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By the end of this section, you will be able to:
- Explain the interrelationships of the anatomy and functions of the hypothalamus and the posterior and anterior lobes of the pituitary gland
- Identify the two hormones released from the posterior pituitary, their target cells, and their principal actions
- Identify the six hormones produced by the anterior lobe of the pituitary gland, their target cells, their principal actions, and their regulation by the hypothalamus
The hypothalamus–pituitary complex can be thought of as the “command center” of the endocrine system. This complex secretes several hormones that directly produce responses in target tissues, as well as hormones that regulate the synthesis and secretion of hormones of other glands. In addition, the hypothalamus–pituitary complex coordinates the messages of the endocrine and nervous systems. In many cases, a stimulus received by the nervous system must pass through the hypothalamus–pituitary complex to be translated into hormones that can initiate a response.
The hypothalamus is a structure of the diencephalon of the brain located anterior and inferior to the thalamus (Figure 1). It has both neural and endocrine functions, producing and secreting many hormones. In addition, the hypothalamus is anatomically and functionally related to the pituitary gland (or hypophysis), a bean-sized organ suspended from it by a stem called the infundibulum (or pituitary stalk). The pituitary gland is cradled within the sellaturcica of the sphenoid bone of the skull. It consists of two lobes that arise from distinct parts of embryonic tissue: the posterior pituitary (neurohypophysis) is neural tissue, whereas the anterior pituitary (also known as the adenohypophysis) is glandular tissue that develops from the primitive digestive tract. The hormones secreted by the posterior and anterior pituitary, and the intermediate zone between the lobes are summarized in Table 1.
|Table 1. Pituitary Hormones|
|Pituitary lobe||Associated hormones||Chemical class||Effect|
|Anterior||Growth hormone (GH)||Protein||Promotes growth of body tissues|
|Anterior||Prolactin (PRL)||Peptide||Promotes milk production from mammary glands|
|Anterior||Thyroid-stimulating hormone (TSH)||Glycoprotein||Stimulates thyroid hormone release from thyroid|
|Anterior||Adrenocorticotropic hormone (ACTH)||Peptide||Stimulates hormone release by adrenal cortex|
|Anterior||Follicle-stimulating hormone (FSH)||Glycoprotein||Stimulates gamete production in gonads|
|Anterior||Luteinizing hormone (LH)||Glycoprotein||Stimulates androgen production by gonads|
|Posterior||Antidiuretic hormone (ADH)||Peptide||Stimulates water reabsorption by kidneys|
|Posterior||Oxytocin||Peptide||Stimulates uterine contractions during childbirth|
|Intermediate zone||Melanocyte-stimulating hormone||Peptide||Stimulates melanin formation in melanocytes|
The posterior pituitary is actually an extension of the neurons of the paraventricular and supraoptic nuclei of the hypothalamus. The cell bodies of these regions rest in the hypothalamus, but their axons descend as the hypothalamic–hypophyseal tract within the infundibulum, and end in axon terminals that comprise the posterior pituitary (Figure 2).
The posterior pituitary gland does not produce hormones, but rather stores and secretes hormones produced by the hypothalamus. The paraventricular nuclei produce the hormone oxytocin, whereas the supraoptic nuclei produce ADH. These hormones travel along the axons into storage sites in the axon terminals of the posterior pituitary. In response to signals from the same hypothalamic neurons, the hormones are released from the axon terminals into the bloodstream.
When fetal development is complete, the peptide-derived hormone oxytocin (tocia- = “childbirth”) stimulates uterine contractions and dilation of the cervix. Throughout most of pregnancy, oxytocin hormone receptors are not expressed at high levels in the uterus. Toward the end of pregnancy, the synthesis of oxytocin receptors in the uterus increases, and the smooth muscle cells of the uterus become more sensitive to its effects. Oxytocin is continually released throughout childbirth through a positive feedback mechanism. As noted earlier, oxytocin prompts uterine contractions that push the fetal head toward the cervix. In response, cervical stretching stimulates additional oxytocin to be synthesized by the hypothalamus and released from the pituitary. This increases the intensity and effectiveness of uterine contractions and prompts additional dilation of the cervix. The feedback loop continues until birth.
Although the mother’s high blood levels of oxytocin begin to decrease immediately following birth, oxytocin continues to play a role in maternal and newborn health. First, oxytocin is necessary for the milk ejection reflex (commonly referred to as “let-down”) in breastfeeding women. As the newborn begins suckling, sensory receptors in the nipples transmit signals to the hypothalamus. In response, oxytocin is secreted and released into the bloodstream. Within seconds, cells in the mother’s milk ducts contract, ejecting milk into the infant’s mouth. Secondly, in both males and females, oxytocin is thought to contribute to parent–newborn bonding, known as attachment. Oxytocin is also thought to be involved in feelings of love and closeness, as well as in the sexual response.
Antidiuretic Hormone (ADH)
The solute concentration of the blood, or blood osmolarity, may change in response to the consumption of certain foods and fluids, as well as in response to disease, injury, medications, or other factors. Blood osmolarity is constantly monitored by osmoreceptors—specialized cells within the hypothalamus that are particularly sensitive to the concentration of sodium ions and other solutes.
In response to high blood osmolarity, which can occur during dehydration or following a very salty meal, the osmoreceptors signal the posterior pituitary to release antidiuretic hormone (ADH). The target cells of ADH are located in the tubular cells of the kidneys. Its effect is to increase epithelial permeability to water, allowing increased water reabsorption. The more water reabsorbed from the filtrate, the greater the amount of water that is returned to the blood and the less that is excreted in the urine. A greater concentration of water results in a reduced concentration of solutes. ADH is also known as vasopressin because, in very high concentrations, it causes constriction of blood vessels, which increases blood pressure by increasing peripheral resistance. The release of ADH is controlled by a negative feedback loop. As blood osmolarity decreases, the hypothalamic osmoreceptors sense the change and prompt a corresponding decrease in the secretion of ADH. As a result, less water is reabsorbed from the urine filtrate.
Interestingly, drugs can affect the secretion of ADH. For example, alcohol consumption inhibits the release of ADH, resulting in increased urine production that can eventually lead to dehydration and a hangover. A disease called diabetes insipidus is characterized by chronic underproduction of ADH that causes chronic dehydration. Because little ADH is produced and secreted, not enough water is reabsorbed by the kidneys. Although patients feel thirsty, and increase their fluid consumption, this doesn’t effectively decrease the solute concentration in their blood because ADH levels are not high enough to trigger water reabsorption in the kidneys. Electrolyte imbalances can occur in severe cases of diabetes insipidus.
The anterior pituitary originates from the digestive tract in the embryo and migrates toward the brain during fetal development. There are three regions: the pars distalis is the most anterior, the pars intermedia is adjacent to the posterior pituitary, and the pars tuberalis is a slender “tube” that wraps the infundibulum.
Recall that the posterior pituitary does not synthesize hormones, but merely stores them. In contrast, the anterior pituitary does manufacture hormones. However, the secretion of hormones from the anterior pituitary is regulated by two classes of hormones. These hormones—secreted by the hypothalamus—are the releasing hormones that stimulate the secretion of hormones from the anterior pituitary and the inhibiting hormones that inhibit secretion.
Hypothalamic hormones are secreted by neurons, but enter the anterior pituitary through blood vessels (Figure 3). Within the infundibulum is a bridge of capillaries that connects the hypothalamus to the anterior pituitary. This network, called the hypophyseal portal system, allows hypothalamic hormones to be transported to the anterior pituitary without first entering the systemic circulation. The system originates from the superior hypophyseal artery, which branches off the carotid arteries and transports blood to the hypothalamus. The branches of the superior hypophyseal artery form the hypophyseal portal system (see Figure 3). Hypothalamic releasing and inhibiting hormones travel through a primary capillary plexus to the portal veins, which carry them into the anterior pituitary. Hormones produced by the anterior pituitary (in response to releasing hormones) enter a secondary capillary plexus, and from there drain into the circulation.
The anterior pituitary produces seven hormones. These are the growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), beta endorphin, and prolactin. Of the hormones of the anterior pituitary, TSH, ACTH, FSH, and LH are collectively referred to as tropic hormones (trope- = “turning”) because they turn on or off the function of other endocrine glands.
The endocrine system regulates the growth of the human body, protein synthesis, and cellular replication. A major hormone involved in this process is growth hormone (GH), also called somatotropin—a protein hormone produced and secreted by the anterior pituitary gland. Its primary function is anabolic; it promotes protein synthesis and tissue building through direct and indirect mechanisms (Figure 4). GH levels are controlled by the release of GHRH and GHIH (also known as somatostatin) from the hypothalamus.
A glucose-sparing effect occurs when GH stimulates lipolysis, or the breakdown of adipose tissue, releasing fatty acids into the blood. As a result, many tissues switch from glucose to fatty acids as their main energy source, which means that less glucose is taken up from the bloodstream.
GH also initiates the diabetogenic effect in which GH stimulates the liver to break down glycogen to glucose, which is then deposited into the blood. The name “diabetogenic” is derived from the similarity in elevated blood glucose levels observed between individuals with untreated diabetes mellitus and individuals experiencing GH excess. Blood glucose levels rise as the result of a combination of glucose-sparing and diabetogenic effects.
GH indirectly mediates growth and protein synthesis by triggering the liver and other tissues to produce a group of proteins called insulin-like growth factors (IGFs). These proteins enhance cellular proliferation and inhibit apoptosis, or programmed cell death. IGFs stimulate cells to increase their uptake of amino acids from the blood for protein synthesis. Skeletal muscle and cartilage cells are particularly sensitive to stimulation from IGFs.
Dysfunction of the endocrine system’s control of growth can result in several disorders. For example, gigantism is a disorder in children that is caused by the secretion of abnormally large amounts of GH, resulting in excessive growth. A similar condition in adults is acromegaly, a disorder that results in the growth of bones in the face, hands, and feet in response to excessive levels of GH in individuals who have stopped growing. Abnormally low levels of GH in children can cause growth impairment—a disorder called pituitary dwarfism (also known as growth hormone deficiency).
The activity of the thyroid gland is regulated by thyroid-stimulating hormone (TSH), also called thyrotropin. TSH is released from the anterior pituitary in response to thyrotropin-releasing hormone (TRH) from the hypothalamus. As discussed shortly, it triggers the secretion of thyroid hormones by the thyroid gland. In a classic negative feedback loop, elevated levels of thyroid hormones in the bloodstream then trigger a drop in production of TRH and subsequently TSH.
The adrenocorticotropic hormone (ACTH), also called corticotropin, stimulates the adrenal cortex (the more superficial “bark” of the adrenal glands) to secrete corticosteroid hormones such as cortisol. ACTH come from a precursor molecule known as pro-opiomelanotropin (POMC) which produces several biologically active molecules when cleaved, including ACTH, melanocyte-stimulating hormone, and the brain opioid peptides known as endorphins.
The release of ACTH is regulated by the corticotropin-releasing hormone (CRH) from the hypothalamus in response to normal physiologic rhythms. A variety of stressors can also influence its release, and the role of ACTH in the stress response is discussed later in this chapter.
Follicle-Stimulating Hormone and Luteinizing Hormone
The endocrine glands secrete a variety of hormones that control the development and regulation of the reproductive system (these glands include the anterior pituitary, the adrenal cortex, and the gonads—the testes in males and the ovaries in females). Much of the development of the reproductive system occurs during puberty and is marked by the development of sex-specific characteristics in both male and female adolescents. Puberty is initiated by gonadotropin-releasing hormone (GnRH), a hormone produced and secreted by the hypothalamus. GnRH stimulates the anterior pituitary to secrete gonadotropins—hormones that regulate the function of the gonads. The levels of GnRH are regulated through a negative feedback loop; high levels of reproductive hormones inhibit the release of GnRH. Throughout life, gonadotropins regulate reproductive function and, in the case of women, the onset and cessation of reproductive capacity.
The gonadotropins include two glycoprotein hormones: follicle-stimulating hormone (FSH) stimulates the production and maturation of sex cells, or gametes, including ova in women and sperm in men. FSH also promotes follicular growth; these follicles then release estrogens in the female ovaries. Luteinizing hormone (LH) triggers ovulation in women, as well as the production of estrogens and progesterone by the ovaries. LH stimulates production of testosterone by the male testes.
As its name implies, prolactin (PRL) promotes lactation (milk production) in women. During pregnancy, it contributes to development of the mammary glands, and after birth, it stimulates the mammary glands to produce breast milk. However, the effects of prolactin depend heavily upon the permissive effects of estrogens, progesterone, and other hormones. And as noted earlier, the let-down of milk occurs in response to stimulation from oxytocin.
In a non-pregnant woman, prolactin secretion is inhibited by prolactin-inhibiting hormone (PIH), which is actually the neurotransmitter dopamine, and is released from neurons in the hypothalamus. Only during pregnancy do prolactin levels rise in response to prolactin-releasing hormone (PRH) from the hypothalamus.
Intermediate Pituitary: Melanocyte-Stimulating Hormone
The cells in the zone between the pituitary lobes secrete a hormone known as melanocyte-stimulating hormone (MSH) that is formed by cleavage of the pro-opiomelanocortin (POMC) precursor protein. Local production of MSH in the skin is responsible for melanin production in response to UV light exposure. The role of MSH made by the pituitary is more complicated. For instance, people with lighter skin generally have the same amount of MSH as people with darker skin. Nevertheless, this hormone is capable of darkening of the skin by inducing melanin production in the skin’s melanocytes. Women also show increased MSH production during pregnancy; in combination with estrogens, it can lead to darker skin pigmentation, especially the skin of the areolas and labia minora. Figure 5 is a summary of the pituitary hormones and their principal effects.
The following video is an animation showing the role of the hypothalamus and the pituitary gland. Which hormone is released by the pituitary to stimulate the thyroid gland?
A YouTube element has been excluded from this version of the text. You can view it online here: pb.libretexts.org/aapii/?p=42
[reveal-answer q=”261011″]Show Answer[/reveal-answer]
[hidden-answer a=”261011″]Thyroid-stimulating hormone.[/hidden-answer]
The hypothalamus–pituitary complex is located in the diencephalon of the brain. The hypothalamus and the pituitary gland are connected by a structure called the infundibulum, which contains vasculature and nerve axons. The pituitary gland is divided into two distinct structures with different embryonic origins. The posterior lobe houses the axon terminals of hypothalamic neurons. It stores and releases into the bloodstream two hypothalamic hormones: oxytocin and antidiuretic hormone (ADH). The anterior lobe is connected to the hypothalamus by vasculature in the infundibulum and produces and secretes six hormones. Their secretion is regulated, however, by releasing and inhibiting hormones from the hypothalamus. The six anterior pituitary hormones are: growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin (PRL).
Answer the question(s) below to see how well you understand the topics covered in the previous section.
Critical Thinking Questions
- Compare and contrast the anatomical relationship of the anterior and posterior lobes of the pituitary gland to the hypothalamus
- Name the target tissues for prolactin.
[reveal-answer q=”122626″]Show Answers[/reveal-answer]
- The anterior lobe of the pituitary gland is connected to the hypothalamus by vasculature, which allows regulating hormones from the hypothalamus to travel to the anterior pituitary. In contrast, the posterior lobe is connected to the hypothalamus by a bridge of nerve axons called the hypothalamic–hypophyseal tract, along which the hypothalamus sends hormones produced by hypothalamic nerve cell bodies to the posterior pituitary for storage and release into the circulation.
- The mammary glands are the target tissues for prolactin.
acromegaly: disorder in adults caused when abnormally high levels of GH trigger growth of bones in the face, hands, and feet
adrenocorticotropic hormone (ACTH): anterior pituitary hormone that stimulates the adrenal cortex to secrete corticosteroid hormones (also called corticotropin)
antidiuretic hormone (ADH): hypothalamic hormone that is stored by the posterior pituitary and that signals the kidneys to reabsorb water
follicle-stimulating hormone (FSH): anterior pituitary hormone that stimulates the production and maturation of sex cells
gigantism: disorder in children caused when abnormally high levels of GH prompt excessive growth
gonadotropins: hormones that regulate the function of the gonads
growth hormone (GH): anterior pituitary hormone that promotes tissue building and influences nutrient metabolism (also called somatotropin)
hypophyseal portal system: network of blood vessels that enables hypothalamic hormones to travel into the anterior lobe of the pituitary without entering the systemic circulation
hypothalamus: region of the diencephalon inferior to the thalamus that functions in neural and endocrine signaling
infundibulum: stalk containing vasculature and neural tissue that connects the pituitary gland to the hypothalamus (also called the pituitary stalk)
insulin-like growth factors (IGF): protein that enhances cellular proliferation, inhibits apoptosis, and stimulates the cellular uptake of amino acids for protein synthesis
luteinizing hormone (LH): anterior pituitary hormone that triggers ovulation and the production of ovarian hormones in females, and the production of testosterone in males
osmoreceptor: hypothalamic sensory receptor that is stimulated by changes in solute concentration (osmotic pressure) in the blood
oxytocin: hypothalamic hormone stored in the posterior pituitary gland and important in stimulating uterine contractions in labor, milk ejection during breastfeeding, and feelings of attachment (also produced in males)
pituitary dwarfism: disorder in children caused when abnormally low levels of GH result in growth retardation
pituitary gland: bean-sized organ suspended from the hypothalamus that produces, stores, and secretes hormones in response to hypothalamic stimulation (also called hypophysis)
prolactin (PRL): anterior pituitary hormone that promotes development of the mammary glands and the production of breast milk
thyroid-stimulating hormone (TSH): anterior pituitary hormone that triggers secretion of thyroid hormones by the thyroid gland (also called thyrotropin)
Endocrine system 2: hypothalamus and pituitary gland
The endocrine system comprises glands and tissues that produce hormones for regulating and coordinating vital bodily functions. This article, the second in an eight-part series, looks at the hypothalamus and pituitary gland
The endocrine system consists of glands and tissues that produce and secrete hormones to regulate and coordinate vital bodily functions. This article, the second in an eight-part series on the endocrine system, explores the anatomy and physiology of the hypothalamus and pituitary gland, and how they work together to regulate and coordinate vital physiological processes in the body through hormonal action. It shows how many of the actions initiated by the hypothalamus are mediated through hormonal secretions produced by the pituitary gland beneath it.
Citation: Bayram-Weston Z et al (2021) Endocrine system 2: hypothalamus and pituitary gland. Nursing Times [online] 117: 6, 49-53.
Authors: Zubeyde Bayram-Weston is senior lecturer in biomedical science Maria Andrade is honorary lecturer in biomedical science John Knight is associate professor in biomedical science all at College of Human and Health Sciences, Swansea University.
- This article has been double-blind peer reviewed
- Scroll down to read the article or download a print-friendly PDF here (if the PDF fails to fully download please try again using a different browser) to see other articles in this series
The first article in this eight-part series on the endocrine system gave an overview of the nature of endocrine glands and highlighted the role of hormones as chemical signals that help maintain the homeostatic balance essential to health the remaining articles will each explore different major endocrine glands and tissues. This article examines the anatomy and physiology of the hypothalamus and pituitary gland, which lie in the cranial cavity of the skull.
The hypothalamus is located at the base of the brain just below the thalamus. A small but vital region of the brain, it is roughly the size of an almond and weighs around 4g (Saper and Lowell, 2014). It accounts for <1% of the total brain mass but performs a multitude of functions that are essential to survival and the enjoyment of life.
The hypothalamus is part of the limbic system, a region of the brain that also includes the thalamus, amygdala, hippocampus and cingulate gyrus. The limbic system is well developed in all higher vertebrates and plays a key role in emotional responses, long-term memory, sense of smell (olfaction) and the acquisition of new skills, as well as contributing to a range of behavioural responses (Wróbel, 2018). The hypothalamus is the location of the thermoregulatory centre, which regulates body temperature (VanPutte et al, 2017) it plays an essential role in water balance, regulation of blood pressure and the sensations of thirst and hunger.
This article focuses on the endocrine functions of the hypothalamus and its role as the key link between the nervous and endocrine systems. The hypothalamus is connected directly to the pituitary gland via a thin stalk, called the infundibulum (Fig 1). Many actions initiated by the hypothalamus are mediated through secretions produced by the pituitary gland beneath it.
The pituitary gland
The pituitary gland is a pea-sized gland that is typically around 0.8-1.0cm in diameter and weighs around 500mg. It resides in the sella turcica (Turkish saddle), a protective pocket in the sphenoid bone of the skull (Fig 1). Increased pituitary size is often indicative of endocrine pathologies, particularly tumours of the pituitary (De Sousa et al, 2015). The pituitary gland comprises two regions (Fig 1):
- Posterior pituitary (neurohypophysis) – neural tissue extends from the hypothalamus through the infundibulum into a larger, bulbous region called the pars nervosa this forms the bulk of the posterior pituitary
- Anterior pituitary (adenohypophysis) – derived from the epithelial tissue of the embryonic oral cavity.
During embryonic development, the roof of the mouth bulges upwards (invaginates) to form a tiny, bubble-like structure known as Rathke’s pouch, which then fuses with the posterior portion of the pituitary gland (Fig 2). Failure of this process to occur normally may lead to an abnormal pituitary structure or the formation of cysts and clefts (Babu et al, 2013).
The anterior pituitary accounts for approximately 70-80% of the total mass of the gland and includes two major parts:
- Pars distalis – larger, bulbous portion
- Pars tuberalis – highly vascular sheath wrapped around the infundibular stalk.
A third (intermediate) region of the pituitary gland is often recognisable this is known as the pars intermedia and is usually present as a thin band of tissue that marks the point where the anterior and posterior pituitaries fuse (Ilahi and Ilahi, 2020).
Hormones of the posterior pituitary
Two major hormones are released from the posterior pituitary:
These hormones are synthesised in the cell bodies of neurons in the hypothalamus and transported down the axons of the neurons running through the infundibulum. ADH and oxytocin are concentrated and stored in the pars nervosa (Fig 3), before being released into the blood when required. Both are peptide hormones and, as they are produced by neurons, they are often called neuropeptides.
ADH plays a vital role in regulating fluid balance and blood pressure. Specialised osmoreceptors located in the hypothalamus continually monitor the solute concentration of the blood. When the body loses water (for example, through sweating during exercise or following vomiting and diarrhoea) dehydration may occur and the plasma solute concentration rises. This is detected by the hypothalamic osmoreceptors, which initiate the release of ADH from the posterior pituitary.
ADH primarily acts on the kidneys, increasing the volume of fluid absorbed from the renal filtrate back into the blood. This reduces the volume of urine produced (hence the name antidiuretic hormone), resulting in the urine being darker and more highly concentrated. By increasing fluid reabsorption back into the blood, ADH helps normalise the solute concentration of the blood (VanPutte et al, 2017).
ADH is also released after a drop in blood volume or pressure. By promoting water reabsorption in the kidney, ADH increases blood volume, which then starts to increase blood pressure. This normalisation of blood pressure is further enhanced by ADH acting as a powerful vasopressor (which promotes the constriction of blood vessels). ADH-induced vasoconstriction, particularly in the peripheral arterioles (small arteries), further increases and normalises blood pressure (Kanbay et al, 2019). As a result, ADH is also known as vasopressin, particularly in the United States.
Reduced secretion of ADH can lead to diabetes insipidus (DI). Patients with DI cannot concentrate their urine, resulting in polyuria. Large volumes of urine (3-20L/day) are usually produced if not treated, this can lead to severe dehydration.
DI is rare, affecting around 1 in 25,000 people two major types are recognised:
- Neurogenic or central DI is caused by the undersecretion (hyposecretion) of ADH by the posterior pituitary. This is most often due to trauma (commonly head injuries), tumours affecting the hypothalamus or pituitary or, more rarely, infections
- Nephrogenic DI is a rarer form, in which patients usually have normal ADH synthesis and secretion, but their kidneys are insensitive to the effects of ADH – most commonly due to kidney disease or drug-induced kidney damage (Kalra et al, 2016).
DI requires careful management. Initially patients may be severely dehydrated, feel nauseous and shivery, and experience headache careful monitoring of water intake and urine output, with ongoing assessment of urine and blood concentration, is essential. Neurogenic DI is usually treated with desmopressin, a synthetic analogue of ADH that acts on the kidneys in the same way to concentrate the urine and increase blood volume. Treatment of nephrogenic DI is more complex and depends on the underlying cause of the disease (The Pituitary Foundation, 2016).
Oxytocin is released into the blood at high concentration towards the end of the gestational period and initiates parturition (childbirth) by stimulating contractions of the myometrium (muscular layer of the uterus). Oxytocin secretion is regulated by a positive feedback mechanism, whereby increased oxytocin stimulates more-powerful myometrial contractions, which in turn stimulate the release of more oxytocin (VanPutte et al, 2017). This is possible because the uterine wall has receptors that monitor the strength of myometrial contractions and generate nerve impulses (action potentials) that are relayed back to the hypothalamus.
Oxytocin also stimulates the ‘letdown reflex’ in lactating mothers here the smooth muscle linings of the milk ducts in the breast contract, making milk available to the baby during suckling. Again, this is regulated by positive feedback, with the mechanical stimulation of the baby’s suckling action triggering the release of more oxytocin (Osilla and Sharma, 2020).
Oxytocin is often referred to as ‘the love hormone’ because it plays an important role in promoting mother/baby bonding it is also thought to facilitate pair bonding between partners. Evidence is also emerging that oxytocin has other psychological effects, such as reducing anxiety, and promoting maternal behaviour (Parmar and Malik, 2017).
Hormones of the anterior pituitary
The anterior pituitary produces a far greater range of hormones than the posterior pituitary. The anterior pituitary’s role in producing a variety of stimulating hormones that regulate the activity of many other endocrine glands is why the pituitary is often referred to as the ‘master gland’. As explained below, this is a misnomer: the release of these stimulating hormones is governed by hormones released from the hypothalamus, which ultimately acts as the true primary orchestrator of endocrine function.
The anterior pituitary’s cells are usually classified into five major types based on the nature of their secretions. These are listed below with their hormonal secretions:
- Somatotrophs – somatotropin or growth hormone (GH)
- Lactotrophs – prolactin
- Thyrotrophs – thyroid-stimulating hormone (TSH)
- Corticotropths – adrenocorticotropic hormone (ACTH) and melanocyte-stimulating hormone (MSH)
- Gonadotrophs – follicle-stimulating hormone (FSH) and luteinising hormone (LH).
As its name suggests, the primary function of GH is to promote bodily growth. Most famously, GH promotes the widening of the growth plates in the epiphyses of the long bones of the skeleton, which results in elongation of the major bones of the arms and legs, progressively increasing height. GH also enhances amino acid uptake from the blood into cells, increasing the rate of protein synthesis in tissues such as muscle this is why it is known as an anabolic hormone.
Thyroid hormones T3 and T4 (thyroxine), which regulate metabolism, are necessary for GH to exert its effects efficiently. The anabolic effects of GH are also enhanced by the presence of other anabolic hormones such as testosterone. As well as promoting bone and muscle growth, GH also stimulates the growth of many of the major internal organs (Devesa et al, 2016).
GH secretion is regulated by two hormones produced by the hypothalamus:
- Growth hormone-releasing hormone stimulates the release of GH
- Growth hormone-inhibiting hormone (GHIH) acts antagonistically to inhibit the release of GH (Table 1).
Deficiency of GH during childhood may result in pituitary dwarfism this is characterised by below-average growth and, commonly, an underdeveloped bridge of the nose and prominent forehead. Unlike achondroplastic dwarfism (a genetic disorder), pituitary dwarfism, although associated with reduced height, is characterised by normal bodily proportions. Recombinant human GH is available to treat children who are deficient in GH. It is usually injected subcutaneously once a day, and growth rate and potential side-effects then carefully monitored (Rose et al, 2014).
Elevated secretion of GH in childhood often leads to gigantism, in which rapid growth of the long bones can result in an adult height of >2.4m. Elevated secretion of GH in adults, after their epiphyseal growth plates have fused, can lead to acromegaly, in which the hands, feet and some facial features (particularly the lower jawbone) can grow abnormally large and usually out of normal proportion (de Herder, 2009).
Prolactin (lactogenic hormone) initiates milk secretion (lactation) in breast tissue. By itself, prolactin has only a weak effect, but during pregnancy prolactin levels increase and it acts synergistically with other hormones – including oestrogens, progesterone and cortisol – to promote the enlargement and engorgement of the breasts in preparation for lactation (Suarez et al, 2015).
It has been hypothesised that the release of prolactin is regulated and fine-tuned by the antagonistic actions of a prolactin-releasing hormone and a prolactin-inhibiting hormone, both of which are thought to be produced by the hypothalamus (Table 1).
Tropic hormones have a stimulating effect on other endocrine glands, inducing the synthesis and secretion of the target hormone(s). Four major tropic hormones are synthesised and secreted by the anterior pituitary, as described below.
Thyroid-stimulating hormone (thyrotrophin)
TSH stimulates the thyroid gland to secrete the iodine-containing hormones T3 and T4. These are primarily responsible for regulating metabolism, with T3 being the more potent. Most cell types in the body have internal receptors for T3 and T4. These hormones are also vital for growth and development, and play key roles in the normal functioning of the cardiovascular, respiratory, skeletal and central nervous systems.
The release of TSH is regulated by thyrotropin-releasing hormone, which is produced by the hypothalamus (Table 1). The fine tuning of T3 and T4 release is regulated by negative feedback, through the sequential secretions of the hypothalamus, anterior pituitary and thyroid gland (Fitzgerald and Bean, 2018). This hormonal cascade is referred to as the hypothalamic-pituitary-thyroid (HPT) axis and will be explored in detail in part 3 of this series.
Adrenocorticotrophic hormone (adrenocorticotropin)
ACTH primarily regulates the production and secretion of cortisol from the adrenal cortex (outer portion of the adrenal gland). Cortisol is a long-term stress hormone and a steroidal hormone synthesised from cholesterol. It is referred to as a glucocorticoid because it is produced by the adrenal cortex and influences the concentration of glucose in the blood (VanPutte et al, 2017). Following periods of chronic stress (including classic biological stressors such as starvation or physical injury), the hypothalamus releases corticotropin-releasing hormone. This initiates the release of ACTH from the anterior pituitary and, subsequently, stimulates the release of cortisol from the adrenal cortex (Table 1).
Cortisol plays a key role in regulating metabolism and, during periods of food deprivation, stimulates the breakdown of protein and fat to generate glucose for use as fuel in glucose-dependent tissues, such as the brain. This process is called gluconeogenesis (literally, the creation of new glucose). Cortisol also influences the sleep/wake cycle, mood and behaviour, and has potent anti-inflammatory/immunosupressant properties (Kandhalu, 2013).
ACTH also helps to regulate the release of other steroid hormones produced by the adrenal cortex, including aldosterone (which regulates the concentration of sodium and potassium in the blood) and the group of testosterone-like hormones known as androgens (Gallo-Payet, 2016). The complex interplay between the hypothalamus, anterior pituitary and the adrenal cortex is referred to as the HPT axis and will be examined in detail in part 4 of this series.
ACTH is also part of the melanocortin group of hormones, which influence skin pigmentation (see below).
MSH is synthesised by the pars intermedia region of the pituitary gland. Although this region marks the boundary where the anterior and posterior portions of the pituitary gland fuse, it is generally considered part of the anterior pituitary. The pars intermedia atrophies (shrinks) with age and, in adults, may only be present as a vestigial remnant or, in some cases, is not recognisable at all. MSH exists in a range of structurally similar forms known as melanocortins, which are all small peptides.
As implied by its name, MSH stimulates the pigment-producing cells (melanocytes) in the epidermis to release the dark pigment known as melanin, which is largely responsible for skin colour. All races are thought to have similar numbers of melanocytes in their epidermis it is the relative activity of these cells and the amount of melanin they synthesise and release that ultimately determines skin colour.
Melanocytes can synthesise MSH when exposed to the ultraviolet (UV) light in sunlight (Tsatmali et al, 2002). This is essential to protect the actively dividing cells of the epidermis from the harmful effects of UV, known to cause DNA damage that can lead to mutations and, potentially, skin cancers. Melanin is excellent at absorbing UV wavelengths of light and, as it accumulates in the epidermis the skin, darkens and develops a protective suntan.
During pregnancy, levels of MSH tend to increase, which, together with changes to the sex hormones oestrogen and progesterone, often leads to hyper-pigmentation around the eye sockets, cheekbones, lips and forehead. This is known as melasma or ‘the mask of pregnancy’ these pigmented areas usually fade gradually after childbirth (Costin and Birlea, 2006).
ACTH (described above) is another hormone that can influence skin pigmentation through the direct stimulation of melanocytes. This is particularly true of certain forms of Cushing’s syndrome, in which excess ACTH often causes regions of dark, hyperpigmented skin this will be discussed further in part 4 of this series.
These act on the gonads (testes and ovaries) to stimulate the production of sex hormones and sperm or ova in males and females respectively (see below). The main gonadrotrophins are FSH and LH the release of both is regulated by gonadotropin-releasing hormone, which is produced by the hypothalamus (Table 1).
In females, each month FSH initiates the development of immature follicles in the ovaries. As each follicle enlarges, it secretes the female sex hormone oestrogen, before maturing into a Graafian follicle, a fluid-filled, pressurised sac containing a mature ovum (egg), primed and ready to rupture. Ovulation is triggered by LH, which initiates rupturing of the follicle and ovarian wall this explosive event propels the ovum into its adjacent fallopian tube.
Following ovulation, the remnants of the Graafian follicle collapse to form a structure known as the corpus luteum (yellow body). This produces the second major female sex hormone, progesterone, which maintains the integrity of the endometrial lining of the uterus to allow for the implantation of a fertilised ovum (VanPutte et al, 2017).
Despite their names being reflective of the role played in the female ovarian cycle, FSH and LH also play crucial roles in male reproductive physiology. FSH is essential in stimulating spermatogenesis, where diploid cells (containing 46 chromosomes) undergo meiotic division to produce vast numbers of haploid spermatozoa (each containing 23 chromosomes).
FSH also stimulates the activity of Sertoli cells (‘nurse’ cells) in the testes these provide nutrition to the developing spermatozoa, allowing maturation into viable gametes that are capable of fertilisation. LH stimulates the interstitial cells (Leydig cells) of the testes to synthesise and release the male sex hormone testosterone (Babu et al, 2004). This powerful anabolic steroid stimulates skeletal muscle development, growth of facial and body hair, expansion of the larynx (causing the deepening of the voice) and spermatogenesis, and is largely responsible for the male sex drive.
The role of the gonadotropins and male and female sex hormones will be discussed further in part 7 of this series.
Role of the hypothalamus
The pituitary gland is often referred to as the master gland but, in fact, it plays more of a ‘middle-management’ role many of its actions are directed by the hypothalamus.
Hypothalamic nuclei and hypothalamic-pituitary portal system
The hypothalamus contains discrete, organised clusters of neurons called the hypothalamic nuclei, which synthesise the hypothalamic releasing and inhibiting hormones that regulate the activity of the anterior pituitary. Both the hypothalamus and pituitary gland are highly vascularised and have a dedicated network of blood vessels called the hypothalamic-pituitary portal system, which ensures rapid and efficient delivery of the releasing and inhibiting hormones from the hypothalamus to the anterior pituitary below (Bear et al, 2021).
Release of hypothalamic hormones
Secretion of the hypothalamic releasing and inhibiting hormones is determined by multiple sensory inputs, which continually monitor the changing physiological status of the body. Multiple parameters monitored continuously and in real time include temperature, pH, solute concentrations and current levels of circulating hormones. The hypothalamus functions as the key bridge between the nervous and endocrine systems, but many of the interactions between the two remain poorly understood.
Table 1 summarises the key hormones of the hypothalamus and pituitary, and their relationships. Some of the better-studied interactions between the hypothalamus, pituitary and peripheral endocrine glands (such as the HPT axis and hypothalamic-pituitary-adrenal axis) will be explored later in this series. Part 3 focuses on the thyroid and parathyroid glands.
- The hypothalamus and pituitary gland both lie in the cranial cavity of the skull
- Two major hormones released by the posterior pituitary gland are antidiuretic hormone and oxytocin
- The anterior pituitary gland produces several stimulating hormones that regulate the activity of other endocrine glands
- Although the pituitary gland is often referred to as the master gland, many of its actions are directed by the hypothalamus
- Clusters of neurons in the hypothalamus synthesise releasing and inhibiting hormones that regulate the activity of the anterior pituitary
Also in this series
Babu R et al (2013) Symptomatic Rathke’s cleft cyst with a co-existing pituitary tumor brief review of the literature. Asian Journal of Neurosurgery 8: 4, 183-187.
Babu SR et al (2004) Evaluation of FSH, LH and testosterone levels in different subgroups of infertile males. Indian Journal of Clinical Biochemistry 19: 1, 45-49.
Bear MH et al (2021) Neuroanatomy, Hypothalamus. StatPearls Publishing.
Costin G-E, Birlea S-A (2006) What is the mechanism for melasma that so commonly accompanies human pregnancy? International Union of Biochemistry and Molecular Biology Life 58: 1, 55-57.
De Herder WW (2009) Acromegaly and gigantism in the medical literature. Case descriptions in the era before and the early years after the initial publication of Pierre Marie (1886). Pituitary 12: 3, 236-244.
De Sousa SMC et al (2015) Pituitary hyperplasia: case series and literature review of an under-recognised and heterogeneous condition. Endocrinology, Diabetes and Metabolism Case Reports 2015: 150017.
Devesa J et al (2016) Multiple effects of growth hormone in the body: is it really the hormone for growth? Clinical Medicine Insights: Endocrinology and Diabetes 9: 47-71.
Fitzgerald SP, Bean NG (2018) Thyroid stimulating hormone (TSH) autoregulation reduces variation in the TSH response to thyroid hormones. Temperature 5: 4, 380-389.
Gallo-Payet N (2016) Adrenal and extra-adrenal functions of ACTH. Journal of Molecular Endocrinology 56: 4, T135-T156.
Kalra S et al (2016) Diabetes insipidus: the other diabetes. Indian Journal of Endocrinology and Metabolism 20: 1, 9-21.
Kanbay M et al (2019) Antidiuretic hormone and serum osmolarity physiology and related outcomes: what is old, what is new, and what is unknown? Journal of Clinical Endocrinology and Metabolism 104: 11, 5406-5420.
Kandhalu P (2013) Effects of cortisol on physical and psychological aspects of the body and effective ways by which one can reduce stress. Berkeley Scientific Journal 18: 1, 14-16.
Osilla EV, Sharma S (2020) Oxytocin. StatPearls Publishing.
Parmar P, Malik S (2017) Oxytocin: the hormone of love. International Organization of Scientific Research Journal of Pharmacy and Biological Sciences 12: 6, 1-9.
Pereira Suarez AL et al (2015) Prolactin in inflammatory response. Advances in Experimental Medicine and Biology 846: 243-264.
The Pituitary Foundation (2016) Diabetes Insipidus. The Pituitary Foundation.
Rose SR et al (2014) Growth hormone therapy guidelines: clinical and managed care perspectives. American Journal of Pharmacy Benefits 6: 5, e134-e146.
Saper CB, Lowell BB (2014) The hypothalamus. Current Biology 24: 23, R1111-1116.
Tsatmali M et al (2002) Melanocyte function and its control by melanocortin peptides. Journal of Histochemistry and Cytochemistry 50: 2, 125-133.
VanPutte CL et al (2017) Seeley’s Anatomy and Physiology. McGraw-Hill.
Wróbel G (2018) The structure of the brain and human behaviour. Pedagogy and Psychology of Sport 4: 1, 37-51.
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The posterior pituitary is significantly different in structure from the anterior pituitary. It is a part of the brain, extending down from the hypothalamus, and contains mostly nerve fibers and neuroglial cells, which support axons that extend from the hypothalamus to the posterior pituitary. The posterior pituitary and the infundibulum together are referred to as the neurohypophysis.
The hormones antidiuretic hormone (ADH), also known as vasopressin, and oxytocin are produced by neurons in the hypothalamus and transported within these axons along the infundibulum to the posterior pituitary. They are released into the circulatory system via neural signaling from the hypothalamus. These hormones are considered to be posterior pituitary hormones, even though they are produced by the hypothalamus, because that is where they are released into the circulatory system. The posterior pituitary itself does not produce hormones, but instead stores hormones produced by the hypothalamus and releases them into the blood stream.
In order for our body to function properly, it has to respond to external stimuli and internal signals. Some are nerve signals while others are chemical signals. The hypothalamus, a region of the brain, serves as the main integrator of these signals. It receives signals and responds by producing hormones. Many of these hormones regulate the synthesis and secretion of hormones by the glands of the endocrine system.
Hormones produced by the hypothalamus are released into the pituitary gland, located at the base of the hypothalamus. The pituitary gland has two distinct parts: the anterior pituitary and the posterior pituitary. Some hormones from the hypothalamus are secreted into the blood. This is the job of the posterior pituitary gland. Other hypothalamic hormones control the production and release of hormones from the anterior pituitary gland.
The hypothalamus synthesizes several hormones that are secreted into the blood via the posterior pituitary gland. Oxytocin is produced and released in females in response to suckling, or breast-feeding. Suckling stimulates nerves that send signals to the hypothalamus. The hypothalamus synthesizes oxytocin, which is released from the posterior pituitary gland. When the oxytocin reaches the mammary gland, the breast, it signals the breast to eject milk. During childbirth, the release of oxytocin causes the muscles of the uterus to contract.
One hormone can have various effects. This is due in part to different target cells expressing the hormone receptor on their surface only under particular conditions so they respond to the hormone only at certain times.
Antidiuretic hormone, or ADH, is also produced by the hypothalamus and released by the posterior pituitary gland. ADH helps control the concentration of solutes in the blood. When the concentration of solutes is too high, nerve cells in the hypothalamus signal to secretory cells in the hypothalamus to synthesize ADH. When the ADH, released by the posterior pituitary, reaches the kidney, it signals target cells to release water into the blood to lower the solute concentration. The solute concentration is lowered, and the nerve cells stop signaling the production of ADH.
This type of negative feedback is common in maintaining homeostasis. Unlike the posterior pituitary, the anterior pituitary doesn't release hormones produced by the hypothalamus. The anterior pituitary is made up of endocrine cells that synthesize and secrete hormones into the blood, under the control of the hypothalamus. The hypothalamus produces and releases two classes of hormones into the blood supply of the anterior pituitary: releasing hormones and inhibiting hormones.
Releasing hormones cause the anterior pituitary to secrete particular hormones. Inhibiting hormones make it stop secreting particular hormones. Each anterior pituitary hormone is controlled by at least one releasing hormone, and some hormones are controlled by both releasing and inhibiting hormones.
Some anterior pituitary hormones are tropic, meaning they cause the synthesis and secretion of hormones by other endocrine glands. For example, the anterior pituitary gland secretes several hormones, including follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH, which stimulate activities of the male and female gonads. The anterior pituitary secretes some nontropic hormones that directly affect the target tissue, including endorphins, which inhibit the perception of pain by the brain. Some of the secreted hormones are both tropic and nontropic. Growth hormone, or GH, is tropic because it promotes the production of growth factors, such as insulinlike growth factor by the liver. Growth hormone also directly stimulates the growth of bones.
Now that we've explored the hypothalamus and the pituitary gland, let's consider the hormone products of some other endocrine glands, and see how they interact with the hypothalamus.
Copyright 2006 The Regents of the University of California and Monterey Institute for Technology and Education
The pituitary gland is one of the principal glands of the endocrine system. It releases at least nine hormones affecting a wide variety of body functions, including growth, reproduction, and levels of electrolytes and water in the body fluids. The pituitary sits near the center of the head, behind the nose and beneath the brain, just below the hypothalamus. The hypothalamus is a brain structure from which the pituitary receives chemical signals that control its action. Nerve endings from the hypothalamus stimulate the posterior portion of the pituitary to secrete oxytocin and antidiuretic hormone (ADH). Capillaries from the hypothalamus carry releasing factors and inhibiting factors to the anterior portion of the pituitary, stimulating or inhibiting release of eight other hormones (see Table 1). All the hormones of the pituitary gland are peptides, small chains of amino acids .
|Hormones Released by the Pituitary Gland|
|Hormone Site of Action||Effects|
|Oxytocin||uterus||stimulates contraction during labor|
|breast||stimulates contraction to express milk|
|Antidiuretic hormone (ADH)||kidney||stimulates retention of water|
|hormone, ACTH)||adrenal cortex||stimulates release of cortisol|
|Thyroid-stimulating hormone (TSH)||thyroid||stimulates release of thyroxine|
|Growth hormone (GH)||bone||stimulates growth|
|Follicle-stimulating hormone (FSH)||female ovaries||stimulates follicle to mature an egg, estrogen|
|male testes stimulates||sperm production|
|Luteinizing hormone (LH)||female ovaries||stimulates ovulation, progesterone production|
|male testes stimulates||testosterone production|
Both the hypothalamus and the pituitary are involved in complex feedback loops with other glands in the body, sending and receiving hormonal signals to maintain homeostasis. Because of its central role in so many systems, pituitary abnormalities can lead to a variety of disorders. Disorders may lead to either hyposecretion or hypersecretion . Deficient growth hormone, for instance, leads to dwarfism, while excess causes gigantism.
Q. Compare and contrast the anatomical relationship of the anterior and posterior lobes of the pituitary gland to the hypothalamus.
A. The anterior lobe of the pituitary gland is connected to the hypothalamus by vasculature, which allows regulating hormones from the hypothalamus to travel to the anterior pituitary. In contrast, the posterior lobe is connected to the hypothalamus by a bridge of nerve axons called the hypothalamic&ndashhypophyseal tract, along which the hypothalamus sends hormones produced by hypothalamic nerve cell bodies to the posterior pituitary for storage and release into the circulation.
Growth and somatotrophin deficiency
Clinical Case 7.3
A 2-year-old boy was referred to the general Pediatric clinic because of ilure to thrive’. He had been born weighing 2.79 kg after a normal pregnancy and delivery. Developmental milestones (such as the age of speaking and walking) were normal. Both parents were about the 25th centile for height. In the clinic, he was noted to be short (well below the 3rd centile, but also dysmorphic with a short body (sitting height SDS -5, subischeal leg length SDS -2). (Box 7.10). He weighed 10.03 kg (3rd centile). He was noted to be kyphotic with a short neck. X-rays revealed shortening of the cervical spine but MR imaging of the spine was normal. An endocrine cause of his short stature was thought unlikely. Review of his clinical appearance and the radiological findings by clinical geneticists failed to suggest an underlying diagnosis. One year later, he was referred to the Pediatric Endocrine clinic for the very practical reason that he was too short to use the toilets at his nursery school. He was indeed very short (Box 7.12) and the skeletal disproportion still present.
Sagittal MR scan of Clinical Case 7.3. Note the short thorax (arrowed), a major factor in his short spine.
Growth Chart of Clinical Case 7.3. Age is plotted on the horizontal (X) axis. Two sets of normal data are plotted. Height (the upper set of curves) is plotted on the left-hand vertical (Y) axis and weight (the lower set of curves) on the right-hand Y-axis. (more. )
The young boy in this case was initially referred with ilure to thrive’, a term generally used for children under the age of 2 years who are failing to put on weight (i.e. lean for their height). To interpret this case it is necessary to understand the use of growth charts (Boxes 7.11 and 7.12). As can be seen from the charts, at initial presentation he was nearer the 3rd centile for weight than he was the 3rd centile for height. Thus, he was not failing to thrive, he was failing to grow. With parents on the 25th centile, he would have been expected, all other things being equal, also to grow along that line.
Growth charts. The growth of a child is multifactorial and complex but, fortunately, predictable. Postnatal growth is rapid in infancy (
15 cm/year rapidly decelerating at age 3 years), a childhood rate of about 6 cm/year (with an adolescent deceleration), (more. )
The fastest relative growth rates occur in embryonic and fetal life when a single fertilized ovum progresses, as in this case, to 2.79 kg of live baby after 40 weeks. This represents an increase in fetal mass of about 44 × 10 7 fold whilst length increases 3850-fold. Post-natal growth never matches this with only a 20-fold increase in mass and 3𠄴-fold increase in length. In early childhood, there is a period of rapid growth followed by a period of steady growth with a mid-childhood acceleration, a pubertal growth spurt and a phase of deceleration to final height. In the involutionary years, there is a period of shrinkage, reflecting the changes of spinal shortening.
Intrauterine growth is regulated by endocrine, maternal and genetic factors, though the determinants of prenatal growth are poorly understood. Fetal plasma GH concentrations are very high and yet infants with GH hormone deficiency, and even those with anencephaly, may have normal body length at birth. Loss of human chorionic somatotrophin (hCS) secreted by the placenta (see below) does not appear to affect intrauterine growth. Mothers lacking the hCS gene have given birth to infants of normal birth weight. In contrast, excessive serum insulin may be associated with increased length in infants of diabetic mothers (see clinical case 2.3). The related insulin-like growth factors (IGFs) are also important in fetal growth (see Box 7.19) and, though their precise role is not established, when IGF-1 is lacking (e.g. Laron dwarfs) the reports of birth length show a wide variability, including normality, suggesting that IGF-1 is not a major factor.
GH and the IGFs. The IGF family consists of 3 members (insulin, IGF-1 and IGF-2) sharing common structural similarities. There are variant forms of the IGFs (see website). IGF-1 and IGF-2 also have metabolic functions but also play important roles in (more. )
Maternal (intrauterine) influences have been difficult to define but poor maternal nutrition is the most important factor leading to low birth weight and length world-wide (Box 7.13). Maternal alcohol ingestion and smoking are other adverse factors on fetal growth, and maternal infections such as rubella, toxoplasmosis and cytomegalovirus lead to many abnormalities, as well as short stature. Congenital HIV infection also retards fetal growth. Intrauterine growth retardation (IUGR) is usually defined as a birth weight of less that the 10th percentile for gestational age but of these about 10% are not truly abnormal.
Causes of poor growth. Genetic short stature - includes normal children born to normal short parents. Intrauterine growth retardation - approximately 2% of infants are small for gestational age. This results from a number of possible factors including (more. )
Long answer question Explain the role of the hypothalamus and pituitary as a coordinated unit in maintaining homeostasis? - Biology
Explain the role of the hypothalamus and pituitary as a coordinated unit in maintaining homeostasis?
Solution Show Solution
i. The hypothalamus controls the secretory activity of the pituitary gland (anterior pituitary) by producing, releasing, and inhibiting hormones.
ii. Anterior pituitary and intermediate lobes are connected to the hypothalamus through the hypophyseal portal system. Various hormones secreted by the hypothalamus reach the pituitary gland through the hypophyseal portal system.
iii. The portal vein collects blood from various parts of the hypothalamus and opens into the anterior lobe of the pituitary. From the pituitary, the vein finally carries the blood into the superior vena cava. It helps in the feedback mechanism for hormonal control.
iv. Also, a negative feedback mechanism takes place in the form of hormones released by the target glands to decrease the secretion of the pituitary gland.
v. In such a negative feedback mechanism, the secretion of ACTH, TSH, and gonadotropins (FSH and LH) decreases when their target gland hormone levels rise.
The inside scoop on pituitary tumors
Tumors on the pituitary gland are quite common, says McAninch. And when a patient consults her about one, she's often able to give this good news: "Most pituitary tumors are not cancerous — and often don't require surgery."
Still, doctors monitor pituitary tumors because they can cause problems. For example, they can press against the optic nerve and disrupt vision, or they can trigger a hormone imbalance.
In many cases, medications can shrink the tumor and bring hormones back into balance or even cause the tumor to go away.
When surgery is required, skull base and pituitary care at Rush includes the care of a multidisciplinary team that includes endocrinologists, neurosurgeons, and ear, nose and throat surgeons.
"The endocrinologists take care of regulating the hormones. And the neurosurgeons and ear, nose and throat surgeons collaborate to safely remove the tumor when surgery is needed. This multidisciplinary approach to pituitary tumors translates to better care for the patient," McAninch says.
The pituitary gland releases hormones on different schedules. Most are released every one to three hours. But some, such as growth hormone and prolactin, follow a circadian rhythm, rising and falling throughout the day. They hit their lowest levels just before you go to sleep each night and peak just before you wake up.