WordNet

of or belonging to endocrine glands or their secretions; "endocrine system" (同)endocrinal
any of various organs that synthesize substances needed by the body and release it through ducts or directly into the bloodstream (同)secretory organ, secretor, secreter

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内分泌(ぶんぴつ)の / 内分泌物;内分泌腺(せん)
(生物体内の)腺(せん)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/26 09:03:21」(JST)

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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. Local chemical messengers, not generally considered part of the endocrine system, include autocrines, which act on the cells that secrete them, and paracrines, which act on a different cell type nearby.

The ability of a target cell^{[disambiguation needed]} to respond to a hormone depends on the presence of receptors, within the cell or on its plasma membrane, to which the hormone can bind.

Hormone receptors are dynamic structures. Changes in number and sensitivity of hormone receptors may occur in response to high or low levels of stimulating hormones.

Blood levels of hormones reflect a balance between secretion and degradation/excretion. The liver and kidneys are the major organs that degrade hormones; breakdown products are excreted in urine and feces.

Hormone half-life and duration of activity are limited and vary from hormone to hormone.

1 Interaction of hormones at target cells
2 Control of hormone release
3 Major endocrine organs
- 3.1 Pituitary gland (hypophysis)
- 3.2 Thyroid gland
- 3.3 Parathyroid glands
- 3.4 Pancreas
- 3.5 Gonads
- 3.6 Pineal gland
4 Other hormone-producing structures
5 Developmental aspects of the endocrine systems
6 References

Interaction of hormones at target cells

Permissiveness is the situation in which a hormone cannot exert its full effects without the presence of another hormone.

Synergism occurs when two or more hormones produce the same effects in a target cell and their results are amplified.

Antagonism occurs when a hormone opposes or reverses the effect of another hormone.

Control of hormone release

Endocrine organs are activated to release their hormones by humoral, neural or hormonal stimuli. Negative feedback is important in regulating hormone levels in the blood.

The nervous system, acting through hypothalamic controls, can in certain cases override or modulate hormonal effects.

Major endocrine organs

Pituitary gland (hypophysis)

Endocrine glands in the human head and neck and their hormones

The pituitary gland hangs from the base of the brain by a stalk and is enclosed by bone. It consists of a hormone-producing glandular portion (anterior pituitary) and a neural portion (posterior pituitary), which is an extension of the hypothalamus. The hypothalamus regulates the hormonal output of the anterior pituitary and synthesizes two hormones that it exports to the posterior pituitary for storage and later release.

Four of the six adenohypophyseal hormones are tropic hormones that regulate the function of other endocrine organs. Most anterior pituitary hormones exhibit a diurnal rhythm of release, which is subject to modification by stimuli influencing the hypothalamus.

Somatotropic hormone or Growth hormone (GH) is an anabolic hormone that stimulates growth of all body tissues but especially skeletal muscle and bone. It may act directly, or indirectly via insulin-like growth factors (IGFs). GH mobilizes fats, stimulates protein synthesis, and inhibits glucose uptake and metabolism. Secretion is regulated by growth hormone releasing hormone (GHRH) and growth hormone inhibiting hormone (GHIH), or somatostatin. Hypersecretion causes gigantism in children and acromegaly in adults; hyposecretion in children causes pituitary dwarfism.

Thyroid-stimulating hormone (TSH) promotes normal development and activity of the thyroid gland. Thyrotropin-releasing hormone (TRH) stimulates its release; negative feedback of thyroid hormone inhibits it.

Adrenocorticotropic hormone (ACTH) stimulates the adrenal cortex to release corticosteroids. ACTH release is triggered by corticotropin-releasing hormone (CRH) and inhibited by rising glucocorticoid levels.

The gonadotropins—follicle-stimulating hormone (FSH) and luteinizing hormone (LH) regulate the functions of the gonads in both sexes. FSH stimulates sex cell production; LH stimulates gonadal hormone production. Gonadotropin levels rise in response to gonadotropin-releasing hormone (GnRH). Negative feedback of gonadal hormones inhibits gonadotropin release.

Prolactin (PRL) promotes milk production in humans females. Its secretion is prompted by prolactin-releasing hormone (PRH) and inhibited by prolactin-inhibiting hormone (PIH).

The neurohypophysis stores and releases two hypothalamic hormones:

Oxytocin stimulates powerful uterine contractions, which trigger labor and delivery of an infant, and milk ejection in nursing women. Its release is mediated reflexively by the hypothalamus and represents a positive feedback mechanism.
Antidiuretic hormone (ADH) stimulates the kidney tubules to reabsorb and conserve water, resulting in small volumes of highly concentrated urine and decreased plasma osmolarity. ADH is released in response to high solute concentrations in the blood and inhibited by low solute concentrations in the blood. Hyposecretion results in diabetes insipidus.

Thyroid gland

The thyroid gland is located in the anterior throat. Thyroid follicles store colloid containing thyroglobulin, a glycoprotein from which thyroid hormone is derived.

Thyroid hormone (TH) includes thyroxine (T4) and triiodothyronine (T3), which increase the rate of cellular metabolism. Consequently, oxygen use and heat production rise.

Secretion of thyroid hormone, prompted by TSH, requires reuptake of the stored colloid by the follicle cells and splitting of the hormones from the colloid for release. Rising levels of thyroid hormone feed back to inhibit the pituitary and hypothalamus.

Most T4 is converted to T3 (the more active form) in the target tissues. These hormones act by turning on gene and protein synthesis.

Graves' disease is the most common cause of hyperthyroidism; hyposecretion causes cretinism in infants and myxoedema in adults.

Calcitonin, produced by the parafollicular cells of the thyroid gland in response to rising blood calcium levels, depresses blood calcium levels by inhibiting bone matrix resorption and enhancing calcium deposit in bone.

Parathyroid glands

The parathyroid glands, located on the dorsal aspect of the thyroid gland, secrete parathyroid hormone (PTH),^[1] which causes an increase in blood calcium levels by targeting bone, the intestine, and the kidneys. PTH is the antagonist of calcitonin. PTH release is triggered by falling blood calcium levels and is inhibited by rising blood calcium levels.

Hyperparathyroidism results in hypercalcaemia and all its effects and in extreme bone wasting. Hypoparathyroidism leads to hypocalcaemia, evidenced by tetany and respiratory paralysis.

Pancreas

The pancreas, located in the abdomen close to the stomach, is both an exocrine and an endocrine gland. The endocrine portion (islets of langerhans) releases insulin and glucagon and smaller amounts of other hormones to the blood.

Glucagon, released by alpha (α) cells when glucose level in blood are low, stimulates the liver to release glucose to the blood.

Insulin is released by beta (β) cells when blood levels of glucose (and amino acids) are rising. It increases the rate of glucose uptake and metabolism by most body cells. Hyposecretion of insulin results in diabetes mellitus; cardinal signs are polyuria, polydipsia, and polyphagia.

Gonads

The ovaries of the female, located in the pelvic cavity, release two main hormones. Secretion of estrogens by the ovarian follicles begins at puberty under the influence of FSH. Estrogens stimulate maturation of the female reproductive system and development of the secondary sexual characteristics. Progesterone is released in response to high blood levels of LH. It works with estrogens in establishing the menstrual cycle.

The testes of the male begin to produce testosterone at puberty in response to LH. Testosterone promotes maturation of the male reproductive organs, development of secondary sex characteristics, and production of sperm by the testes.

Pineal gland

The pineal gland is located in the diencephalon. Its primary hormone is melatonin, which influences daily rhythms and may have an antigonadotropic effect in humans.

Other hormone-producing structures

Many body organs not normally considered endocrine organs contain isolated cell clusters that secrete hormones. Examples include the heart (atrial natriuretic peptide); gastrointestinal tract organs (gastrin, secretin, and others); the placenta (hormones of pregnancy—estrogen, progesterone, and others); the kidneys (erythropoietin and renin); the thymus; skin (cholecalciferol); and adipose tissue (leptin and resistin).

Developmental aspects of the endocrine systems

Endocrine glands derive from all three germ layers. Those derived from mesoderm produce steroidal hormones; the others produce the amino acid–based hormones.

The natural decrease in function of the female’s ovaries during late middle age results in menopause. The efficiency of all endocrine glands seems to decrease gradually as aging occurs. This leads to a generalized increase in the incidence of diabetes mellitus and a lower metabolic rate.

References

^ Endocrinology: Tissue Histology. University of Nebraska at Omaha.

UpToDate Contents

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1. 原発性副甲状腺機能亢進症の副甲状腺診査 parathyroid exploration for primary hyperparathyroidism
2. 唾液腺腫瘍：疫学、診断、評価、および病期分類 salivary gland tumors epidemiology diagnosis evaluation and staging
3. 甲状腺の外科解剖学 surgical anatomy of the thyroid gland
4. 視床下部下垂体軸 hypothalamic pituitary axis
5. 妊娠に対する母体の内分泌系および代謝の適応 maternal endocrine and metabolic adaptation to pregnancy

English Journal

Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4).

Thakker RV.Author information Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford OX3 7LJ, United Kingdom. Electronic address: rajesh.thakker@ndm.ox.ac.uk.AbstractMultiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2 (previously MEN2A) due to mutations of a tyrosine kinase receptor encoded by the rearranged during transfection (RET) protoncogene; MEN3 (previously MEN2B) due to RET mutations; and MEN4 due to cyclin-dependent kinase inhibitor (CDNK1B) mutations. Each MEN type is associated with the occurrence of specific tumors. Thus, MEN1 is characterized by the occurrence of parathyroid, pancreatic islet and anterior pituitary tumors; MEN2 is characterized by the occurrence of medullary thyroid carcinoma (MTC) in association with phaeochromocytoma and parathyroid tumors; MEN3 is characterized by the occurrence of MTC and phaeochromocytoma in association with a marfanoid habitus, mucosal neuromas, medullated corneal fibers and intestinal autonomic ganglion dysfunction, leading to megacolon; and MEN4, which is also referred to as MENX, is characterized by the occurrence of parathyroid and anterior pituitary tumors in possible association with tumors of the adrenals, kidneys, and reproductive organs. This review will focus on the clinical and molecular details of the MEN1 and MEN4 syndromes. The gene causing MEN1 is located on chromosome 11q13, and encodes a 610 amino-acid protein, menin, which has functions in cell division, genome stability, and transcription regulation. Menin, which acts as scaffold protein, may increase or decrease gene expression by epigenetic regulation of gene expression via histone methylation. Thus, menin by forming a subunit of the mixed lineage leukemia (MLL) complexes that trimethylate histone H3 at lysine 4 (H3K4), facilitates activation of transcriptional activity in target genes such as cyclin-dependent kinase (CDK) inhibitors; and by interacting with the suppressor of variegation 3-9 homolog family protein (SUV39H1) to mediate H3K methylation, thereby silencing transcriptional activity of target genes. MEN1-associated tumors harbor germline and somatic mutations, consistent with Knudson's two-hit hypothesis. Genetic diagnosis to identify individuals with germline MEN1 mutations has facilitated appropriate targeting of clinical, biochemical and radiological screening for this high risk group of patients for whom earlier implementation of treatments can then be considered. MEN4 is caused by heterozygous mutations of CDNK1B which encodes the 196 amino-acid CDK1 p27Kip1, which is activated by H3K4 methylation.
Molecular and cellular endocrinology.Mol Cell Endocrinol.2014 Apr 5;386(1-2):2-15. doi: 10.1016/j.mce.2013.08.002. Epub 2013 Aug 8.
Multiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2 (previou
PMID 23933118

Fate and plasticity of renin precursors in development and disease.

Gomez RA1, Belyea B, Medrano S, Pentz ES, Sequeira-Lopez ML.Author information 1Department of Pediatrics, University of Virginia School of Medicine, 409 Lane Road, Room 2001, Charlottesville, VA, 22908, USA, rg@virginia.edu.AbstractRenin-expressing cells appear early in the embryo and are distributed broadly throughout the body as organogenesis ensues. Their appearance in the metanephric kidney is a relatively late event in comparison with other organs such as the fetal adrenal gland. The functions of renin cells in extra renal tissues remain to be investigated. In the kidney, they participate locally in the assembly and branching of the renal arterial tree and later in the endocrine control of blood pressure and fluid-electrolyte homeostasis. Interestingly, this endocrine function is accomplished by the remarkable plasticity of renin cell descendants along the kidney arterioles and glomeruli which are capable of reacquiring the renin phenotype in response to physiological demands, increasing circulating renin and maintaining homeostasis. Given that renin cells are sensors of the status of the extracellular fluid and perfusion pressure, several signaling mechanisms (β-adrenergic receptors, Notch pathway, gap junctions and the renal baroreceptor) must be coordinated to ensure the maintenance of renin phenotype-and ultimately the availability of renin-during basal conditions and in response to homeostatic threats. Notably, key transcriptional (Creb/CBP/p300, RBP-J) and posttranscriptional (miR-330, miR125b-5p) effectors of those signaling pathways are prominent in the regulation of renin cell identity. The next challenge, it seems, would be to understand how those factors coordinate their efforts to control the endocrine and contractile phenotypes of the myoepithelioid granulated renin-expressing cell.
Pediatric nephrology (Berlin, Germany).Pediatr Nephrol.2014 Apr;29(4):721-6. doi: 10.1007/s00467-013-2688-0. Epub 2013 Dec 15.
Renin-expressing cells appear early in the embryo and are distributed broadly throughout the body as organogenesis ensues. Their appearance in the metanephric kidney is a relatively late event in comparison with other organs such as the fetal adrenal gland. The functions of renin cells in extra rena
PMID 24337407

Japanese Journal

症例報告副甲状腺摘出術後の残存異所性副甲状腺腺腫により副甲状腺機能亢進症が持続した血液透析患者の1例

鈴木孝尚,大塚篤史,石井保夫 [他]
日本内分泌・甲状腺外科学会雑誌 = Official journal of the Japan Association of Endocrine
NAID 40020299248

Transcriptional Control of Steroid Biosynthesis Genes in the Drosophila Prothoracic Gland by Ventral Veins Lacking and Knirps

Danielsen E. Thomas,Moeller Morten E.,Dorry Elad,Komura-Kawa Tatsuya,Fujimoto Yoshinori,Troelsen Jesper T.,Herder Rachel,O'Connor Michael B.,Niwa Ryusuke,Rewitz Kim F.
PLOS genetics 10(6), e1004343, 2014-06
… Specialized endocrine cells produce and release steroid hormones that govern development, metabolism and reproduction. … In Drosophila, the steroid producing endocrine cells are located in the prothoracic gland (PG) that releases the steroid hormone ecdysone. … Vvl is highly expressed in the PG during embryogenesis and is enriched in the gland during larval development, suggesting that Vvl might function as a master transcriptional regulator in this tissue. …
NAID 120005466790

Related Pictures

★リンクテーブル★

リンク元	「内分泌腺」
拡張検索	「endocrine gland neoplasm」「endocrine-gland-derived vascular endothelial growth factor」
関連記事	「endocrine」

「内分泌腺」

Endocrine glands
	The major endocrine glands: 1 Pineal gland 2 Pituitary gland 3 Thyroid gland 4 Thymus 5 Adrenal gland 6 Pancreas 7 Ovary (female) 8 Testis (male)
Details
Latin	glandulae endocrinae
Identifiers
Code	TH H2.00.02.0.03072
TA	A11.0.00.000
FMA	71653
	Anatomical terminology