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Flashcards in Membrane Carriers Deck (23):

What is a carrier vs a channel? How do they compare in size / speed?

Carrier - bind the solutes and moves via conformation change - slower than channel, especially when not using facilitated diffusion

Channel: Allow diffusion, do not undergo conformational change, much faster


How is it useful that carriers are reversible?

They can go both directions, although they normally go one direction under physiological conditions. Coupled carriers can utilize energy to push against gradients and create electrochemical gradients


What is competitive vs non-competitive inhibition?

Competitive - chemically related solute competes for active site
Non-competitive inhibition - ligand binds to a separate part of site but is not transported


How can the transport of carriers be described?

In terms of enzyme kinetics. They have high temperature coefficients (act faster every 10 degrees Q10). Described by Michaelis-Menten Kinetics


What is active vs passive transport?

Active - utilizes energy, either ATP or electrochemical gradient, to move solute

Passive - driving force is difference in electrochemical potential of transported species. Cannot create or maintain a concentration gradient with this (used for polar + charged solutes)


What type of carrier is the GLUT? How can it be described?

D-glucose carrier - facilitated diffusion (passive transport)

Net flux driven by desire to equilibrate glucose across cellular compartments. The transporter allows diffusion much faster than simple diffusion.

Transport described by simple Michaelis-Menten kinetics


What is Km? What does it measure?

The concentration of substrate for which an enzyme works at 1/2 Vmax. It measures affinity.


Why is facilitated diffusion hyperbolic, and simple diffusion linear?

Simple diffusion - only a function of extracellular glucose concentration

Facilitated diffusion - a function of carrier affinity as well as extracellular glucose concentration


What is the simple enzyme kinetics equation?

v = (Vmax) / (1 + (Km / C))

C = concentration of substrate
Km = concentration of substrate for 1/2 Vmax
v = rate of unidirectional influx


Why do GLUT2 transporters in the liver have a higher Km than GLUT4 transporters in skeletal muscle / adipose?

Because you want to keep liver D-glucose carriers sensitive until higher glucose levels. If you want more uptake of glucose in other tissues, simply increase the absolute number of carriers at the cell surface.


What is primary active transport vs secondary active transport?

Primary - Expend ATP to directly move something / create a gradient
Secondary - Use electrochemical gradient created from ATP expenditure to symport / antiport a solute against its concentration gradient


What is the normal stoichiometry for Na,K-ATPase?

3 Na+ out
2 K+ in


What is the pump / leak model?

Metabolic energy used to create ion gradients. Energy is stored in gradients. Energy leaks out when it is utilize for active transport of other solutes.

I.e. co-transport of Na+ and amino acids
Na+/H+ exchanger to regulate pH
Regulation of Ca+2 via Na+/Ca+2 exchanger


What are the subunits of the Na,K-ATPase and why is this important?

Beta-subunit stabilizes alpha subunit
Alpha subunit binds the ions, has the ATPase, and binds digitalis (cardiac glycoside)

There are 4 isoforms of alpha and 3 of beta, so many types of these carriers


What is the function of digitalis, and why does hypokalemia increase its toxicity?

Medicine given in heart failure which partially inhibits Na+,K+ATPase by binding E2 confirmation, competing with K+. It decreases the Na+ gradient, allowing less Ca+2 to be pumped out, increasing the amount of muscle contraction

Hypokalemia is bad when using digitalis because there is not enough competition by K+ at the E2 site, making it dangerous.


What are PMCA and SERCA?

PMCA - Ca-ATPase in plasma membrane
SERCA - Ca-ATPase in endoplasmic reticulum

Keep ICF Calcium 10^4 lower than ECF


What are the two types of secondary active transport?

1. Cotransport - symport
2. Exchange - antiport


Where is the Na+/glucose transporter and what is it an example of?

Transporter on apical surface of enterocytes. It is secondary active transport via a symporter.

Na+ moves into the cell with glucose, which is moving up its concentration gradient. Glucose is high in the cell and freely diffuses down its concentration gradient at the basal surface.


How does SGLT1 differ from SGLT2/3?

SGLT1 can move glucose up a bigger gradient since it expends two Na+ to cotransport glucose, rather than 1


Assuming the absolute ratios of the chemical gradient where the same for sodium and glucose, why does the Na+/glucose symporter still function?

The cell has a negative membrane potential inside of about -60 mV. This creates an electrical affinity for Na+ at as well which accounts for the 10x difference.


How does the Ca+2/Na+ exchanger (NCX) work? How does this differ in action potential.

At normal resting membrane potential (~-50- -80mV), it pumps 3 Na+ in while pumping out 1 Ca+2.

However, during action potential, the energy of the calcium gradient becomes greater since the membrane potential is less negative, and it is more favorable to move positive charges out. This results in a calcium influx into the cell with Na+ pumped out.


How does each additional sodium pumped in contribute to the favorability of the gradient?

Since it is exponential, the 10-fold sodium gradient is cubed, accounting for a 1000 fold gradient supported by the chemical gradient alone. Multiply this by 10 because when 3 are pumped in, the charge also increases slightly. This accounts for 10x more

10*1000 = 10,000, which is the 10^4 calcium gradient which is supported.


Why does digitalis work so effectively?

Since the Ca+2/Na+ exchanger is reversible, only a small decrease in the sodium gradient leads for the Ca+2 to start flowing back into the heart muscle.

Digitalis destroys the outward pumping of sodium by the Na+/K+ ATPase