From Wikipedia, the free encyclopedia
Endocrine hormone molecules are secreted (released) directly into the bloodstream, whereas exocrine hormones (or ectohormones) are secreted directly into a duct, and, from the duct, they flow either into the bloodstream or from cell to cell by diffusion in a process known as paracrine signalling.
Recently it has been found that a variety of exogenous modern chemical compounds have hormone-like effects on both humans and wildlife. Their interference with the synthesis, secretion, transport, binding, action, or elimination of natural hormones in the body are responsible of homeostasis, reproduction, development, and/or behavioural changes sameway as the endogenous produced hormones."[1]
Hormones as a signal
Hormonal signaling involves the following:[citation needed]- Biosynthesis of a particular hormone in a particular tissue
- Storage and secretion of the hormone
- Transport of the hormone to the target cell(s)
- Recognition of the hormone by an associated cell membrane or intracellular receptor protein
- Relay and amplification of the received hormonal signal via a signal transduction process: This then leads to a cellular response. The reaction of the target cells may then be recognized by the original hormone-producing cells, leading to a down-regulation in hormone production. This is an example of a homeostatic negative feedback loop.
- Degradation of the hormone.
Interactions with receptors
Most hormones initiate a cellular response by initially combining with either a specific intracellular or cell membrane associated receptor protein. A cell may have several different receptors that recognize the same hormone and activate different signal transduction pathways, or a cell may have several different receptors that recognize different hormones and activate the same biochemical pathway.For many hormones, including most protein hormones, the receptor is membrane-associated and embedded in the plasma membrane at the surface of the cell. The interaction of hormone and receptor typically triggers a cascade of secondary effects within the cytoplasm of the cell, often involving phosphorylation or dephosphorylation of various other cytoplasmic proteins, changes in ion channel permeability, or increased concentrations of intracellular molecules that may act as secondary messengers (e.g., cyclic AMP). Some protein hormones also interact with intracellular receptors located in the cytoplasm or nucleus by an intracrine mechanism.
For hormones such as steroid or thyroid hormones, their receptors are located intracellularly within the cytoplasm of their target cell. To bind their receptors, these hormones must cross the cell membrane. They can do so because they are lipid-soluble. The combined hormone-receptor complex then moves across the nuclear membrane into the nucleus of the cell, where it binds to specific DNA sequences, effectively amplifying or suppressing the action of certain genes, and affecting protein synthesis.[2] However, it has been shown that not all steroid receptors are located intracellularly. some are associated with the plasma membrane.[3]
An important consideration, dictating the level at which cellular signal transduction pathways are activated in response to a hormonal signal, is the effective concentration of hormone-receptor complexes that are formed. Hormone-receptor complex concentrations are effectively determined by three factors:
- The number of hormone molecules available for complex formation
- The number of receptor molecules available for complex formation
- The binding affinity between hormone and receptor.
Physiology of hormones
Most cells are capable of producing one or more molecules, which act as signaling molecules to other cells, altering their growth, function, or metabolism. The classical hormones produced by cells in the endocrine glands mentioned so far in this article are cellular products, specialized to serve as regulators at the overall organism level. However, they may also exert their effects solely within the tissue in which they are produced and originally released.The rate of hormone biosynthesis and secretion is often regulated by a homeostatic negative feedback control mechanism. Such a mechanism depends on factors that influence the metabolism and excretion of hormones. Thus, higher hormone concentration alone cannot trigger the negative feedback mechanism. Negative feedback must be triggered by overproduction of an "effect" of the hormone.
Hormone secretion can be stimulated and inhibited by:
- Other hormones (stimulating- or releasing -hormones)
- Plasma concentrations of ions or nutrients, as well as binding globulins
- Neurons and mental activity
- Environmental changes, e.g., of light or temperature
A recently identified class of hormones is that of the "hunger hormones" - ghrelin, orexin, and PYY 3-36 - and "satiety hormones" - e.g., cholecystokinin, leptin, nesfatin-1, obestatin.
To release active hormones quickly into the circulation, hormone biosynthetic cells may produce and store biologically inactive hormones in the form of pre- or prohormones. These can then be quickly converted into their active hormone form in response to a particular stimulus.
Effects of hormones
Hormones have the following effects on the body:- stimulation or inhibition of growth
- mood swings
- induction or suppression of apoptosis (programmed cell death)
- activation or inhibition of the immune system
- regulation of metabolism
- preparation of the body for mating, fighting, fleeing, and other activity
- preparation of the body for a new phase of life, such as puberty, parenting, and menopause
- control of the reproductive cycle
- hunger cravings
Chemical classes of hormones
Vertebrate hormones fall into three chemical classes:- Peptide hormones consist of chains of amino acids. Examples of small peptide hormones are TRH and vasopressin. Peptides composed of scores or hundreds of amino acids are referred to as proteins. Examples of protein hormones include insulin and growth hormone. More complex protein hormones bear carbohydrate side-chains and are called glycoprotein hormones. Luteinizing hormone, follicle-stimulating hormone and thyroid-stimulating hormone are glycoprotein hormones. There's also another type of hydrophilics hormones. They are called nonpeptide hormones. Although they don't have peptide connections, they are assimilated as peptide hormones.
- Lipid and phospholipid-derived hormones derive from lipids such as linoleic acid and arachidonic acid and phospholipids. The main classes are the steroid hormones that derive from cholesterol and the eicosanoids. Examples of steroid hormones are testosterone and cortisol. Sterol hormones such as calcitriol are a homologous system. The adrenal cortex and the gonads are primary sources of steroid hormones. Examples of eicosanoids are the widely studied prostaglandins.
- Monoamines derived from aromatic amino acids like phenylalanine, tyrosine, tryptophan by the action of aromatic amino acid decarboxylase enzymes. Examples of monoamines are thyroxine and adrenaline.
Pharmacology
Many hormones and their analogues are used as medication. The most commonly prescribed hormones are estrogens and progestagens (as methods of hormonal contraception and as HRT), thyroxine (as levothyroxine, for hypothyroidism) and steroids (for autoimmune diseases and several respiratory disorders). Insulin is used by many diabetics. Local preparations for use in otolaryngology often contain pharmacologic equivalents of adrenaline, while steroid and vitamin D creams are used extensively in dermatological practice.A "pharmacologic dose" of a hormone is a medical usage referring to an amount of a hormone far greater than naturally occurs in a healthy body. The effects of pharmacologic doses of hormones may be different from responses to naturally occurring amounts and may be therapeutically useful. An example is the ability of pharmacologic doses of glucocorticoid to suppress inflammation.
Important human hormones
See: List of human hormonesSee also
References
- ^ Crisp TM, Clegg ED, Cooper RL, Wood WP, Anderson DG, Baetcke KP, Hoffmann JL, Morrow MS, Rodier DJ, Schaeffer JE, Touart LW, Zeeman MG, Patel YM (1998). "Environmental endocrine disruption: An effects assessment and analysis". Environ. Health Perspect. 106 (Suppl 1): 11–56. PMID 9539004.
- ^ Beato M, Chavez S and Truss M (1996). "Transcriptional regulation by steroid hormones". Steroids 61 (4): 240–251. doi:10.1016/0039-128X(96)00030-X. PMID 8733009.
- ^ Hammes SR (2003). "The further redefining of steroid-mediated signaling". Proc Natl Acad Sci USA 100 (5): 21680–2170. doi:10.1073/pnas.0530224100. PMID 12606724.
No comments:
Post a Comment