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The endocrine system is the collection of glands of an organism that secrete hormones directly into the circulatory system to be carried towards distant target organs. In humans, the major endocrine glands include the pineal gland, pituitary gland, pancreas, ovaries, testes, thyroid gland, parathyroid gland, and adrenal glands. In vertebrates, the hypothalamus is the neural control center for all endocrine systems. The field of study dealing with the endocrine system and its disorders is endocrinology, a branch of internal medicine.[1]

Endocrine system
Illu endocrine system New.png
Main glands of the endocrine system. Note that the thymus is no longer considered part of the endocrine system, as it does not produce hormones.
Details
Identifiers
Latin Systema endocrinum
FMA 9668
Anatomical terminology

Special features of endocrine glands are, in general, their ductless nature, their vascularity, and commonly the presence of intracellular vacuoles or granules that store their hormones. In contrast, exocrine glands, such as salivary glands, sweat glands, and glands within the gastrointestinal tract, tend to be much less vascular and have ducts or a hollow lumen. A number of glands that signal each other in sequence are usually referred to as an axis, for example, the hypothalamic-pituitary-adrenal axis.

In addition to the specialized endocrine organs mentioned above, many other organs that are part of other body systems, such as bone, kidney, liver, heart and gonads, have secondary endocrine functions. For example, the kidney secretes endocrine hormones such as erythropoietin and renin. Hormones can consist of either amino acid complexes, steroids, eicosanoids, leukotrienes, or prostaglandins.[1]

The endocrine system is in contrast to the exocrine system, which secretes its hormones to the outside of the body using ducts. As opposed to endocrine factors that travel considerably longer distances via the circulatory system, other signaling molecules, such as paracrine factors involved in paracrine signalling diffuse over a relatively short distance.

The word endocrine derives from the Greek words ἐνδο- endo- "inside, within," and κρίνειν krinein "to separate, distinguish".

Contents

StructureEdit

Major endocrine systemsEdit

The human endocrine system consists of several systems that operate via feedback loops. Several important feedback systems are mediated via the hypothalamus and pituitary.[2]

GlandsEdit

Endocrine glands are glands of the endocrine system that secrete their products, hormones, directly into the blood rather than through a duct. The major glands of the endocrine system include the pineal gland, pituitary gland, pancreas, ovaries, testes, thyroid gland, parathyroid gland, hypothalamus and adrenal glands. The hypothalamus and pituitary gland are neuroendocrine organs.

CellsEdit

DevelopmentEdit

FunctionEdit

HormonesEdit

A hormone is any member of a class of signaling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behaviour. Hormones have diverse chemical structures, mainly of 3 classes: eicosanoids, steroids, and amino acid/protein derivatives (amines, peptides, and proteins). The glands that secrete hormones comprise the endocrine system. The term hormone is sometimes extended to include chemicals produced by cells that affect the same cell (autocrine or intracrine signalling) or nearby cells (paracrine signalling).

Hormones are used to communicate between organs and tissues for physiological regulation and behavioral activities, such as digestion, metabolism, respiration, tissue function, sensory perception, sleep, excretion, lactation, stress, growth and development, movement, reproduction, and mood.[3][4]

Hormones affect distant cells by binding to specific receptor proteins in the target cell resulting in a change in cell function. When a hormone binds to the receptor, it results in the activation of a signal transduction pathway. This may lead to cell type-specific responses that include rapid non-genomic effects or slower genomic[disambiguation needed] responses where the hormones acting through their receptors activate gene transcription resulting in increased expression of target proteins. Amino acid–based hormones (amines and peptide or protein hormones) are water-soluble and act on the surface of target cells via second messengers; steroid hormones, being lipid-soluble, move through the plasma membranes of target cells (both cytoplasmic and nuclear) to act within their nuclei.

Cell signallingEdit

The typical mode of cell signaling in the endocrine system is endocrine signaling, that is, using the circulatory system to reach distant target organs. However, there are also other modes, i.e., paracrine, autocrine, and neuroendocrine signaling. Purely neurocrine signaling between neurons, on the other hand, belongs completely to the nervous system.

AutocrineEdit

Autocrine signaling is a form of signaling in which a cell secretes a hormone or chemical messenger (called the autocrine agent) that binds to autocrine receptors on the same cell, leading to changes in the cells.

ParacrineEdit

Some endocrinologists and clinicians include the paracrine system as part of the endocrine system, but there is not consensus. Paracrines are slower acting, targeting cells in the same tissue or organ. An example of this is somatostatin which is released by some pancreatic cells and targets other pancreatic cells.[1]

JuxtacrineEdit

Juxtacrine signaling is a type of intercellular communication that is transmitted via oligosaccharide, lipid, or protein components of a cell membrane, and may affect either the emitting cell or the immediately adjacent cells.[5]

It occurs between adjacent cells that possess broad patches of closely opposed plasma membrane linked by transmembrane channels known as connexons. The gap between the cells can usually be between only 2 and 4 nm.[6]

Clinical significanceEdit

DiseaseEdit

 
Disability-adjusted life year for endocrine disorders per 100,000 inhabitants in 2002.[7]
  no data
  less than 80
  80–160
  160–240
  240–320
  320–400
  400–480
  480–560
  560–640
  640–720
  720–800
  800–1000
  more than 1000

Diseases of the endocrine system are common,[8] including conditions such as diabetes mellitus, thyroid disease, and obesity. Endocrine disease is characterized by irregulated hormone release (a productive pituitary adenoma), inappropriate response to signaling (hypothyroidism), lack of a gland (diabetes mellitus type 1, diminished erythropoiesis in chronic renal failure), or structural enlargement in a critical site such as the thyroid (toxic multinodular goitre). Hypofunction of endocrine glands can occur as a result of loss of reserve, hyposecretion, agenesis, atrophy, or active destruction. Hyperfunction can occur as a result of hypersecretion, loss of suppression, hyperplastic or neoplastic change, or hyperstimulation.

Endocrinopathies are classified as primary, secondary, or tertiary. Primary endocrine disease inhibits the action of downstream glands. Secondary endocrine disease is indicative of a problem with the pituitary gland. Tertiary endocrine disease is associated with dysfunction of the hypothalamus and its releasing hormones.[citation needed]

As the thyroid, and hormones have been implicated in signaling distant tissues to proliferate, for example, the estrogen receptor has been shown to be involved in certain breast cancers. Endocrine, paracrine, and autocrine signaling have all been implicated in proliferation, one of the required steps of oncogenesis.[9]

Other common diseases that result from endocrine dysfunction include Addison’s disease, Cushing’s disease and Grave’s disease. Cushing's disease and Addison's disease are pathologies involving the dysfunction of the adrenal gland. Dysfunction in the adrenal gland could be due to primary or secondary factors and can result in hypercortisolism or hypocortisolism . Cushing’s disease is characterized by the hypersecretion of the adrenocorticotropic hormone (ACTH) due to a pituitary adenoma that ultimately causes endogenous hypercortisolism by stimulating the adrenal glands.[10] Some clinical signs of Cushing’s disease include obesity, moon face, and hirsutism.[11] Addison's disease is an endocrine disease that results from hypocortisolism caused by adrenal gland insufficiency. Adrenal insufficiency is significant because it is correlated with decreased ability to maintain blood pressure and blood sugar, a defect that can prove to be fatal.[12]

Graves' disease involves the hyperactivity of the thyroid gland which produces the T3 and T4 hormones.[11] Graves' disease effects range from excess sweating, fatigue, heat intolerance and high blood pressure to swelling of the eyes that causes redness, puffiness and in rare cases reduced or double vision.[6]

Other animalsEdit

A neuroendocrine system has been observed in all animals with a nervous system and all vertebrates have an hypothalamus-pituitary axis.[13] All vertebrates have a thyroid, which in amphibians is also crucial for transformation of larvae into adult form.[14][15] All vertebrates have adrenal gland tissue, with mammals unique in having it organized into layers.[16] All vertebrates have some form of renin-angiotensin axis, and all tetrapods have aldosterone as primary mineralocorticoid.[17][18]

Additional imagesEdit

See alsoEdit

ReferencesEdit

  1. ^ a b c Marieb, Elaine (2014). Anatomy & physiology. Glenview, IL: Pearson Education, Inc. ISBN 978-0321861580. 
  2. ^ Sherwood, L. (1997). "Human Physiology: From Cells to Systems". Wadsworth Pub Co. ISBN 0495391840. 
  3. ^ Neave N (2008). Hormones and behaviour: a psychological approach. Cambridge: Cambridge Univ. Press. ISBN 978-0521692014. Lay summaryProject Muse. 
  4. ^ "Hormones". MedlinePlus. U.S. National Library of Medicine. 
  5. ^ Gilbert, Scott F. (2000-01-01). "Juxtacrine Signaling". 
  6. ^ a b Vander, Arthur (2008). Vander's Human Physiology: the mechanisms of body function. Boston: McGraw-Hill Higher Education. pp. 332–333. 
  7. ^ "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002. 
  8. ^ Kasper (2005). Harrison's Principles of Internal Medicine. McGraw Hill. p. 2074. ISBN 0-07-139140-1. 
  9. ^ Bhowmick NA, Chytil A, Plieth D, Gorska AE, Dumont N, Shappell S, Washington MK, Neilson EG, Moses HL (2004). "TGF-beta signaling in fibroblasts modulates the oncogenic potential of adjacent epithelia". Science. 303 (5659): 848–51. doi:10.1126/science.1090922. PMID 14764882. 
  10. ^ Buliman A, Tataranu LG, Paun DL, Mirica A, Dumitrache C (2016). "Cushing's disease: a multidisciplinary overview of the clinical features, diagnosis, and treatment". Journal of Medicine & Life. 9 (1): 12–18. 
  11. ^ a b Vander, Arthur (2008). Vander's Human Physiology: the mechanisms of body function. Boston: McGraw-Hill Higher Education. pp. 345-347
  12. ^ Inder, Warrick J.; Meyer, Caroline; Hunt, Penny J. (2015-06-01). "Management of hypertension and heart failure in patients with Addison's disease". Clinical Endocrinology. 82 (6): 789–792. doi:10.1111/cen.12592. ISSN 1365-2265. 
  13. ^ Hartenstein V (September 2006). "The neuroendocrine system of invertebrates: a developmental and evolutionary perspective". The Journal of Endocrinology. 190 (3): 555–70. doi:10.1677/joe.1.06964. PMID 17003257. 
  14. ^ Dickhoff, Walton W.; Darling, Douglas S. (1983). "Evolution of Thyroid Function and Its Control in Lower Vertebrates". American Zoologist. 23 (3): 697–707. doi:10.1093/icb/23.3.697. JSTOR 3882951. 
  15. ^ Galton, Valerie Anne (1 January 1988). "The Role of Thyroid Hormone in Amphibian Development". Integrative and Comparative Biology. 28 (2): 309–18. doi:10.1093/icb/28.2.309. JSTOR 3883279. 
  16. ^ Pohorecky LA, Wurtman RJ (March 1971). "Adrenocortical control of epinephrine synthesis". Pharmacological Reviews. 23 (1): 1–35. PMID 4941407. 
  17. ^ Wilson JX (1984). "The renin-angiotensin system in nonmammalian vertebrates". Endocrine Reviews. 5 (1): 45–61. doi:10.1210/edrv-5-1-45. PMID 6368215. 
  18. ^ Colombo L, Dalla Valle L, Fiore C, Armanini D, Belvedere P (April 2006). "Aldosterone and the conquest of land". Journal of Endocrinological Investigation. 29 (4): 373–9. doi:10.1007/bf03344112. PMID 16699307. 

External linksEdit