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The hypothalamus produces gonadotrophin releasing hormone (GnRH) that induces gonadotroph cells in the anterior pituitary gland to release FSH that induces development of ovarian follicles which contain an ovum, and LH that induces ovulation of the mature Graffian ovarian follicles.
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Hypothalamic Cell Models
Metabolism and satiety
The hypothalamus-pituitary system in nonmammalian vertebrates
E The hypothalamus of reptiles
Disorders of the Endocrine System
Hypothalamus
Studies on Estradiol-binding in Mammalian Tissues
3. Hypothalamus
Endocrine, nutritional, and metabolic diseases
Incoming signals
Genetic Factors in Mouse Obesity
Anatomy of Teleosts and elasmobranchs
Endocrine system
Endocrinology
Hypothalamus
Corticotropic axis
A brief discussion of the hypothalamus and pituitary glands
What are the releasing and inhibiting hormones of the hypothalamus?
What is the function of releasing and inhibiting hormone?
What hormone requires a releasing hormone from the hypothalamus?
What activities does the hypothalamus control?
From: Animal Agriculture, 2020
Hypothalamic Cell Models
Prasad Dalvi, … Denise D. Belsham, in Cellular Endocrinology in Health and Disease (Second Edition), 2021
Abstract
The hypothalamus is a vital and an integral part of the central nervous
system as it regulates a wide range of physiological and psychological processes, including energy homeostasis, reproduction, circadian rhythms, as well as emotional and behavioral patterns. Structurally, the hypothalamus is a complex neuroendocrine tissue composed of an array of unique neuronal cell types that express critical neuromodulators required to mediate hypothalamic function. Until recently, the properties of these hypothalamic neurons were challenging to study, primarily because of
the heterogeneity and complex neuronal architecture of the neuroendocrine hypothalamus. However, hypothalamic neuronal cell models have proved to be a useful in vitro tool in understanding hypothalamic function and disorders. This chapter discusses the hypothalamic cell models that have been generated to date primarily to study mechanisms underlying the function of individual hypothalamic neurons in order to gain a more complete understanding of the overall physiology and
A. Rodríguez, … G. Frühbeck, in Satiation, Satiety and the Control of Food Intake, 2013
Abstract:
The hypothalamus is a centre of convergence and integration of multiple nutrient-related signals.
Important short-term signals are conveyed by hormones, cytokines and/or fuel substrates, which are sensed through a variety of cellular mechanisms in order to maintain energy homeostasis. Nevertheless, there are also long-term signals secreted from the adipose tissue (adipokines) that inform the hypothalamus about the size of adipose tissue depots. The present chapter reviews how short- and long-term mechanisms operate in concert to provide an appropriate regulation of satiety, and focuses on
emerging knowledge of the metabolic effects of adipokines on energy homeostasis.
The hypothalamus-pituitary system in nonmammalian vertebrates
David O. Norris PhD, James A. Carr PhD, in Vertebrate Endocrinology (Sixth Edition), 2021
E The hypothalamus of reptiles
The reptilian hypothalamus is depicted in Fig. 5.7. In
reptiles, there is no longer a PON, but the medial and lateral POAs are present. The PON of anamniotes has separated into the supraoptic nucleus (SON) and paraventricular nucleus (PVN) characteristic of all amniote vertebrates. These paired nuclei consist of peptidergic NS neurons that produce the octapeptide neurohormones AVT and MST. Their axons terminate in the pars nervosa. The hypothalamus is separated into anterior, dorsal, and posterior hypothalamic areas, paraventricular organs, periventricular nucleus, and both ventral and dorsal medial nuclei. The IFN, also called the ARC, is considered homologous to the VH of the amphibian IFN and the ARC nucleus (= IFN) of birds as well as to the major hypophysiotropic area of the mammalian hypothalamus. Aminergic and peptidergic NS
fibers originate in this nucleus and terminate in the median eminence.
Figure 5.7. Hypothalamus of a reptile, the Japanese forest rat snake
(Elaphe conspicillata).
(A) Sagittal section. (B–D) Cross sections at levels indicated in part A. AHA, DHA, LHA, PHA, Anterior dorsal, lateral, and posterior hypothalamic areas, respectively; DMN, dorsomedial nucleus; PVN, ventricular nucleus; PVO, paraventricular organ; VMN, ventromedial nucleus. See Figs 5.5 and 5.6 for other abbreviations.
Adapted with permission from Matsumoto, A., Ishii, S., 1989.
Atlas of Endocrine Organs: Vertebrates and Invertebrates. Springer-Verlag, Berlin.
Stephen M. Reed DVM, Dipl ACVIM, … Debra C. Sellon DVM, PhD, Dipl ACVIM, in Equine Internal Medicine (Fourth Edition), 2018
Hypothalamus
The hypothalamus is located in the ventral diencephalon and below the thalamus. It is part of the
limbic system (with the hippocampus, amygdala, thalamic nuclei, mammillary body toàn thân, limbic cortex, and other structures) and mediates autonomic, endocrine, and behavioral functions. It is the master regulator of numerous physiologic processes.529,530 It generates and receives humoral and neural information; coordinates different levels of autonomic communication between the CNS and central and peripheral organs; and regulates body toàn thân temperature, hunger, thirst,
circadian and circannual rhythmicity, sleep, reproductive drive, sexual dimorphism, growth, behavior, metabolic activity, and other essential functions.529-531 The hypothalamus connects via neural circuits to other structures of the CNS but also sends and receives humoral information. A good example of hypothalamic humoral connection is with the pituitary gland via the portal system in the median eminence.529,530
Histologically, the hypothalamus is arranged in a series of nuclei with magnocellular and parvocellular neurons that secrete releasing (e.g., corticotropin-releasing hormone [CRH], thyrotropin-releasing hormone [TRH], growth hormone–releasing hormone [GHRH], gonadotropin-releasing hormone [GnRH]) and inhibitory (e.g., somatostatin, dopamine) factors into the pituitary portal system to control hormone synthesis and secretion by the adenohypophysis (e.g.,
adrenocorticotropic hormone [ACTH], growth hormone [GH], thyroid-stimulating hormone [TSH], prolactin).532,533 The hypothalamus also produces peptides that are stored in the neurohypophysis (e.g., oxytocin, vasopressin), as well as factors that modulate melanotrope activity in the pituitary pars intermedia (e.g., dopamine, serotonin, TRH). The hypothalamus is responsive to peripheral hormones (leptin, ghrelin, insulin, steroids, thyroid hormones), metabolites (glucose),
electrolytes (sodium), neural stimuli (light, smell, touch, vascular pressure, pheromones, temperature, input from the thorax, gastrointestinal tract, and reproductive tract), cytokines, and microbial products. The level at which hypothalamic neurons are stimulated or suppressed is dictated by set-points specific to each function (e.g., thermoregulation, thirst, osmolality, blood pressure).532,533
Peptides and large molecules are
sensed or gain access to hypothalamic neurons through circumventricular organs, including the subfornical organ and the organum vasculosum of the lamina terminalis. These structures have a fenestrated endothelium and lack an effective blood-brain barrier allowing the hypothalamus to continuously sample systemic circulation and relay information to different parts of the CNS and are essential for feedback regulatory mechanisms that modulate neuroendocrine function.533
R.J.B. King, … M. Vértes, in Schering Workshop on Steroid Hormone ‘Receptors’, Berlin, December 7 to 9, 1970, 1971
3. Hypothalamus
The hypothalamus is thought to regulate both the development and continuation of the estrus cycle in female rats and we have studied the role of 3H-estradiol binding in relation to these functions [45, 46]. Both the anterior and posterior hypothalamus contain nuclear and
cytoplasmic receptors(Fig. 12) and more binding occurs in the anterior than posterior part of the hypothalamus. It is not known if this is due to more receptor sites per cell or to a greater number of receptive cells per unit weight of tissue. The neonatal administration of androgen to female rats alters the function of the preoptic region of the hypothalamus producing permanent alteration in ovarian, uterine and vaginal function [4] and we wondered if this was mediated
via the 3H-estradiol binding mechanism. At 28 days of age, the anterior hypothalamus from androgenised female rats had a lower nuclear and higher cytoplasmic uptake of 3H-estradiol in vivo, an effect that was not obtained with posterior hypothalamus or cortex. By 60 days of age, androgenisation had decreased binding in both these subcellular fractions (Fig. 13). Because of the 26 day gap between androgen and 3H-estradiol injection these
effects cannot be due to competition between the two steroids for receptor sites. In any case, testosterone does not compete with 3H-estradiol in either the anterior or posterior hypothalamus. The exact mechanism whereby androgen produces this effect on the anterior hypothalamus is not known but it could be explained by a primary defect in either the transport or nuclear acceptor mechanism giving the results seen in the 28 day old animals; by 60 days this might lead to an overall drop
in receptor sites. Such an hypothesis would require proof that prolonged lack of nuclear retention leads to an overall decrease in binding. Such evidence is not available. How does androgen exert this effect? Kato [18] has shown that the hypothalamic estradiol binding mechanism is not functional in neonatal rats so androgenisation may affect the development of the receptor mechanism rather than blocking an existing function. We would also like to know if the androgenisation
effect is similar to the mechanism whereby the cycling activity of the preoptic nucleus in males is switched off on day 4/5 of life. Could this be explained by the presence of androgen receptors in both neonatal male and female hypothalamus which are switched off by androgen in the female?
Fig. 12. Cytoplasmic and nuclear receptors in anterior and posterior hypothalamus. Regions of the brain were labelled with 1 nM 3H-estradiol and washed twice with unlabelled medium. The
hypothalamus was removed as a block limited anteriorly about 1 mm before the optic chiasma, laterally by the hypothalamic fissures and posteriorly by a line just behind the mamillary bodies. Its depth was about 2 mm. The block was divided into anterior and posterior portions by section through the infundibulum. The tissue was homogenised as described in fig. 7Fig. 12a 105 xg supernatant. Fig. 12b 0.3 M KC1 extract of 105 xg/pellet.
anterior hypothalamus; – posterior hypothalamus;
cortex.
Fig. 13. Effect of neonatal androgenisation on 3H-estradiol uptake by brain and pituitary. Female rats received 1 mg testosterone propionate on the 2nd day of life. At either 28 (Fig. 13a) or 60 days (Fig. 13b) of age, the animals were injected with 0.1 μg 3H-estradiol/100 g body toàn thân weight 1 hr before death. Hypothalamus was separated into anterior and posterior portions as described in fig.
12, homogenised in 10 mM Tris 1 mM EDTA pH 7.4 and separated into 700 xg pellet and supernatant. The 700 xg pellet was extracted with 0.3 M KCl for 15 min. The supernatant was treated with an equal volume of protamine sulphate (7 mg/ml water) for 10 min and the pellet sedimented at 103 xg for 10 min.
androgen treated. Results are expressed as the mean ± S.D. of at least 4 estimations. The S.D. has been omitted in those cases where it was too small for visual
display. Significance of the difference between treated and control groups • p. <0.05; ○ p. < 0.01; ▪ p. < 0.001.
Anastasia P. Nesterova, … Anton Yuryev, in Disease Pathways, 2020
Incoming signals
The hypothalamus secretes thyrotropin-releasing hormone (TRH) that in turn induces the secretion of thyroid-stimulating hormone (TSH) from the
anterior pituitary gland.
Fig. 16. Pathway 1: Decreased secretion of thyroid hormones.
TSH stimulates the thyroid gland to produce the thyrotrophic hormones thyroxine (T4) and to a lesser extent triiodothyronine (T3). T4 synthesis relies on the availability of sufficient levels of iodine. T4 has low biological activity, and it is converted into the more active T3 by the selenium-dependent deiodinase in peripheral tissues. Therefore, iodine and selenium are essential for the production of thyroid hormones.
Circulating
levels of T3 and T4 provide negative feedback regulation of TRH and TSH production. Both thyroid hormones, through their nuclear receptors (THRB and THRA), directly inhibit the synthesis and release of TSH in pituitary cells. Also, T3 inhibits the preprocessing of the TRH protein in the hypothalamus.
The destruction of thyroid follicles by autoreactive CD4 T cells in Hashimoto’s thyroiditis is considered the most common cause of dysfunctional secretion
of thyroid hormones. Overall the molecular mechanisms leading to decreased thyroid hormone production are not well understood.
TOM BRODY, in Nutritional Biochemistry (Second Edition), 1999
Genetic Factors in Mouse Obesity
Several strains of mice have been discovered that are naturally genetically obese. The genetic defects have been traced to specific genes and to changes in the corresponding polypeptides. These polypeptides occur in various tissues in the body toàn thân, but one thing they have in common is that they all act in the hypothalamus.
Thus, an appreciation of the genetic factors of mouse obesity requires some background in the physiology of the hypothalamus.
Physiology of the Hypothalamus
The hypothalamus has long been suspected as being an important regulator of feeding behavior. Work during the 1950s revealed that physical damage inflicted to parts of the hypothalamus
result in increases or decreases in food intake and body toàn thân weight. A cross-section of the hypothalamus of the rat is shown in Figure 7.14.
FIGURE 7.14. Cross-section of the hypothalamus of the rat and
regions used to trigger hunger and satiety. The hypothalamus contains regions called the ventromedial hypothalamus (VMH) and the ventrolateral hypothalamus (LH). Lesions in the ventromedial region cause overeating and obesity. Lesions in the ventrolateral region cause less eating and loss in weight. The arcuate nucleus (ARN) of the hypothalamus is the site of synthesis of melanocortin hormones, where these hormones include POMC (pro-opiomelanocortin), ACTH, MSH, and LPH. POMC is a 265-amino-acid
polypeptide that is the precursor of ACTH (39 amino acids), MSH (13 amino acids), and LPH (39 amino acids). The arcuate nucleus is also the site of synthesis of neuropeptide Y. Neurones extend from the arcuate nucleus (site of NPY synthesis) and convey NPY to the dorsomedial hypothalamic nucleus (DMH) and paraventricular nucleus (not shown). The DMH is also involved in melanocortin metabolism, since MC4 receptors (which bind melanocortin) occur in the ventromedial nucleus (VMH). The VMH and LH
are connected via the DMH. Other structures are the corpus callosum (CC), cerebral cortex (CCX), hippocampus (HI), and optic tract (T).
(Redrawn by permission from Schwartz et al. 1992.)
The hypothalamus contains regions called the ventromedial hypothalamus and the ventrolateral hypothalamus. The following commentary serves to emphasize the importance of the
hypothalamus in the control of eating. Lesions (intentional damage) in the ventromedial region cause overeating and obesity, and provoke a decline in glucagon secretion. The ventromedial region is called the satiety center of the brain. The normal function of the ventromedial region is to inhibit the activity of the lateral region. Electrical stimulation of the ventromedial region provokes increased glucagon secretion and an increase in the activity of
glycogen phosphorylase (and thus glycogen breakdown) in the liver. This effect is mediated by nerves leading to the liver. Lesions in the ventrolateral region cause less eating and loss in weight. The ventrolateral region is called the feeding center of the brain. The satiety center acts by inhibiting the activity of the feeding center. Electric stimulation of the ventrolateral region of the
hypothalamus provokes an increase in activity of liver glycogen synthase (Rohner-Jeanrenaud, 1995; Lynch et al. 1997).
The study of obesity has been aided by the occurrence of certain strains of mice that are genetically obese. These mice arose spontaneously in various animal colonies over the past few decades. Five separate strains have been maintained and bred. Their names and abbreviations are: (1) obese (ob), (2)
The names of these strains are used to refer to the strain of mouse, to the genetic makeup, to the specific gene that may be affected, and to the protein (if any) made by the gene. In recent years, the specific genes that are responsible for obesity have been identified for these strains. The obese gene (ob gene) codes
for leptin, a hormone that circulates in the bloodstream. The hormone, in humans, is 116 amino acids long (Considine et al. 1995). The diabetes gene (db gene) codes for the leptin receptor, i.e., for a membrane-bound protein. The protein is rather large and consists of 1178 amino acids (Caro et al. 1996).
… Bernardo Baldisserotto, in Biology and Physiology of Freshwater Neotropical Fish, 2020
Endocrine system
The hypothalamus, which functions as an interface between the nervous and endocrine systems, resides ventrally to the thalamus in the lower portion of the brain (Fig. 2.25). The hypothalamus produces several hormones (Ogawa and Parhar, 2013; Biran et al., năm ngoái), and is connected to another endocrine structure, the pituitary gland. The pituitary is parted into neurohypophysis and adenohypophysis, the last one comprising the rostral pars
distalis, proximal pars distalis, and pars intermedia. Some neurosecretory cells of the hypothalamus have their axons ending at the neurohypophysis, which stores and releases the hormones produced by these cells (Table 2.2) to the rest of the body toàn thân. Teleosts do not have the hypothalamic-pituitary-portal vascular system, which carries the blood passing through the hypothalamus directly to the adeno-hypophysis. However, hypothalamic neurosecretory cells release hormones that influence
the production and release of adenohypophysial hormones (Table 2.2).
Fig. 2.25. Simplified representation of the
localization of some endocrine structures. C, caudal neurosecretory system (urophysis); D, digestive tract; K, kidney; G, gonads (ovary or testis); H, hypothalamus-pituitary; He, heart; i, interrenal cells; L, liver; P, pancreas; Pi, pineal; Sc, Stannius corpuscles; T, thyroid follicles; U, ultimobranchial gland.
(Modified from Baldisserotto, B. 2013. Fisiologia de Peixes
Aplicada à Piscicultura. EDUFSM, Santa Maria.)
Table 2.2. Main endocrine organs of Teleosts, hormones and their main functions
Organ
Hormones
Functions
Brain/hypothalamus
Kisspeptin
Regulator of reproduction
Hypothalamus
Arginine vasotocin (AVT)
It stimulates spawning reflexes and reproductive behavior, adrenocorticotropic hormone (ACTH) release, contraction of the smooth muscle of the blood vessels of the gills, decreases the formation and elimination of urine
Isotocin
It increases spermatozoids in sperm
Melanin-concentrating hormone (MCH)
It stimulates the aggregation of pigments in melanophores, xanthophores, and erythrophores
Gonadotropin-releasing hormone (GNRH)
It stimulates the release of gonadotropins
Dopamine
It inhibits the release of gonadotropins
Corticotropin-releasing hormone (CRH)
It stimulates the release of ACTH and melanocyte-stimulating hormone (α-MSH)
Thyrotropin-releasing hormone (TRH)
It stimulates the release of thyrotropin and α-MSH
Somatostatin
It inhibits the release of the growth hormone (GH)
Growth hormone-releasing hormone (GHRH)
It stimulates the release of GH
Prolactin-releasing peptide (or factor) (PRRP)
It stimulates the release of prolactin
Adenohypophysis
Growth hormone (GH)
It stimulates the secretion of insulin growth factors (IGF-I and IGF-II)
Prolactin
It stimulates osmoregulatory adaptations to freshwater
Somatolactin
It is related to physiological responses to stress, regulation of calcium, phosphate, and acid-base equilibrium
Adrenocorticotropic hormone or corticotropin (acth)
It stimulates cortisol secretion and proliferation of interrenal cells
Follicle-stimulating hormone or gonadotropin I (GTH I)
It stimulates estradiol release by the ovarium, gonadal growth, gametogenesis, and the vitellogenin uptake by the oocyte
Luteinizing hormone or gonadotropin II (GTH II)
It stimulates final gamete maturation and release
Thyroid-stimulating hormone or thyrotropin (TSH)
It stimulates thyroid growth and secretion
Melanocyte-stimulating hormone (α-MSH)
It stimulates melanin production and pigment dispersion in the skin
Parathyroid hormone-related protein (PTHRP)
Hipercalcemic effect
Thyroid
Triiodothyronine (T3) and thyroxine (T4)
They stimulate metabolism, growth, and metamorphosis
Chromaffin cells
Adrenaline (epinephrine) and noradrenaline (norepinephrine)
They stimulate physiological changes related to acute stress
Interrenal cells
Cortisol
immunosuppression, hyperglycemia, osmoregulatory adaptations to seawater
Pancreas
Insulin
It stimulates the synthesis and storage of nutrients in the cells
Movements and secretions of gastrointestinal tract
Heart
Natriuretic peptides (or factors
Vasodilation and reduction of blood pressure, also stimulates diuresis
Pineal
Melatonin
Synchronization of reproductive period
Ultimobranchial gland
Calcitonin
Hypocalcemia
Stannius corpuscles
Stanniocalcin
Antihypercalcemic
Caudal neurosecretory system
Urotensin I (UI)
It stimulates ACTH and cortisol release, freshwater adaptation (?)
Urotensin II (UII)
It stimulates contraction of smooth muscles, freshwater adaptation (?)
The adenohypophysis produces several hormones that act directly in some organs, but others regulate the production and release of hormones from endocrine glands (Whittington and Wilson, 2013; Martos-Sitcha et al., năm trước. Prado-Lima and Val, năm ngoái; Ah and Khairnar, 2018). These endocrine glands and other organs that release hormones are in Table 2.2 and Fig. 2.25.
Amitava Dasgupta Ph.D, DABCC, Amer Wahed M.D, FRCPath (UK), in Clinical Chemistry, Immunology and Laboratory Quality Control
(Second Edition), 2021
Hypothalamus
The hypothalamus produces thyrotropin-releasing hormone (TRH), corticotrophin hormone (CRH), gonadotropin-releasing hormone (GnRH), growth hormone-releasing hormone (GRH), and somatostatin (growth hormone inhibitory hormone). These hormones act on the anterior pituitary resulting in release of various other hormones, including
thyroid-stimulating hormone (TSH), adrenocorticotropin (ACTH), FSH, LH, and GH. Somatostatin inhibits the release of GH. Dopamine (also known as prolactin inhibitory hormone), a neurotransmitter, is also produced by the hypothalamus. Dopamine can inhibit GH secretion.
The supra optic and paraventricular nuclei of the hypothalamus produce antidiuretic hormone (ADH; also known as vasopressin) and oxytocin. These hormones are stored in the posterior pituitary
and act on certain body toàn thân parts rather than acting on pituitary like other tropic hormones. ADH acts on the collecting ducts of the renal tubules and causes absorption of water. ADH secretion is linked to serum osmolality, and increased serum osmolality results in increased secretion of ADH. Lesions of the hypothalamus may result in inadequate ADH secretion, also known as cranial diabetes insipidus. Failure of ADH to act on the collecting ducts results in nephrogenic diabetes insipidus. Causes of
nephrogenic diabetes insipidus include hypercalcemia, hypokalemia, and lithium therapy. In both types of diabetes insipidus, polyuria with low osmolality is common symptoms. Please see Chapter 5 for more detail.
Oxytocin is a nonapeptide hormone (nine amino acids) primarily synthesized in the magnocellular neurons of paraventricular and supraoptic nuclei of hypothalamus, and most of oxytocin produced is transported to the posterior
pituitary where it is released to regulate parturition and lactation. In addition, oxytocin plays an important role in the development of the capacity to form social bonds, the mediation of the positive aspects of early-life nurturing on adult bonding capacity, and the maintenance of social bonding [2]. Hormones released by hypothalamus and their characteristics are listed in Table 2.
Table 2. Characteristics of hormones released by hypothalamus.
Kamyar M. Hedayat, Jean-Claude Lapraz, in The Theory of
Endobiogeny, 2019
A brief discussion of the hypothalamus and pituitary glands
The hypothalamus contains the master regulating hormones of the endocrine system. In the classical endocrine consideration, hypothalamic hormones stimulate pituitary hormones in a vertical feed forward action and are inhibited in turn by these hormones through feedback. While this is certainly
true, the role of the hypothalamus is more complex. It is itself subjected to regulation by the pineal gland.1 It is the origin of classical hormones which are in turn neurotransmitters (TRH, histamine),2 regulators of the global energy economy (pro-opiomelanocortin, αMSH),3 consolidators of dreams and memory (growth hormone releasing hormone),4, 5 and many other divergent tasks. Thus, we find
that a more complete consideration of hypothalamic hormones must include these various activities.
The pituitary gland consists of three lobes: anterior, intermediate, and posterior. The anterior lobe contains the majority of pituitary hormones and includes all those that regulate the four endocrine axes: corticotropic (POMC, ATCH, β-lipotropin), gonadotropic (FSH, LH), thyrotropic (TSH), and somatotropic (GH).6 The intermediate lobe
is exclusively dedicated to POMC derivatives of the corticotropic axis (MSH family, endorphins, γ-lipotropin, ACTH).7 The posterior pituitary contains two key and unique hormones: vasopressin and oxytocin.8 According to the theory of Endobiogeny, pituitary hormones have direct inter- and intra-axial peripheral activities that complement the activity of its peripheral glands. This is where the notion of the axial arrangement of hormones in
alternating catabolic and anabolic functions (Chapter 4) reveals a logic that allows us to develop a coherence theory of complex systems regulation. For example, catabolic ACTH stimulates the “adjacent” axial hormone anabolic FSH, and anabolic FSH stimulates its “adjacent” axial hormone TSH, etc. (Chapter 10). What is more, pituitary hormones have extra-axial activity on other endocrine glands and nonendocrine glands. In the assessment of clinical disorders of
adaptation, it is important to evaluate the role of central factors, peripheral factors, and central-peripheral interactions, both within each axis and across axes as they relate to one another in a coherent and logical manner.
The relationship of the hypothalamus to the pituitary is functional in nature. The hypothalamus is not adjoining the pituitary. Its hormones are discharged by nerve terminals into the hypophyseal portal drainage system
that baths the anterior pituitary cells. Thus, all hypothalamic hormones are neurohormones. An overview of the general relationship reveals a few interesting observations:6 (1) prolactin is the only pituitary hormone not regulated by a hypothalamic hormone within its own axis. It is regulated by the hormone TRH9 and the neurotransmitter dopamine,10 (2) the cells that produce growth hormone take up about 50% of the
anterior pituitary,11 and (3) approximately two-thirds of the total volume of the anterior pituitary is dedicated exclusively to somatotropic hormones, indicating their crucial role in global functioning (Table 6.1).11
What are the releasing and inhibiting hormones of the hypothalamus?
The corticotropin-releasing hormone stimulates the release of adrenocorticotropic hormone from the anterior pituitary. Somatostatin inhibits the release of both growth hormone and thyroid-stimulating hormone, and various intestinal hormones.
What is the function of releasing and inhibiting hormone?
Releasing hormones and inhibiting hormones are hormones whose main purpose is to control the release of other hormones, either by stimulating or inhibiting their release.
What hormone requires a releasing hormone from the hypothalamus?
Thyrotropin-releasing hormone (TSH) is produced in the hypothalamus and stimulates the release stimulates the thyroid gland to produce thyroid hormones. Too much TSH is rare and will cause hyperthyroidism (too much thyroid hormone).
What activities does the hypothalamus control?
The hypothalamus helps manage your body toàn thân temperature, hunger and thirst, mood, sex drive, blood pressure and sleep.
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