Unit 2- Lesson 3: Assisted Membrane Transport

Terms in this set (50)

A limited number of carrier binding sites are available within a particular plasma membrane for a specific substance. Therefore, there is a limit to the amount of a substance a carrier can transport across the membrane in a given time.

Transport Maximum: This limit is known as the transport maximum (Tm). Until the Tm is reached, the number of carrier binding sites occupied by a substance and, accordingly, the substance's rate of transport across the membrane are directly related to its concentration. The more of a substance available for transport, the more will be transported. When the Tm is reached, the carrier is saturated (all binding sites are occupied) and the rate of the substance's transport across the membrane is maximal. Further increases in the substance's concentration are not accompanied by corresponding increases in the rate of transport (G Figure 3-15, p. 70).
As an analogy, consider a ferry boat that can maximally carry 100 people across a river during one trip in an hour. If 25 people are on hand to board the ferry, 25 will be transported that hour. Doubling the number of people on hand to 50 will double the rate of transport to 50 people that hour. Such a direct relationship will exist between the number of people waiting to board (the concentration) and the rate of transport until the ferry is fully occupied (its Tm is reached). The ferry can maximally transport 100 people per hour. Even if 150 people are waiting to board, still only 100 will be transported per hour.

Saturation of carriers is a critical rate-limiting factor in the transport of 3 selected substances across the kidney membranes during urine formation and across the intestinal membranes during absorption of digested foods. Furthermore, it is sometimes possible to regulate (e.g., by hormones) the rate of carrier-mediated transport by varying the affinity (attraction) of the binding site for its passenger or by varying the number of binding sites. For example, the hormone insulin greatly increases the carrier-mediated transport of glucose into most cells of the body by promoting an increase in the number of glucose carriers in the cell's plasma membrane. Deficient insulin action (diabetes mellitus) drastically impairs the body's ability to take up and use glucose as the primary energy source.
The most notable example of facilitated diffusion is the transport of glucose into cells.

Glucose is in higher concentration in the blood than in the tissues. Fresh supplies of this nutrient are regularly added to the blood by eating and by using reserve energy stores in the body.
Simultaneously, the cells metabolize glucose almost as rapidly as it enters the cells from the blood.

As a result, a continuous gradient exists for net diffusion of glucose into the cells.
However, glucose cannot cross cell membranes on its own. Because it is polar, it is not lipid soluble and so is too large to fit through a channel. Without the glucose carrier molecules to facilitate membrane transport of glucose, the cells would be deprived of glucose, their preferred source of fuel.

The carrier-binding sites involved in facilitated diffusion can bind with their passenger molecules when exposed to either side of the membrane (G Figure 3-14). Passenger binding triggers the carrier to flip its conformation and drop off the passenger on the opposite side of the membrane. Because passengers are more likely to bind with the carrier on the high-concentration side than on the low-concentration side, the net movement always proceeds down the concentration gradient from higher to lower concentration. As is characteristic of mediated transport, the rate of facilitated diffusion is limited by saturation of the carrier binding sites, unlike the rate of simple diffusion, which is always directly proportional to the concentration gradient.