Page 676 - Fundamentals of anatomy physiology

Insulin
Insulin is a peptide hormone released by beta cells when blood
glucose concentrations exceed normal levels (70–110 mg/dL).
Elevated levels of some amino acids, including arginine and
leucine, also stimulate secretion of insulin. This hormone af-
fects cellular metabolism in a series of steps that begins when
insulin binds to receptor proteins on the plasma membrane of
a target cell. Binding activates the receptor, which functions as
a kinase, attaching phosphate groups to intracellular enzymes.
These enzymes then produce primary and secondary effects
in the cell. The biochemical details of these effects remain
unresolved.
One of the most important effects is the enhancement of
glucose absorption and utilization. Insulin receptors are pres-
ent in most plasma membranes, and cells that have them are
called insulin dependent. However, cells in the brain and kidneys,
cells in the lining of the digestive tract, and red blood cells
lack insulin receptors. These cells are called insulin independent,
because they can absorb and utilize glucose without insulin
stimulation.
The effects of insulin on its target cells include the following:
Accelerating Glucose Uptake (All Target Cells). This effect re-
sults from an increase in the number of glucose transport
proteins in the plasma membrane. These proteins move
glucose into the cell by facilitated diffusion, which follows
the concentration gradient for glucose and does not
require ATP.
Accelerating Glucose Utilization (All Target Cells) and
Enhanced ATP Production. This effect occurs for two reasons:
(1) The rate of glucose use is proportional to its availability,
so when more glucose enters the cell, more is used.
(2) Second messengers activate a key enzyme involved in
the initial steps of glycolysis.
Stimulating Glycogen Formation (Skeletal Muscles and Liver
Cells). When excess glucose enters these cells, it is stored as
glycogen.
Stimulating Amino Acid Absorption and Protein Synthesis. This
helps to maintain glucose levels by preventing the conver-
sion of amino acids to glucose.
Stimulating Triglyceride Formation in Adipose Tissue. Insulin
stimulates the absorption of fatty acids and glycerol by
adipocytes, which store these components as triglycer-
ides. Adipocytes also increase their absorption of glucose,
and excess glucose is used in the synthesis of additional
triglycerides.
To summarize, the pancreas secretes insulin when glu-
cose is abundant. The hormone stimulates glucose utilization
to support growth and to build carbohydrate (glycogen) and
lipid (triglyceride) reserves. The accelerated use of glucose soon
brings circulating glucose levels within normal limits.
Chapter 18 The Endocrine System 663
&T i p s Tr i c k s
The function of insulin is to get glucose into cells.
Glucagon
When glucose concentrations decrease below normal, alpha
cells release glucagon to mobilize energy reserves. When gluca-
gon binds to a receptor in the target cell’s plasma membrane,
the hormone activates adenylate cyclase. As we have seen, cAMP
acts as a second messenger that activates cytoplasmic enzymes
(p. 640). The primary effects of glucagon are as follows:
Stimulating the Breakdown of Glycogen in Skeletal Muscle and
Liver Cells. The glucose molecules released are either me-
tabolized for energy (in skeletal muscle fibers) or released
into the bloodstream (by liver cells).
Stimulating the Breakdown of Triglycerides in Adipose Tissue.
The adipocytes then release the fatty acids into the blood-
stream for use by other tissues.
18 Stimulating the Production and Release of Glucose by the Liver.
Liver cells absorb amino acids from the bloodstream, con-
vert them to glucose, and release the glucose into the circu-
lation. This process of glucose synthesis in the liver is called
gluconeogenesis (gloo-ko. -ne. -o. -JEN-e-sis).
The results are a reduction in glucose use and the release of
more glucose into the bloodstream. Blood glucose concentra-
tions soon increase toward normal levels.
Pancreatic alpha cells and beta cells monitor blood glucose
concentrations, and they secrete glucagon and insulin without
endocrine or nervous instructions. Yet because the alpha cells
and beta cells are highly sensitive to changes in blood glucose
levels, any hormone that affects blood glucose concentrations
indirectly affects the production of both insulin and glucagon.
Autonomic activity also influences insulin production: Para-
sympathetic stimulation enhances insulin release, and sym-
pathetic stimulation inhibits it. Information about insulin,
glucagon, and other pancreatic hormones is summarized in
Table 18–5.
Diabetes Mellitus
Whether glucose is absorbed by the digestive tract or manu-
factured and released by the liver, very little glucose leaves the
body once it has entered the bloodstream. The kidneys reab-
sorb virtually all glucose, so glucose does not appear in the
urine. However, in diabetes mellitus, glucose accumulates in
the blood and urine as a result of faulty glucose metabolism.
Diabetes mellitus can be caused by genetic abnormalities,
and some of the genes responsible have been identified. Muta-
tions that result in inadequate insulin production, the synthesis
of abnormal insulin molecules, or the production of defective
receptor proteins produce comparable symptoms. Under these