Why is this named primary active transport?

Na+/K+-ATPase is an enzyme and transporter involved with the transport of three sodium ions out of the cell and at the same time the transport of two potassium ions into the cell.

For this coupled process, each time, one ATP is cleaved.

This is considered as primary active transport as the molecules are pumped against a concentration gradient, and this needs each time ATP cleavage


Describe the concept of secondary active transport into cells! Why is this transport also named co-transport and what are the conditions for this to happen?

Secondary active transport has the concept that a specific transport is coupled to a primary active transport system.

The secondary transport needs a transporter that participates in the co-transport of the ions used by the primary active transporter. The gradient of this ion concentration is used to transport another molecule into the cell.

Secondary active transport can take place with a co-transport of sodium ions, when at the same time Na+/K+ -ATPase is active inside the cell.


Is SGLT a transporter that performs facilitated passive transport, primary active transport or secondary active transport? What is transported into the intestinal mucosal cell by SGLT in addition to glucose or galactose, respectively?

SGLT is a transporter involved with secondary active transport.

SGLT 1 transports two sodium ions together with one dietary glucose into the intestinal mucosal cells. SGLT 1 can also transport two sodium ions together with one dietary galactose into the intestinal mucosal cells.

In both cases, a sodium ion gradient is formed by Na+/K+-ATPase.


Which transporter is used for the release of glucose, galactose and fructose from the intestinal cells into the portal vein? What is the concept, and is this performed by facilitated transport or by secondary active transport?

The release of glucose, galactose and fructose from the intestinal cells into the
portal vein is performed by GLUT-2.

This glucose transporter can handle large amounts of monosaccharides, and with that it is perfect to facilitate the transport of dietary monosaccharides from intestinal mucosal cells into the portal vein.

This transport is performed by facilitated transport, which uses a transporter protein (GLUT-2) and follows the gradient of the monosaccharide concentrations.

[As the concentration in the intestinal mucosal cells is high after uptake of dietary monosaccharides, the concentration gradient allows the sugars to use GLUT-2 in order to move into the portal vein.]


In addition to glucose and galactose uptake from the intestinal lumen, which other molecules from a different food group are taken up by a respective sodium ion co-transport?

Dietary amino acids are taken up using sodium ion co-transport. They use several
transporters that are specific for different groups of amino acids.


The transport via a gated channel is mostly grouped as passive transport, although cleavage of some ATP is involved. How can you describe the role of ABC transporters?

An ABC transporter contains ATP-binding cassettes and are often channel proteins which do not need continuous ATP cleavage.

Some ATP is cleaved in order to open the channel, and then many
molecules flow through the open channel with the concentration gradient.


Which gated channel is deficient in cystic fibrosis, and which ion normally flows through this channel? What is the abbreviation for this channel? How is this channel gated and which enzyme is needed to eventually open it?

Cystic fibrosis is due to a deficiency of a specific chloride ion channel in
epithelial cells. This channel is named CFTR which stands for cystic fibrosis
transmembrane conductance regulator.

CFTR is an ABC transporter and is a ligand-gated channel controlled by
phosphorylation performed by protein kinase A


Why is the mucus in patients with cystic fibrosis thick in the intestine and in the lung?

The defective CFTR does not allow the accumulated chloride ions to be released by epithelial cells. This leads to less efflux of water as well.

That leads also to less sodium ions that enter the extra cellular space, and as a result, water does not follow and we find thick mucus.


Why can the sweat test be used to diagnose cystic fibrosis?

In sweat glands, a defective CFTR leads to impaired re-uptake of chloride ions.
Sodium ions get trapped by ionic bonds, and that is why children with cystic
fibrosis often have a salty skin on their forehead.