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Anterior pituitary

This illustration zooms in on the hypothalamus and the attached pituitary gland. The anterior pituitary is highlighted. Three neurosecretory cells are secreting hormones into a web-like network of arteries within the infundibulum. The artery net is labeled the primary capillary plexus of the hypophyseal portal system. The superior hypophysel artery enters the primary capillary plexus from outside of the infundibulum. The hypophyseal portal vein runs down from the primary capillary plexus, through the infundibulum, and connects to the secondary capillary plexus of the hypophyseal portal system. The secondary capillary plexus is located within the anterior pituitary. The hormones released from the neurosecretory cells of the hypothalamus travel through the primary capillary plexus, down the hypophyseal portal vein, and into the secondary capillary plexus. There, the hypothalamus hormones stimulate the anterior pituitary to release its hormones. The anterior pituitary hormones leave the primary capillary plexus from a single vein at the bottom of the anterior lobe.
The anterior pituitary manufactures seven hormones. The hypothalamus produces separate hormones that stimulate or inhibit hormone production in the anterior pituitary. Hormones from the hypothalamus reach the anterior pituitary via the hypophyseal portal system.

The anterior pituitary produces seven hormones. These are the growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), beta endorphin, and prolactin. Of the hormones of the anterior pituitary, TSH, ACTH, FSH, and LH are collectively referred to as tropic hormones (trope- = “turning”) because they turn on or off the function of other endocrine glands.

Growth hormone

The endocrine system regulates the growth of the human body, protein synthesis, and cellular replication. A major hormone involved in this process is growth hormone (GH)    , also called somatotropin—a protein hormone produced and secreted by the anterior pituitary gland. Its primary function is anabolic; it promotes protein synthesis and tissue building through direct and indirect mechanisms ( [link] ). GH levels are controlled by the release of GHRH and GHIH (also known as somatostatin) from the hypothalamus.

Hormonal regulation of growth

This flow chart illustrates the hormone cascade that stimulates human growth. In step 1, the hypothalamus releases growth hormone-releasing hormone (GHRH). GHRH travels into the primary capillary plexus of the anterior pituitary, where it stimulates the anterior pituitary to release growth hormone (GH). The release of growth hormone causes three types of effects. In the glucose-sparing effect, GH stimulates adipose cells to break down stored fat, fueling the growth effects (discussed next). The target cells for the glucose-sparing effects are adipose cells. In the growth effects, GH increases the uptake of amino acids from the blood and enhances cellular proliferation while also reducing apoptosis. The target cells for the growth effects are bone cells, muscle cells, nervous system cells, and immune system cells. In the diabetogenic effect, GH stimulates the liver to break down glycogen into glucose, fueling the growth effects. The liver also releases IGF in response to GH. The IGF further stimulates the growth effects but also negatively feeds back to the hypothalamus. When high IGF one levels are perceived by the hypothalamus, it releases growth hormone inhibiting hormone (GHIH). GHIH inhibits GH release by the anterior pituitary.
Growth hormone (GH) directly accelerates the rate of protein synthesis in skeletal muscle and bones. Insulin-like growth factor 1 (IGF-1) is activated by growth hormone and indirectly supports the formation of new proteins in muscle cells and bone.

A glucose-sparing effect occurs when GH stimulates lipolysis, or the breakdown of adipose tissue, releasing fatty acids into the blood. As a result, many tissues switch from glucose to fatty acids as their main energy source, which means that less glucose is taken up from the bloodstream.

GH also initiates the diabetogenic effect in which GH stimulates the liver to break down glycogen to glucose, which is then deposited into the blood. The name “diabetogenic” is derived from the similarity in elevated blood glucose levels observed between individuals with untreated diabetes mellitus and individuals experiencing GH excess. Blood glucose levels rise as the result of a combination of glucose-sparing and diabetogenic effects.

GH indirectly mediates growth and protein synthesis by triggering the liver and other tissues to produce a group of proteins called insulin-like growth factors (IGFs) . These proteins enhance cellular proliferation and inhibit apoptosis, or programmed cell death. IGFs stimulate cells to increase their uptake of amino acids from the blood for protein synthesis. Skeletal muscle and cartilage cells are particularly sensitive to stimulation from IGFs.

Dysfunction of the endocrine system’s control of growth can result in several disorders. For example, gigantism    is a disorder in children that is caused by the secretion of abnormally large amounts of GH, resulting in excessive growth. A similar condition in adults is acromegaly    , a disorder that results in the growth of bones in the face, hands, and feet in response to excessive levels of GH in individuals who have stopped growing. Abnormally low levels of GH in children can cause growth impairment—a disorder called pituitary dwarfism    (also known as growth hormone deficiency).

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Source:  OpenStax, Anatomy & Physiology. OpenStax CNX. Feb 04, 2016 Download for free at http://legacy.cnx.org/content/col11496/1.8
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