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Chapter 16
hormone. The
beta cells
(or B cells) are the source of insulin,
and the
alpha cells
(or A cells) of glucagon. There is at least
one other molecule—somatostatin—secreted by still other
islet cells called
delta cells
(or D cells). Pancreatic somatosta-
tin is the same peptide chemically as the hypothalamic soma-
tostatin, which controls growth hormone secretion from the
anterior pituitary. The physiological functions of pancreatic
somatostatin in humans are not fully established, but the pep-
tide is known to be capable of inhibiting the secretion of both
insulin and glucagon. Thus, it may act as a paracrine regula-
tor of pancreatic secretion of these two hormones, preventing
oversecretion of either.
Insulin
Insulin
—sometimes called the “storage hormone”—is the
most important controller of organic metabolism. Its secre-
tion, and thus its plasma concentration, is increased during
the absorptive state and decreased during the postabsorptive
state.
The metabolic effects of insulin are exerted mainly on
muscle cells (both cardiac and skeletal), adipose tissue cells,
and liver cells.
Figure 16–4
summarizes the most important
responses of these target cells. Compare the top portion of
this fi gure to Figure 16–1 and to the left panel of Figure 16–3
and you will see that the responses to an increase in insulin
are the same as the events of the absorptive-state pattern.
Conversely, the effects of a reduction in plasma insulin are
the same as the events of the postabsorptive pattern in Figure
16–2 and the right panel of Figure 16–3. The reason for these
correspondences is that an increased plasma concentration of
insulin is the major cause of the absorptive-state events, and a
decreased plasma concentration of insulin is the major cause
of the postabsorptive events.
Like all peptide hormones, insulin induces its effects by
binding to specifi c receptors on the plasma membranes of its
target cells. This binding triggers signal transduction pathways
that infl uence the plasma membrane transport proteins and
intracellular enzymes of the target cell. For example, in muscle
cells and adipose tissue cells, an increased insulin concentration
stimulates cytoplasmic vesicles that contain a particular type of
glucose transporter (GLUT-4) in their membrane to fuse with
the plasma membrane (
Figure 16–5
). The increased number
of plasma membrane glucose transporters resulting from this
fusion then causes a greater rate of glucose movement from the
extracellular fl
uid into the cells by facilitated diffusion. Recall
from Chapter 4 that glucose enters virtually all body cells by
facilitated diffusion. There are multiple subtypes of glucose
transporters that mediate this process, however, and the sub-
type GLUT-4, which is regulated by insulin, is found mainly
in muscle and adipose tissue cells. Of great signifi cance is that
the cells of the brain express a different subtype of GLUT,
one that has very high affi nity for glucose and whose activ-
ity is not insulin-dependent. This ensures that even if plasma
insulin levels are very low, as in prolonged fasting, cells of the
brain can continue to transport glucose from the blood and
maintain CNS function.
A description of the many enzymes whose activities
and/or concentrations are infl uenced by insulin is beyond the
(a)
(b)
Adipocytes
Glucose uptake and utilization
Net triglyceride synthesis
Liver
Glucose uptake
Net glycogen synthesis
Net triglyceride synthesis
No ketone synthesis
Muscle
Glucose uptake and utilization
Net glycogen synthesis
Net amino acid uptake
Net protein synthesis
Plasma insulin
Adipocytes
Glucose uptake and utilization
Net triglyceride catabolism and
release of glycerol and
fatty acids
Liver
Glucose release due to net
glycogen catabolism and
gluconeogenesis
Ketone synthesis and release
Muscle
Glucose uptake and utilization
Net glycogen catabolism
Net protein catabolism
Net amino acid release
Fatty acid uptake and utilization
Plasma insulin
Figure 16–4
Summary of overall target-cell responses to (a) an increase or (b) a decrease in the plasma concentration of insulin. The responses in (a) are
virtually identical to the absorptive state events of Figure 16–1 and the left panel of Figure 16–3; the responses in (b) are virtually identical to
the postabsorptive state events of Figure 16–2 and the right panel of Figure 16–3.
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