The endocrine system uses chemical messengers called hormones as a means of controlling the flow of information between the different tissues and organs of the body. It does not act alone, however, but interacts with the nervous system to coordinate and integrate the activity of body cells. Hormones regulate and integrate body functions. Hormones act on specific target cells, but they cause a variety of effects on tissues. Hormones do not transport other substances; hormones are transported and present in body fluids at all times. The endocrine system uses hormones released into the blood and transported throughout the body to influence the activity of body tissues. Tissue and organ responses to endocrine hormones tend to take much longer than the response to neurotransmitters, but once initiated, they tend to be much more prolonged than those induced by the nervous system. The glands of the endocrine system are widely scattered throughout the body.
Takes longer to respond to innervations but has prolonged actions when they arrive
Glands are widely scattered throughout the body
Responds to neurotransmitter molecules within milliseconds
Releases hormones into the blood that is transported throughout the body
Sends signals to neurons over a short distance to muscles
When hormones act locally on cells other than those that produced the hormone, the action is called paracrine. Paracrine action is not synonymous with autoregulation, and action on the same cells that produced the hormone is autocrine action.
Action on nearby target cells
Action on a distant target cell
Act locally on cells other than those that produce the hormone
Paracrine actions are hormonal interactions with local cells other than those that produce the hormone; autocrine actions are with self-cells (cells from which they were produced). Both autocrine and paracrine hormonal actions affect target cells. Neither paracrine nor autocrine actions affect cell storage.
Hormones can exert autocrine action on the cells from which they were produced. Retinoids are compounds with hormone-like actions. Juxtacrine action involves a chemical messenger imbedded in a plasma membrane that interacts with a specific receptor on a juxtaposed cell. Arachidonic acid is a precursor for eicosanoid compounds (similar to retinoids).
Hormones are divided into three categories according to their structures: amines and amino acids; polypeptides, proteins, and glycoproteins; and steroids. The amine and amino acid hormones include norepinephrine and epinephrine, which are derived from a single amino acid (i.e., tyrosine). The peptide, polypeptide, protein, and glycoprotein hormones can be as small as thyrotropin-releasing hormone (TRH), which contains three amino acids, and as large, and as large and complex as growth hormone (GH) and follicle-stimulating hormone (FSH). Steroid hormones, such as the glucocorticoids, are derivatives of cholesterol.
Peptides & Polypeptides
Amines and amino acids
Insulin is a peptide hormone; as such, its synthesis and release are vesicle mediated. Glucocorticoids (such as cortisol), androgens (such as testosterone), and estrogens are synthesized by non–vesicle-mediated pathways.
Glucocorticoids, androgens, estrogens, and mineralocorticoids (aldosterone is an example of a mineralocorticoid) are all hormones synthesized by non–vesicle-mediated pathways. Epinephrine and insulin are synthesized by vesicle-mediated pathways.
Some hormones, such as steroids and thyroid hormone, are bound to protein carriers for transportation to the target cell destination. The extent of carrier binding influences the rate at which hormones leave the blood and enter the cells. Cholesterol is a precursor for steroid hormone. Prohormones have an extra amino acid and are converted to hormones in the Golgi complex.
Continuous inactivation of secreted hormones is necessary to prevent accumulation that could disrupt the feedback mechanism. Increased secretion stimulates production of more receptor sites. Metabolic waste absorption is not a function of the endocrine system.
Free receptor sites
Absorb metabolic waste
Steroid hormones are bound to protein carriers for transport and are inactive in the bound state. Unbound adrenal and gonadal steroid hormones are conjugated in the liver, which renders them inactive, and then excreted in the bile or urine. Thyroid hormones also are transported by carrier molecules. The free hormone is rendered inactive by the removal of amino acids in the tissues, and the hormone is conjugated in the liver and eliminated in the bile. The catecholamine production is measured by some of their metabolites. In general, peptide hormones also have a short life span in the circulation. Their major mechanism of degradation is through binding to cell surface receptors, with subsequent uptake and degradation by peptide-splitting enzymes in the cell membrane or inside the cell.
Gonadal steroid hormones
Unbound adrenal hormones
Target cell response varies with the number and affinity of the relevant receptors. The number of hormone receptors on a cell may be altered for any of several reasons. Antibodies may destroy or block the receptor proteins. Increased or decreased hormone levels often induce changes in the activity of the genes that regulate receptor synthesis. For example, decreased hormone levels often produce an increase in receptor numbers by means of a process called up-regulation; this increases the sensitivity of the body to existing hormone levels. Likewise, sustained levels of excess hormone often bring about a decrease in receptor numbers by down-regulation, producing a decrease in hormone sensitivity.
A sustained excess hormone level brings about a decrease in receptor numbers.
It may take days to weeks before a hormone can react to target cells.
The role antibodies may have on receptor proteins.
How any given hormone can change its affinity to supply a need to all cells.
A decreased hormone level may produce increased receptor numbers.
cAMP is one of the most common second messengers, whose role is to generate an intracellular signal in response to cell surface receptor activation by a hormone. cAMP does not mediate hormone synthesis, act as a receptor itself, or inactivate hormones.
Acting as a high-affinity receptor on the surface of target cells
Acting as a second messenger to mediate hormone action on target cells
Inactivating hormones to prevent excess accumulation
Mediating hormone synthesis by non–vesicle-mediated pathways
Hormones that utilize nuclear receptors enter the target cell (i.e., cross the cell membrane) and bind to receptors in the cell nucleus that are gene regulatory proteins. These hormones do not selectively utilize second messengers, and they do not interact with surface receptors. They are not both lipid and water soluble.
Both lipid solubility and water solubility
The selective use of a second messenger
The ability to regulate surface receptor affinity
The ability to cross the cell membrane of target cells
The thiazolidinedione medications, which are used in the treatment of type 2 diabetes mellitus, act at the level of nuclear PPAR-gamma receptors to promote glucose uptake and utilization by adipose tissue cells. These drugs do not increase release of insulin from the pancreas, increase BMR, or promote weight loss.
Increase in basal metabolic rate
Stimulation of the beta cells in the pancreas
Weight loss by shrinking fat cells
The hypophysis (pituitary plus hypothalamus) and hypothalamus stimulatory hormones regulate the release and synthesis of anterior pituitary hormones. The levels of hormones such as insulin and antidiuretic hormone (ADH) are regulated by feedback mechanisms that monitor substances such as glucose (insulin) and water (ADH) in the body. The levels of many of the hormones are regulated by feedback mechanisms that involve the hypothalamic–pituitary–target cell system.
The cytokine–interleukin regulatory mechanism
The hypothalamic–pituitary–target cell system
Basal metabolic rate
The angiotensin I to angiotensin II to aldosterone system
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