Endocrine system
Endocrine system | |
---|---|
Details | |
Identifiers | |
Latin | systema endocrinum |
MeSH | D004703 |
FMA | 9668 |
Anatomical terminology |
The endocrine system[1] is a messenger system in an organism comprising feedback loops of hormones that are released by internal glands directly into the circulatory system and that target and regulate distant organs. In vertebrates, the hypothalamus is the neural control center for all endocrine systems.
In
Glands that signal each other in sequence are often referred to as an axis, such as the hypothalamic–pituitary–adrenal axis. In addition to the specialized endocrine organs mentioned above, many other organs that are part of other body systems have secondary endocrine functions, including bone, kidneys, liver, heart and gonads. For example, the kidney secretes the endocrine hormone erythropoietin. Hormones can be amino acid complexes, steroids, eicosanoids, leukotrienes, or prostaglandins.[3]
The endocrine system is contrasted both to
Structure
Major endocrine systems
The human endocrine system consists of several systems that operate via
- TRH – TSH – T3/T4
- GnRH – LH/FSH – sex hormones
- CRH – ACTH – cortisol
- Renin – angiotensin – aldosterone
- Leptin vs. ghrelin
Glands
Endocrine glands are
The hypothalamus and the anterior pituitary are two out of the three endocrine glands that are important in cell signaling. They are both part of the HPA axis which is known to play a role in cell signaling in the nervous system.
Hypothalamus: The hypothalamus is a key regulator of the autonomic nervous system. The endocrine system has three sets of endocrine outputs[5] which include the magnocellular system, the parvocellular system, and autonomic intervention. The magnocellular is involved in the expression of oxytocin or vasopressin. The parvocellular is involved in controlling the secretion of hormones from the anterior pituitary.
Anterior Pituitary: The main role of the anterior pituitary gland is to produce and secrete tropic hormones.[6] Some examples of tropic hormones secreted by the anterior pituitary gland include TSH, ACTH, GH, LH, and FSH.
Cells
There are many types of cells that make up the endocrine system and these cells typically make up larger tissues and organs that function within and outside of the endocrine system.
- Hypothalamus
- Anterior pituitary gland
- Pineal gland
- Posterior pituitary gland
- The posterior pituitary gland is a section of the pituitary gland. This organ does not produce any hormone but stores and secretes hormones such as antidiuretic hormone (ADH) which is synthesized by supraoptic nucleus of hypothalamus and oxytocin which is synthesized by paraventricular nucleus of hypothalamus. ADH functions to help the body to retain water; this is important in maintaining a homeostatic balance between blood solutions and water. Oxytocin functions to induce uterine contractions, stimulate lactation, and allows for ejaculation.[7][8]
- Thyroid gland
- T4 in response to elevated levels of TRH, produced by the hypothalamus, and subsequent elevated levels of TSH, produced by the anterior pituitary gland, which further regulates the metabolic activity and rate of all cells, including cell growth and tissue differentiation.
- Parathyroid gland The endocrine system can control all emotions and can control temperature.
- Thymus Gland
- Adrenal glands
- Pancreas
- Pancreas contain nearly 1 to 2 million islets of Langerhans (a tissue which consists cells that secrete hormones) and acini. Acini secretes digestive enzymes.[9]
- Alpha cells
- The alpha cells of the pancreas secrete hormones to maintain homeostatic blood sugar. Insulin is produced and excreted to lower blood sugar to normal levels. Glucagon, another hormone produced by alpha cells, is secreted in response to low blood sugar levels; glucagon stimulates glycogen stores in the liver to release sugar into the bloodstream to raise blood sugar to normal levels.[10]
- Beta cells
- 60% of the cells present in islet of Langerhans are beta cells. Beta cells secrete insulin. Along with glucagon, insulin helps in maintaining glucose levels in our body. Insulin decreases blood glucose level ( a hypoglycemic hormone) whereas glucagon increases blood glucose level.[9]
- Delta cells
- F Cells
- Alpha cells
- Pancreas contain nearly 1 to 2 million islets of Langerhans (a tissue which consists cells that secrete hormones) and acini. Acini secretes digestive enzymes.[9]
- Ovaries
- Testis
Development
The fetal endocrine system is one of the first systems to develop during prenatal development.
Adrenal glands
The fetal adrenal cortex can be identified within four weeks of gestation. The adrenal cortex originates from the thickening of the intermediate mesoderm. At five to six weeks of gestation, the mesonephros differentiates into a tissue known as the genital ridge. The genital ridge produces the steroidogenic cells for both the gonads and the adrenal cortex. The adrenal medulla is derived from ectodermal cells. Cells that will become adrenal tissue move retroperitoneally to the upper portion of the mesonephros. At seven weeks of gestation, the adrenal cells are joined by sympathetic cells that originate from the neural crest to form the adrenal medulla. At the end of the eighth week, the adrenal glands have been encapsulated and have formed a distinct organ above the developing kidneys. At birth, the adrenal glands weigh approximately eight to nine grams (twice that of the adult adrenal glands) and are 0.5% of the total body weight. At 25 weeks, the adult adrenal cortex zone develops and is responsible for the primary synthesis of steroids during the early postnatal weeks.
Thyroid gland
The thyroid gland develops from two different clusterings of embryonic cells. One part is from the thickening of the pharyngeal floor, which serves as the precursor 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 day of gestation, the foramen cecum, a thin, flask-like diverticulum of the median anlage develops. At approximately 24 to 32 days of gestation the median anlage develops into a bilobed structure. By 50 days of gestation, the medial and lateral anlage have fused together. At 12 weeks of gestation, the fetal thyroid is capable of storing iodine for the production of TRH, TSH, and free thyroid hormone. At 20 weeks, the fetus is able to implement feedback mechanisms for the production of thyroid hormones. During fetal development, T4 is the major thyroid hormone being produced while triiodothyronine (T3) and its inactive derivative, reverse T3, are not detected until the third trimester.
Parathyroid glands
A lateral and ventral view of an embryo showing the third (inferior) and fourth (superior) parathyroid glands during the 6th week of embryogenesis
Once the embryo reaches four weeks of gestation, the parathyroid glands begins to develop. The human embryo forms five sets of endoderm-lined pharyngeal pouches. The third and fourth pouch are responsible for developing into the inferior and superior parathyroid glands, respectively. The third pharyngeal pouch encounters the developing thyroid gland and they migrate down to the lower poles of the thyroid lobes. The fourth pharyngeal pouch later encounters the developing thyroid gland and migrates to the upper poles of the thyroid lobes. At 14 weeks of gestation, the parathyroid glands begin to enlarge from 0.1 mm in diameter to approximately 1 – 2 mm at birth. The developing parathyroid glands are physiologically functional beginning in the second trimester.
Studies in mice have shown that interfering with the HOX15 gene can cause parathyroid gland aplasia, which suggests the gene plays an important role in the development of the parathyroid gland. The genes, TBX1, CRKL, GATA3, GCM2, and SOX3 have also been shown to play a crucial role in the formation of the parathyroid gland. Mutations in TBX1 and CRKL genes are correlated with DiGeorge syndrome, while mutations in GATA3 have also 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 role in parathyroid development. These mutations also lead to varying degrees of hypopituitarism.
Pancreas
The human fetal
While the fetal pancreas has functional beta cells by 14 to 24 weeks of gestation, the amount of insulin that is released into the bloodstream is relatively low. In a study of pregnant women carrying fetuses in the mid-gestation and near term stages of development, the fetuses did not have an increase in plasma insulin levels in response to injections of high levels of glucose. In contrast 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 adult 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 pregnant women was shown to increase the cord blood and maternal glucagon concentrations, demonstrating a fetal response to amino acid exposure.
As such, while the fetal pancreatic alpha and beta islet cells have fully developed and are capable of hormone synthesis during the remaining fetal maturation, the islet cells are relatively immature in their capacity to produce glucagon and insulin. This is thought to be a result of the relatively stable levels of fetal
During fetal development, the storage of glycogen is controlled by fetal
Gonads
The reproductive system begins development at four to five weeks of gestation with germ cell 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 differentiation begins 42 days following conception.
Male gonadal development
For males, the
The testicles descend during prenatal development in a two-stage process that begins at eight weeks of gestation and continues through the middle of the third trimester. 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 factor 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 nerve, and calcitonin gene-related peptide. During the second and third trimester, testicular development concludes with the diminution of the fetal Leydig cells and the lengthening and coiling of the seminiferous cords.
Female gonadal development
For females, the ovaries become morphologically visible by the 8th week of gestation. The absence of testosterone results in the diminution of the Wolffian structures. The Müllerian structures remain and develop into the fallopian tubes, uterus, and the upper region of the vagina. The urogenital sinus develops into the urethra and lower region of the vagina, the genital tubercle develops into the clitoris, the urogenital folds develop into the labia minora, and the urogenital swellings develop into the labia majora. At 16 weeks of gestation, the ovaries produce FSH and LH/hCG receptors. At 20 weeks of gestation, the theca cell precursors are present and oogonia mitosis is occurring. At 25 weeks of gestation, 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 assortment of genes and proteins - such as WNT4, RSPO1, FOXL2, and various estrogen receptors - have been shown to prevent the development of testicles or the lineage of male-type cells.
Pituitary gland
The
The functional development of the anterior pituitary involves spatiotemporal regulation of transcription factors expressed in pituitary stem cells and dynamic gradients of local 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. Other essential proteins necessary for pituitary cell proliferation are
Six weeks into gestation, the
Function
Hormones
A
Hormones are used to communicate between
Hormones affect distant cells by binding to specific
Cell signalling
The typical mode of
Autocrine
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.
Paracrine
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.[3]
Juxtacrine
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.[14]
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.[15]
Clinical significance
Disease
. Endocrine disease is characterized by misregulated hormone release (a productiveEndocrinopathies 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.[18]
As the
Other 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. 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.[20] Some clinical signs of Cushing's disease include obesity, moon face, and hirsutism.[21] 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.[22]
Graves' disease involves the hyperactivity of the thyroid gland which produces the T3 and T4 hormones.
Other animals
A neuroendocrine system has been observed in all
Additional images
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Female endocrine system
-
Male endocrine system
See also
- Endocrine disease
- Endocrinology
- List of human endocrine organs and actions
- Neuroendocrinology
- Nervous system
- Paracrine signalling
- Releasing hormones
- Tropic hormone
References
- ^ "Anatomy of the Endocrine System". www.hopkinsmedicine.org. November 19, 2019. Retrieved June 14, 2022.
- ISBN 978-1259589287.
- ^ ISBN 978-0-321-86158-0.
- ISBN 978-0-495-39184-5.
- S2CID 18782796.
- ^ "Chapter 3. Anterior Pituitary Gland". Endocrine Physiology (4 ed.). McGraw Hill. 2013.
- PMID 18669612.
- )
- ^ a b "267 Endocrine System Facts". Facts Legend. September 19, 2018.
- PMID 30252386.
- ^ "Leydig cell | anatomy". Britannica. Retrieved June 14, 2022.
- ISBN 978-0-521-69201-4.
- Claire L. Gibson (Winter 2010). "Hormones and Behaviour: A Psychological Approach". Perspectives in Biology and Medicine (Review). 53 (1): 152–155. S2CID 72100830.
- Claire L. Gibson (Winter 2010). "Hormones and Behaviour: A Psychological Approach". Perspectives in Biology and Medicine (Review). 53 (1): 152–155.
- ^ "Hormones". MedlinePlus. U.S. National Library of Medicine.
- ISBN 0-87893-243-7.
- ^ ISBN 978-0-07-304962-5.
- ^ "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002.
- ISBN 978-0-07-139140-5.
- OCLC 632070527.
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- ^ ISBN 978-0-07-304962-5.
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- JSTOR 3882951.
- JSTOR 3883279.
- PMID 4941407.
- PMID 6368215.
- S2CID 25316873.
External links
- Media related to Endocrine system at Wikimedia Commons