Regulation and Integration of the Body
Te final sign,
, refers to excessive hunger and
food consumption, a sign that the person is “starving in the
land of plenty.” Although plenty of glucose is available, the
body cannot use it and consumes its fat and protein stores for
energy metabolism instead.
Table 16.4
summarizes the conse-
quences of insulin deficiency. DM is the focus of
A Closer Look
on pp. 624–625.
, or excessive insulin secretion, results in
low blood glucose levels, or
. Tis condition
triggers the release of hyperglycemic hormones, which cause
anxiety, nervousness, tremors, and weakness. Insufficient glu-
cose delivery to the brain causes disorientation, progressing to
convulsions, unconsciousness, and even death. In rare cases, hy-
perinsulinism results from an islet cell tumor. More commonly,
it is caused by an overdose of insulin and is easily treated by
ingesting sugar.
Check Your Understanding
You’ve just attended a football game with your friend,
Sharon, who is diabetic. While Sharon drank only one beer
during the game, she is having trouble walking straight, her
speech is slurred, and she is not making sense. What does
it mean when we say Sharon is diabetic? What is the most
likely explanation for Sharon’s current behavior? How could
you help her?
Diabetes mellitus and diabetes insipidus are both due to
lack of a hormone. Which hormone causes which? What
symptom do they have in common? What would you find in
the urine of a patient with one but not the other?
For answers, see Appendix H.
The Gonads and Placenta
Describe the functional roles of hormones of the testes,
ovaries, and placenta.
Te male and female
produce steroid sex hormones,
identical to those produced by adrenal cortical cells (see Fig-
ure 16.1). Te major distinction is the source and relative
amounts produced. As described earlier, gonadotropins regu-
late the release of gonadal hormones.
Te paired
are small, oval organs located in the female’s
abdominopelvic cavity. Besides producing ova, or eggs, the ova-
ries produce several hormones, most importantly
tĕ-rōn). Alone, the estrogens are responsi-
ble for maturation of the reproductive organs and the appearance
of the secondary sex characteristics of females at puberty. Acting
with progesterone, estrogens promote breast development and cy-
clic changes in the uterine mucosa (the menstrual cycle).
Te male
, located in an extra-abdominal skin pouch
called the scrotum, produce sperm and male sex hormones,
tĕ-rōn). During puberty, tes-
tosterone initiates the maturation of the male reproductive
organs and the appearance of secondary sex characteristics
and sex drive. In addition, testosterone is necessary for normal
sperm production and maintains the reproductive organs in
their mature functional state in adult males.
other nutrients, and blood levels of these substances drop, insu-
lin secretion is suppressed.
Other hormones also influence insulin release. For example,
any hyperglycemic hormone (such as glucagon, epinephrine,
growth hormone, thyroxine, or glucocorticoids) called into action
as blood glucose levels drop indirectly stimulates insulin release by
promoting glucose entry into the bloodstream. Somatostatin and
sympathetic nervous system activation depress insulin release.
As you can see, blood glucose levels represent a balance of
humoral, neural, and hormonal influences. Insulin is the major
hypoglycemic factor that counterbalances the many hypergly-
cemic hormones.
Homeostatic Imbalance
Diabetes mellitus (DM)
results from either hyposecretion or hy-
poactivity of insulin. When insulin is absent, the result is
type 1
diabetes mellitus
. If insulin is present, but its effects are deficient,
the result is
type 2 diabetes mellitus
. In either case, blood glucose
levels remain high a±er a meal because glucose is unable to enter
most tissue cells. Ordinarily, when blood glucose levels rise, hy-
perglycemic hormones are not released, but when hyperglycemia
becomes excessive, the person begins to feel nauseated, which
precipitates the fight-or-flight response. Tis response results,
inappropriately, in all the reactions that normally occur in the
hypoglycemic (fasting) state to make glucose available—that is,
glycogenolysis, lipolysis (breakdown of fat), and gluconeogenesis.
Consequently, high blood glucose levels soar even higher, and ex-
cess glucose begins to be lost from the body in urine (
When sugars cannot be used as cellular fuel, more fats are
mobilized, resulting in high fatty acid levels in the blood, a
condition called lipidemia. In severe cases of diabetes mellitus,
blood levels of fatty acids and their metabolites (acetoacetic
acid, acetone, and others) rise dramatically. Te fatty acid me-
tabolites, collectively called
tōnz) or
ketone bod-
, are organic acids. When they accumulate in the blood, the
blood pH drops, resulting in
, and ketone bodies
begin to spill into the urine (
Severe ketoacidosis is life threatening. Te nervous system
responds by initiating rapid deep breathing (hyperpnea) to blow
off carbon dioxide from the blood and increase blood pH. (We
will explain the physiological basis of this mechanism in Chap-
ter 22.) If untreated, ketoacidosis disrupts heart activity and
oxygen transport, and severe depression of the nervous system
leads to coma and death.
Te three cardinal signs of diabetes mellitus are polyuria,
polydipsia, and polyphagia. Excessive glucose in the blood leads
to excessive glucose in the kidney filtrate where it acts as an
osmotic diuretic (that is, it inhibits water reabsorption by the
kidney tubules), resulting in
, a huge urine output that
decreases blood volume and causes dehydration.
Serious electrolyte losses also occur as the body rids itself of
excess ketone bodies. Ketone bodies are negatively charged and
carry positive ions out with them, so sodium and potassium
ions are also lost. Te electrolyte imbalance leads to abdominal
pain and possibly vomiting, and the stress reaction spirals even
higher. Dehydration stimulates hypothalamic thirst centers,
, or excessive thirst.
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