Function of Hormones
The physiologic
functions of hormones can be divided into three general areas: (1) growth and
differentiation, (2) maintenance of homeostasis, and (3) reproduction.
Growth
Multiple
hormones and nutritional factors mediate the complex phenomenon of growth.
Short stature may be caused by GH deficiency, hypothyroidism, Cushing’s
syndrome, precocious puberty, malnutrition, chronic illness, or genetic
abnormalities that affect the epiphyseal growth plates (e.g., FGFR3 or SHOX
mutations). Many factors (GH, IGF-I, TH) stimulate growth, whereas others (sex
steroids) lead to epiphyseal closure. Understanding these hormonal interactions
is important in the diagnosis and management of growth disorders. For example,
delaying exposure to high levels of sex steroids may enhance the efficacy of GH
treatment.
Maintenance
of Hormone
Though virtually all hormones affect
homeostasis, the most important among these are the following:
1. TH controls about 25% of basal metabolism in most tissues.
2. Cortisol exerts a permissive action for many hormones in addition to its own direct effects.
3. PTH regulates calcium and phosphorus levels.
4. Vasopressin regulates serum osmolality by controlling renal free-water clearance.
5. Mineralocorticoids control vascular volume and serum electrolyte (Na+, K+) concentrations.
6. Insulin maintains euglycemia in the fed and fasted states.
1. TH controls about 25% of basal metabolism in most tissues.
2. Cortisol exerts a permissive action for many hormones in addition to its own direct effects.
3. PTH regulates calcium and phosphorus levels.
4. Vasopressin regulates serum osmolality by controlling renal free-water clearance.
5. Mineralocorticoids control vascular volume and serum electrolyte (Na+, K+) concentrations.
6. Insulin maintains euglycemia in the fed and fasted states.
The defense
against hypoglycemia is an impressive example of integrated hormone action. In
response to the fasted state and falling blood glucose, insulin secretion is
suppressed, resulting in decreased glucose uptake and enhanced glycogenolysis,
lipolysis, proteolysis, and gluconeogenesis to mobilize fuel sources. If
hypoglycemia develops (usually from insulin administration or sulfonylureas),
an orchestrated counterregulatory response occurs glucagon and epinephrine
rapidly stimulate glycogenolysis and gluconeogenesis, whereas GH and cortisol
act over several hours to raise glucose levels and antagonize insulin action.
Although
free-water clearance is primarily controlled by vasopressin, cortisol and TH
are also important for facilitating renal tubular responses to vasopressin. PTH
and vitamin D function in an interdependent manner to control calcium
metabolism. PTH stimulates renal synthesis of 1,25-dihydroxyvitamin D, which
increases calcium absorption in the gastrointestinal tract and enhances PTH
action in bone. Increased calcium, along with vitamin D, feeds back to suppress
PTH, thereby maintaining calcium balance.
Depending on the
severity of a given stress and whether it is acute or chronic, multiple
endocrine and cytokine pathways are activated to mount an appropriate
physiologic response. In severe acute stress such as trauma or shock, the
sympathetic nervous system is activated and catecholamines are released,
leading to increased cardiac output and a primed musculoskeletal system.
Catecholamines also increase mean blood pressure and stimulate glucose
production. Multiple stress-induced pathways converge on the hypothalamus,
stimulating several hormones including vasopressin and corticotropin-releasing
hormone (CRH).These hormones, in addition to cytokines (tumor necrosis factor
α, IL-2, IL-6), increase ACTH and GH production. ACTH stimulates the adrenal
gland, increasing cortisol, which in turn helps to sustain blood pressure and
dampen the inflammatory response. Increased vasopressin acts to conserve free
water.
Reproduction
The stages of reproduction include
1) sex determination during fetal development;
2) sexual maturation during puberty;
3) conception, pregnancy, lactation, and child-rearing;
4) cessation of reproductive capability at menopause.
Each of these stages involves an orchestrated interplay of multiple hormones, a phenomenon well illustrated by the dynamic hormonal changes that occur during each 28-day menstrual cycle. In the early follicular phase, pulsatile secretion of LH and FSH stimulates the progressive maturation of the ovarian follicle. This results in gradually increasing estrogen and progesterone levels, leading to enhanced pituitary sensitivity to GnRH, which, when combined with accelerated GnRH secretion, triggers the LH surge and rupture of the mature follicle. Inhibin, a protein produced by the granulosa cells, enhances follicular growth and feeds back to the pituitary to selectively suppress FSH, without affecting LH. Growth factors such 9 as EGF and IGF-I modulate follicular responsiveness to gonadotropins. Vascular endothelial growth factor and prostaglandins play a role in follicle vascularization and rupture.
During
pregnancy, the increased production of prolactin, in combination with
placentally derived steroids (e.g., estrogen and progesterone), prepares the
breast for lactation. Estrogens induce the production of progesterone
receptors, allowing for increased responsiveness to progesterone. In addition
to these and other hormones involved in lactation, the nervous system and
oxytocin mediate the suckling response and milk release.
The stages of reproduction include
1) sex determination during fetal development;
2) sexual maturation during puberty;
3) conception, pregnancy, lactation, and child-rearing;
4) cessation of reproductive capability at menopause.
Each of these stages involves an orchestrated interplay of multiple hormones, a phenomenon well illustrated by the dynamic hormonal changes that occur during each 28-day menstrual cycle. In the early follicular phase, pulsatile secretion of LH and FSH stimulates the progressive maturation of the ovarian follicle. This results in gradually increasing estrogen and progesterone levels, leading to enhanced pituitary sensitivity to GnRH, which, when combined with accelerated GnRH secretion, triggers the LH surge and rupture of the mature follicle. Inhibin, a protein produced by the granulosa cells, enhances follicular growth and feeds back to the pituitary to selectively suppress FSH, without affecting LH. Growth factors such 9 as EGF and IGF-I modulate follicular responsiveness to gonadotropins. Vascular endothelial growth factor and prostaglandins play a role in follicle vascularization and rupture.

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