Page 268 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

P. 268

Abnormalities of Endocrinal Regulatory Circuit
Hormones are usually part of regulatory cir- Hormone release regulated by the hypothala-
cuits. Disorder of one element in such a circuit mus and pituitary. The plasma concentration
leads to characteristic changes in its other ele- of hormones that are under the influence of
ments. the hypothalamus and pituitary gland is al-
ways regulated (→ B1). Liberins (releasing hor-
Pituitary-independent release of hormones is mones), formed in the hypothalamus, cause
usually regulated by those parameters that the release of tropins in the pituitary. These
are influenced by the particular hormone, the stimulate the release of the respective hor-
latter acting on the target organs, whose func- mone in the periphery. The hormone and to
tions in turn lead to a reduction in the stimuli some extent also the effect produced by the
leading to hormone release (regulatory circuit hormone finally inhibit the release of liberins
with negative feedback). Insulin release serves in the hypothalamus and of tropins in the pi-
as an example (→ A1): raised plasma glucose tuitary. The example illustrates the regulation
concentration stimulates the release of insulin, of cortisol from the adrenal cortex.
the effect of which on the target organ, for ex- Reduced release of peripheral hormones
ample, the liver (increased glycolysis; inhi- may be due to a loss of function in the hypo-
Hormones tion), leads to a reduction in plasma glucose gland. The primary cause of an increased re-
thalamus, pituitary, or peripheral hormonal
bition of gluconeogenesis and glycogen forma-
lease of peripheral hormones can be an inade-
concentration.
If the insulin release is inappropriately high
(→ p. 257 A3) of liberins, tropins, or peripheral
9 for a given plasma glucose concentration (hy- quately high orthotopic or ectopic release
perinsulinism), this will lead to hypoglycemia. hormones.
In addition to an insulin-producing tumor, the If there is an increase in liberin release
cause may be an overlap of regulatory circuits, (→ B2), liberin, tropin, and peripheral hor-
in that some amino acids also stimulate insu- mone concentrations are raised.
lin release, and some of the insulin effects If there is a primary increase in tropin re-
(stimulation of protein synthesis, inhibition of lease, the concentrations of tropins and of the
proteolysis) can produce a reduction in the peripheral hormone will be raised, but that of
plasma concentration of amino acids. An ab- liberins reduced (→ B3).
normal breakdown of amino acids, for exam- If there is a primary rise in peripheral hor-
ple, one due to an enzyme defect, can trigger mone release, the release of liberins and tro-
hypoglycemia via a rise in amino acid concen- pins is suppressed (→ B4).
tration in the blood and subsequent stimula- In an analogous manner, a primary deficien-
tion of insulin release (→ A2). cy of liberins will lead to tropin and peripheral
If there is a defective hormonal gland hormone deficiency, while a primary lack of
(→ A3), the hormone level and thus the hor- tropins will result in a reduced release of pe-
monal effect is reduced. In the example illus- ripheral hormones, with increased release of
trated an insufficiency of the beta cells results liberins; a primary deficiency of peripheral
in hyperglycemia. hormones will lead to increased release of
In addition, when the responsiveness of the liberins and tropins.
target organs is reduced (→ A4), the hormonal
effect is decreased. In this way liver failure can
result in hyperglycemia, which in turn will
raise plasma insulin concentration. However,
the abnormal breakdown of amino acids in liv-
er failure can cause hypoglycemia through hy-
peraminoacidemia and by stimulating insulin
release (see above; → A2).
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