Endocrine system

The body ‘s hormone-producing glands

The endocrine system is a messenger system comprising feedback loops of the hormones released by inner glands of an organism immediately into the circulative system, regulating distant target organs. In vertebrates, the hypothalamus is the neural control center for all endocrine systems. In humans, the major endocrine glands are the thyroid gland and the adrenal gland glands. The study of the endocrine system and its disorders is known as endocrinology. Glands that signal each early in sequence are much referred to as an axis, such as the hypothalamic-pituitary-adrenal axis. In addition to the speciate hormone organs mentioned above, many other organs that are depart of other torso systems have junior-grade endocrine functions, including bone, kidneys, liver, heart and gonads. For case, the kidney secretes the endocrine gland hormone erythropoietin. Hormones can be amino acid complexes, steroids, eicosanoids, leukotrienes, or prostaglandins. [ 1 ]

Reading: Endocrine system

The endocrine gland system can be contrasted to both exocrine glands, which secrete hormones to the outside of the body, and paracrine signalling between cells over a relatively short distance. Endocrine glands have no ducts, are vascular, and normally have intracellular vacuoles or granules that store their hormones. In contrast, exocrine glands, such as salivary glands, fret glands, and glands within the gastrointestinal nerve pathway, tend to be a lot less vascular and have ducts or a hollow lumen. Endocrinology is a branch of internal music. [ 1 ]

structure [edit ]

major endocrine gland systems [edit ]

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

Glands [edit ]

Endocrine glands are glands of the endocrine system that secrete their products, hormones, directly into interstitial spaces and then absorbed into blood rather than through a duct. The major glands of the endocrine gland organization include the pineal gland, pituitary gland, pancreas, ovaries, testes, thyroid gland, parathyroid gland gland, hypothalamus and adrenal glands. The hypothalamus and pituitary gland are neuroendocrine organs. The hypothalamus and the anterior pituitary are two out of the three hormone glands that are crucial in cell signaling. They are both part of the HPA bloc which is known to play a role in cell sign in the nervous system. hypothalamus : The hypothalamus is a key regulator of the autonomic anxious system. The hormone arrangement has three sets of endocrine gland outputs [ 3 ] which include the magnocellular system, the parvocellular organization, and autonomic intervention. The magnocellular is involved in the formula of oxytocin or vasopressin. The parvocellular is involved in controlling the secretion of hormones from the front tooth pituitary. anterior Pituitary : The main role of the front tooth pituitary gland is to produce and secret tropical hormones. [ 4 ] Some examples of tropic hormones secreted by the anterior pituitary gland include TSH, ACTH, GH, LH, and FSH .

Cells [edit ]

There are many types of cells that make up the hormone system and these cells typically make up larger tissues and organs that function within and outside of the endocrine gland organization .

Development [edit ]

The fetal endocrine system is one of the first systems to develop during prenatal development .

Adrenal glands [edit ]

The fetal adrenal gland lens cortex can be identified within four weeks of pregnancy. The adrenal lens cortex originates from the node of the intermediate mesoderm. At five to six weeks of gestation, the mesonephros differentiates into a tissue known as the gonadal ridge. The gonadal ridge produces the steroidogenic cells for both the gonads and the adrenal gland lens cortex. The adrenal myelin is derived from ectodermal cells. Cells that will become adrenal gland tissue move retroperitoneally to the upper part of the mesonephros. At seven weeks of pregnancy, the adrenal cells are joined by sympathetic cells that originate from the neural crest to form the adrenal medulla. At the end of the one-eighth workweek, the adrenal gland glands have been encapsulated and have formed a clear-cut organ above the developing kidneys. At birth, the adrenal glands weight approximately eight to nine grams ( doubly that of the adult adrenal gland glands ) and are 0.5 % of the full body weight unit. At 25 weeks, the pornographic adrenal gland lens cortex partition build up and is responsible for the primary coil deduction of steroids during the early postnatal weeks .

Thyroid gland [edit ]

The thyroid gland gland develops from two unlike clusterings of embryonic cells. One separate is from the thickening of the pharyngeal floor, which serves as the harbinger of the thyroxine ( T4 ) producing follicular cells. The other part is from the caudal extensions of the fourth pharyngobranchial pouches which results in the parafollicular calcitonin-secreting cells. These two structures are apparent by 16 to 17 days of gestation. Around the 24th sidereal day of pregnancy, the foramen cecum, a thin, flask-like diverticulum of the median primordium develops. At approximately 24 to 32 days of gestation the median primordium develops into a bilobate social organization. By 50 days of pregnancy, the medial and lateral pass primordium have fused together. At 12 weeks of pregnancy, the fetal thyroid is capable of storing tincture of iodine for the output of TRH, TSH, and free thyroid gland hormone. At 20 weeks, the fetus is able to implement feedback mechanism for the production of thyroid hormones. During fetal exploitation, T4 is the major thyroid hormone being produced while triiodothyronine ( T3 ) and its nonoperational derivative, rearward T3, are not detected until the third shipshape .

Parathyroid glands [edit ]

A lateral and adaxial scene of an embryo showing the third ( inferior ) and fourth ( superior ) parathyroid gland glands during the 6th week of embryogenesis once the embryo reaches four weeks of gestation, the parathyroid gland glands begins to develop. The human embryo forms five sets of endoderm -lined guttural pouches. The third base and fourth bulge are responsible for developing into the inferior and superior parathyroid gland glands, respectively. The third base guttural pouch encounters the developing thyroid gland and they migrate down to the lower poles of the thyroid gland lobe. The fourth guttural bulge late encounters the developing thyroid gland and migrates to the upper poles of the thyroid lobe. At 14 weeks of pregnancy, the parathyroid gland glands begin to enlarge from 0.1 mm in diameter to approximately 1 – 2 millimeter at give birth. The developing parathyroid gland glands are physiologically functional get down in the second trimester. Studies in mice have shown that interfering with the HOX15 gene can cause parathyroid gland gland aplasia, which suggests the gene plays an important character in the development of the parathyroid gland gland. The genes, TBX1, CRKL, GATA3, GCM2, and SOX3 have besides been shown to play a all-important function in the formation of the parathyroid gland gland. Mutations in TBX1 and CRKL genes are correlated with DiGeorge syndrome, while mutations in GATA3 have besides resulted in a DiGeorge-like syndrome. Malformations in the GCM2 gene have resulted in hypoparathyroidism. Studies on SOX3 gene mutations have demonstrated that it plays a character in parathyroid gland development. These mutations besides lead to varying degrees of hypopituitarism .

Pancreas [edit ]

The human fetal pancreas begins to develop by the fourth week of pregnancy. Five weeks subsequently, the pancreatic alpha and beta cells have begun to emerge. Reaching eight to ten weeks into development, the pancreas starts producing insulin, glucagon, somatostatin, and pancreatic polypeptide. During the early on stages of fetal development, the number of pancreatic alpha cells outnumbers the numeral of pancreatic beta cells. The alpha cells reach their extremum in the center stage of gestation. From the middle stage until term, the beta cells continue to increase in issue until they reach an approximate 1:1 proportion with the alpha cells. The insulin concentration within the fetal pancreas is 3.6 pmol/g at seven to ten weeks, which rises to 30 pmol/g at 16–25 weeks of gestation. Near term, the insulin concentration increases to 93 pmol/g. The hormone cells have dispersed throughout the body within 10 weeks. At 31 weeks of growth, the islets of Langerhans have differentiated. While the fetal pancreas has functional beta cells by 14 to 24 weeks of gestation, the total of insulin that is released into the bloodstream is relatively low. In a study of pregnant women carrying fetuses in the mid-gestation and approach term stages of exploitation, the fetuses did not have an addition in plasma insulin levels in response to injections of high levels of glucose. In line to insulin, the fetal plasma glucagon levels are relatively high and continue to increase during development. At the mid-stage of gestation, the glucagon concentration is 6 μg/g, compared to 2 μg/g in pornographic humans. Just like insulin, fetal glucagon plasma levels do not change in response to an infusion of glucose. however, a study of an infusion of alanine into meaning women was shown to increase the cord blood and enate glucagon concentrations, demonstrating a fetal reply to amino acerb exposure. As such, while the fetal pancreatic alpha and beta isle cells have fully developed and are able of hormone deduction during the remaining fetal growth, the isle cells are relatively young in their capacity to produce glucagon and insulin. This is thought to be a result of the relatively stable levels of fetal serum glucose concentrations achieved via enate transfer of glucose through the placenta. On the other hand, the stable fetal serum glucose levels could be attributed to the absence of pancreatic signaling initiated by incretins during feeding. In accession, the fetal pancreatic islets cells are unable to sufficiently produce camp and quickly degrade camp by phosphodiesterase necessity to secrete glucagon and insulin. During fetal development, the repositing of glycogen is controlled by fetal glucocorticoids and placental lactogen. fetal insulin is responsible for increasing glucose uptake and lipogenesis during the stages leading up to parentage. Fetal cells contain a higher total of insulin receptors in comparison to adults cells and fetal insulin receptors are not downregulated in cases of hyperinsulinemia. In comparison, fetal haptic glucagon receptors are lowered in comparison to adult cells and the glycemic effect of glucagon is blunted. This irregular physiologic change aids the increase rate of fetal development during the final shipshape. ailing managed maternal diabetes mellitus is linked to fetal macrosomia, increased risk of spontaneous abortion, and defects in fetal development. Maternal hyperglycemia is besides linked to increased insulin levels and beta cell hyperplasia in the post-term baby. Children of diabetic mothers are at an increased risk for conditions such as : polycythemia, nephritic vein thrombosis, hypocalcemia, respiratory distress syndrome, jaundice, cardiomyopathy, congenital heart disease, and improper organ development .

Gonads [edit ]

The generative system begins development at four to five weeks of pregnancy with microbe cellular telephone migration. The bipotential gonad results from the collection of the medioventral region of the urogenital ridge. At the five-week point, the developing gonads break away from the adrenal primordium. Gonadal specialization begins 42 days following creation .

male gonadal development [edit ]

For males, the testes form at six fetal weeks and the sertoli cells begin developing by the eight workweek of gestation. SRY, the sex-determining venue, serves to differentiate the Sertoli cells. The Sertoli cells are the charge of origin for anti-Müllerian hormone. once synthesized, the anti-Müllerian hormone initiates the ipsilateral regression of the Müllerian nerve pathway and inhibits the development of female internal features. At 10 weeks of gestation, the Leydig cells begin to produce androgen hormones. The androgen hormone dihydrotestosterone is creditworthy for the development of the male external genitalia. The testicles descend during prenatal exploitation in a two-stage work that begins at eight weeks of pregnancy and continues through the middle of the third base spare. During the transabdominal stage ( 8 to 15 weeks of gestation ), the gubernacular ligament contracts and begins to thicken. The craniosuspensory ligament begins to break down. This stage is regulated by the secretion of insulin-like 3 ( INSL3 ), a relaxin-like agent produced by the testicles, and the INSL3 G-coupled receptor, LGR8. During the transinguinal phase ( 25 to 35 weeks of gestation ), the testicles descend into the scrotum. This stage is regulated by androgens, the genitofemoral boldness, and calcitonin gene-related peptide. During the second base and one-third spare, testicular development concludes with the decline of the fetal Leydig cells and the lengthen and handbuild of the seminiferous cords .

Female gonadal growth [edit ]

For females, the ovaries become morphologically visible by the 8th workweek of pregnancy. The absence of testosterone results in the diminution of the Wolffian structures. The Müllerian structures remain and develop into the fallopian pipe, uterus, and the upper region of the vagina. The urogenital venous sinus develops into the urethra and lower region of the vagina, the genital nodule develops into the clitoris, the urogenital folds develop into the labium minora, and the urogenital swellings develop into the labium majora. At 16 weeks of gestation, the ovaries produce FSH and LH/hCG receptors. At 20 weeks of pregnancy, the theca cell precursors are present and oogonia mitosis is occurring. At 25 weeks of pregnancy, the ovary is morphologically defined and folliculogenesis can begin. Studies of gene expression show that a specific complement of genes, such as follistatin and multiple cyclin kinase inhibitors are involved in ovarian development. An categorization of genes and proteins – such as WNT4, RSPO1, FOXL2, and versatile estrogen receptors – have been shown to prevent the development of testicles or the lineage of male-type cells .

pituitary gland [edit ]

The pituitary gland is formed within the rostral neural plate. The Rathke ’ s pouch, a cavity of ectodermal cells of the oropharynx, forms between the fourth and fifth workweek of gestation and upon full moon development, it gives rise to the anterior pituitary gland. By seven weeks of pregnancy, the anterior pituitary vascular organization begins to develop. During the first 12 weeks of gestation, the anterior pituitary undergoes cellular differentiation. At 20 weeks of gestation, the hypophyseal portal vein organization has developed. The Rathke ’ s pouch grows towards the third ventricle and fuses with the diverticulum. This eliminates the lumen and the structure becomes Rathke ’ sulfur cleft. The posterior pituitary lobe is formed from the diverticulum. Portions of the pituitary tissue may remain in the nasopharyngeal midplane. In rare cases this results in functioning ectopic hormone-secreting tumors in the nasopharynx. The functional development of the anterior pituitary involves spatiotemporal regulation of arrangement factors expressed in pituitary stem cells and dynamic gradients of local anesthetic soluble factors. The coordination of the dorsal gradient of pituitary morphogenesis is dependent on neuroectodermal signals from the infundibular bone morphogenetic protein 4 ( BMP4 ). This protein is responsible for the development of the initial invagination of the Rathke ’ s pouch. early essential proteins necessary for pituitary cell proliferation are Fibroblast growth factor 8 ( FGF8 ), Wnt4, and Wnt5. Ventral developmental pattern and the formulation of transcription factors is influenced by the gradients of BMP2 and sonic porcupine protein ( SHH ). These factors are essential for coordinating early patterns of cellular telephone proliferation.

Six weeks into gestation, the corticotroph cells can be identified. By seven weeks of gestation, the front tooth pituitary is able of secreting ACTH. Within eight weeks of gestation, somatotroph cells begin to develop with cytoplasmic expression of human emergence hormone. once a fetus reaches 12 weeks of development, the thyrotrophs begin formulation of Beta subunits for TSH, while gonadotrophs being to express beta-subunits for LH and FSH. Male fetuses predominately produced LH-expressing gonadotrophs, while female fetuses produce an adequate expression of LH and FSH expressing gonadotrophs. At 24 weeks of pregnancy, prolactin-expressing lactotrophs begin to emerge .

function [edit ]

Hormones [edit ]

A hormone is any of a classify of signaling molecules produced by cells in glands in multicellular organisms that are transported by the circulatory system to target aloof organs to regulate physiology and behavior. Hormones have diverse chemical structures, chiefly of 3 classes : eicosanoids, steroids, and amino acid / protein derivatives ( amines, peptides, and proteins ). The glands that secrete hormones comprise the hormone system. The term hormone is sometimes extended to include chemicals produced by cells that affect the same cell ( autocrine or intracrine sign ) or nearby cells ( paracrine signalling ). Hormones are used to communicate between organs and tissues for physiological regulation and behavioral activities, such as digestion, metabolism, breathing, tissue routine, sensory perception, sleep, body waste, lactation, stress, growth and development, motion, reproduction, and mood. [ 9 ] [ 10 ] Hormones affect distant cells by binding to specific receptor proteins in the prey cell resulting in a change in cell function. This may lead to cell type-specific responses that include rapid changes to the natural process of existing proteins, or slower changes in the formulation of target genes. Amino acid–based hormones ( amines and peptide or protein hormones ) are water-soluble and act on the come on of target cells via bespeak transduction pathways ; steroid hormones, being lipid-soluble, move through the plasma membranes of target cells to act within their nucleus .

Cell signalling [edit ]

The typical modality of cellular telephone signalling in the endocrine organization is endocrine gland signaling, that is, using the circulative system to reach distant target organs. however, there are besides early modes, i.e., paracrine, autocrine, and neuroendocrine signal. strictly neurocrine signaling between neurons, on the other handwriting, belongs completely to the anxious system .

Autocrine [edit ]

Autocrine signal is a mannequin 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 .

Paracrine [edit ]

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

Juxtacrine [edit ]

Juxtacrine signal is a type of intercellular communication that is transmitted via oligosaccharide, lipid, or protein components of a cell membrane, and may affect either the emit cell or the immediately adjacent cells. [ 11 ] It occurs between adjacent cells that own broad patches of closely opposed plasma membrane linked by transmembrane channels known as connexons. The col between the cells can normally be between lone 2 and 4 nanometer. [ 12 ]

clinical significance [edit ]

disease [edit ]

Diseases of the endocrine system are common, [ 14 ] including conditions such as diabetes mellitus, thyroid disease, and fleshiness. Endocrine disease is characterized by misregulated hormone spill ( a generative pituitary adenoma ), inappropriate response to signaling ( hypothyroidism ), miss of a gland ( diabetes mellitus type 1, diminished erythropoiesis in chronic kidney failure ), or geomorphologic enlargement in a critical site such as the thyroid gland ( toxic multinodular goiter ). Hypofunction of hormone glands can occur as a leave of passing of reservation, hyposecretion, agenesis, atrophy, or active end. Hyperfunction can occur as a consequence of hypersecretion, loss of inhibition, hyperplastic or neoplastic change, or hyperstimulation. Endocrinopathies are classified as primary, secondary, or tertiary. primary coil endocrine disease inhibits the action of downriver glands. secondary hormone disease is indicative mood of a problem with the pituitary gland. third endocrine disease is associated with dysfunction of the hypothalamus and its turn hormones. [ 15 ] As the thyroid, and hormones have been implicated in signaling distant tissues to proliferate, for exercise, 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 ask steps of oncogenesis. [ 16 ] early common diseases that result from endocrine dysfunction include Addison ‘s disease, Cushing ‘s disease and Graves ‘ disease. Cushing ‘s disease and Addison ‘s disease are pathologies involving the dysfunction of the adrenal gland gland. dysfunction in the adrenal gland could be due to primary or secondary coil 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. [ 17 ] Some clinical signs of Cushing ‘s disease include fleshiness, lunar month front, and hirsuteness. [ 18 ] Addison ‘s disease is an hormone disease that results from hypocortisolism caused by adrenal gland gland insufficiency. adrenal gland insufficiency is significant because it is correlated with decrease ability to maintain rake imperativeness and blood carbohydrate, a defect that can prove to be fatal. [ 19 ] Graves ‘ disease involves the hyperactivity of the thyroid gland gland which produces the T3 and T4 hormones. [ 18 ] Graves ‘ disease effects range from surfeit sweat, fatigue, heat intolerance and high blood pressure to well of the eyes that causes inflammation, ostentation and in rare cases reduced or double vision. [ 12 ]

other animals [edit ]

A neuroendocrine system has been observed in all animals with a nervous system and all vertebrates have a hypothalamus-pituitary axis. [ 20 ] All vertebrates have a thyroid gland, which in amphibians is besides crucial for transformation of larva into adult form. [ 21 ] [ 22 ] All vertebrates have adrenal gland gland tissue, with mammals unique in having it organized into layers. [ 23 ] All vertebrates have some form of a renin–angiotensin axis, and all tetrapods have aldosterone as a primary mineralocorticoid. [ 24 ] [ 25 ]

extra images [edit ]

See besides [edit ]

References [edit ]

  • Media related to Endocrine system at Wikimedia Commons

Leave a Reply

Your email address will not be published.