Anatomy and Physiology - Introduction to Biomedical Engineering - page 128

LOW BLOOD
GLUCOSE

HIGH BLOOD
GLUCOSE

PANCREAS

GLUCAGON RELEASED BY
ALPHA CELLS OF PANCREAS

INSULIN RELEASED BY
BETA CELLS OF PANCREAS

LIVER RELEASES
GLUCOSE INTO BLOOD

FAT CELLS TAKE IN
GLUCOSE FROM BLOOD

ACHIEVE NORMAL
BLOOD GLUCOSE LEVELS
FIGURE 3.40 Two negative feedback mechanisms help control the level of glucose in the blood. When blood
glucose levels are higher than the body's set point (stimulus), beta cells (receptors) in the pancreatic islets produce
insulin (messenger), which facilitates glucose transport across plasma membranes and enhances the conversion of
glucose into glycogen for storage in the liver (effector). This causes the level of glucose in the blood to drop. When
the level equals the body's set point, the beta cells stop producing insulin. When blood glucose levels are lower
than the body's set point (stimulus), alpha cells (receptors) in the pancreatic islets produce glucagon (messenger),
which stimulates the liver (effector) to convert glycogen into glucose. This causes the level of glucose in the blood
to increase. When the level equals the body's set point, the alpha cells stop producing glucagon.

pancreas. When glucose levels are high, beta cells in the islets produce insulin, which
facilitates glucose transport across plasma membranes and into cells and enhances the
conversion of glucose into glycogen that is stored in the liver. During periods of fasting,
or whenever the concentration of blood glucose drops below normal (70-110 mg/dl),
alpha cells produce glucagon, which stimulates the liver to convert glycogen into glucose
and the formation of glucose from noncarbohydrate sources such as amino acids and
lactic acid. When glucose levels return to normal, the effector cells in the pancreatic islets
stop producing their respective hormone—that is, insulin or glucagon. Some biomedical