branes of various body cells (including liver cells)have recep-
tors for apolipo protein-B. When the liver releases LDL particles
into the blood, cells with apolipoprotein-B receptors can rec-
ognize the LDL particles and bind them. Formation of such a
receptor-ligand combination stimulates the cell membrane to
indent and form a vesicle around the LDL particle. The vesicle
carries the LDL particle to a lysosome, where enzymes digest it
and release the cholesterol molecules for cellular use.
the particle, and slowly draw it inside the cell. The part of the
membrane surrounding the solid detaches from the cell’s sur-
face, forming a vesicle containing the particle
(f g. 3.30)
. Such
a vesicle may be several micrometers in diameter.
Usually, a lysosome joins a newly formed vesicle, and lys-
osomal digestive enzymes decompose the contents
(f g. 3.31)
The products of this decomposition may then diffuse out of
the lysosome and into the cytoplasm, where they may be used
as raw materials in metabolic processes. Exocytosis may expel
any remaining residue. In this way, phagocytic cells dispose of
foreign objects, such as dust particles; remove damaged cells
or cell parts that are no longer functional; or destroy disease-
causing microorganisms. Phagocytosis is an important line of
defense against infection.
Pinocytosis and phagocytosis engulf nonspeci± cally. In
contrast is the more discriminating
receptor-mediated endo-
which moves very specific types of particles into
the cell. This process involves protein molecules that extend
through the cell membrane and are exposed on its outer sur-
face. These proteins are receptors to which speci± c molecules
from the fl uid surroundings of the cell can bind. Molecules
that can bind to the receptor sites selectively enter the cell;
other types of molecules are left outside
(f g. 3.32)
. Molecules
that bind speci± cally to receptors are called
Entry of cholesterol molecules into cells illustrates receptor-
mediated endocytosis. Cholesterol molecules synthesized in
liver cells are packaged into large spherical particles called
density lipoproteins
(LDL). An LDL particle has a coating that
contains a binding protein called
The mem-
A cell may
take in a solid particle from its
surroundings by phagocytosis.
lysosome envelopes a vesicle
that contains a phagocytized
particle, its digestive enzymes
may destroy the particle. The
products of this intracellular
digestion diF
use into the
cytoplasm. Exocytosis may expel
any residue.
More than 25 million people in the United States take cholesterol-
lowering drugs called statins. The drugs inhibit an enzyme, HMG-CoA
reductase, which cells use to produce cholesterol—in addition to
cholesterol we eat. ²eedback is at play. When levels of the enzyme
drop with taking the drug, liver cells are stimulated to make more
LDL receptors. With statin use not only does the body make less cho-
lesterol, but the more abundant LDL receptors remove cholesterol
from the bloodstream more e³
ciently. Combined with a low-fat diet,
taking a statin powerfully lowers blood serum cholesterol.
The idea to limit cholesterol synthesis inside the body came from
studies of rare individuals with an inherited disease that prevents
their cells from making LDL receptors. Excess cholesterol is deposited
under the skin, appearing as yellowish lumps behind the knees. These
individuals die of heart disease before age 20. Japanese researchers
developed the ´
rst statin based on understanding the relationship
between HMG-CoA reductase and the number of LDL receptors. The
rst statin was approved in the United States in 1987. Today the more
than a dozen statin drugs diF
er by potency.
previous page 127 David Shier Hole's Human Anatomy and Physiology 2010 read online next page 129 David Shier Hole's Human Anatomy and Physiology 2010 read online Home Toggle text on/off