GH increases lipolysis (lipid breakdown) and the release of fatty acids from adipocytes into the blood. Fatty acids then can be used as energy sources to drive chemical reactions, including anabolic reactions, by other cells. GH also increases glucose synthesis by the liver, which releases glucose into the blood. The increased use of lipids as an energy source accompanies a decrease in glucose usage. Overall, GH activates the use of lipids to promote growth and protein synthesis.
(From Seeley's Anatomy and Physiology, 10th edition.)
That passage has gotten me confused. So more lipids are used by cells instead of glucose, yet the body releases more glucose into the blood in response to GH. What would be the point, or benefit, of this occurring?
Great question… and an important point about glucose and lipid utilization! The body can't turn fat into sugar, but it can turn sugar into fat. The more technical way to say this is that the body can't convert acetyl-CoA into glucose, but it can convert glucose into acetyl-CoA.
The enzyme that converts glucose to acetyl-CoA, pyruvate dehydrogenase, catalyzes an irreversible chemical reaction. Pyruvate dehydrogenase converts pyruvate into acetyl-CoA, which can be used in the Krebs Cycle, fatty acid synthesis, etc. Once acetyl-CoA is produced it cannot be converted back into glucose (carbohydrate) within the body. This is important because certain cells/tissues can use only glucose for energy production, while other cells/tissues like the liver can use both glucose and lipid for energy production.
This is where your question becomes very important, because the liver is the predominate organ that maintains glucose homeostasis (i.e. maintains blood glucose concentration) in-between meals or during periods of fasting. In periods of fasting, the liver uses free fatty acids released by adipose tissue for energy/ATP production in order to produce glucose through gluconeogenesis, an anabolic process that requires energy.
So, growth hormone increases fatty acid release from adipose tissue stores for uptake by the liver. The liver takes up the fatty acids from the plasma and uses them to produce glucose for release into the circulation for glucose-dependent tissues to use. During this time of fasting, tissues that can use fatty acids and glucose tend to switch to fatty acids as their energy source, while tissues that only can use glucose will continue to rely on glucose production from the liver for their energy source.
Here is a nice summary (open source) from National Library of Medicine explaining in more depth the basis for why fatty acids are oxidized to provide ATP for gluconeogenesis - "Energy Metabolism in the Liver".
Also, George Cahill, a famous physician-scientist at Harvard University who studied metabolism and starvation has an excellent review of fuel flux under fasting and starvation conditions that demonstrates the above mentioned principles as well "Fuel Metabolism in Starvation" - namely that free fatty acids released from adipose tissue are oxidized in the liver and used for anabolic processes in the liver, such as gluconeogenesis that maintains blood glucose concentrations.
It is an important participant in the control of several complex physiological processes, including growth and metabolism.
Growth hormone is also of great interest as a drug used in both humans and animals.
Physiological effects of somatotropin
A critical concept to understand the activity of growth hormone is that it has two different types of effects:
- The direct effects are the result of the binding of the growth hormone to its receptor in the target cells.
- Fat cells (adipocytes), for example, have growth hormone receptors, and growth hormone stimulates them to break down triglycerides and suppresses their ability to absorb and accumulate circulating lipids.
- Indirect effects are mediated primarily by a growth factor similar to insulin I (IGF-I), a hormone secreted by the liver and other tissues in response to growth hormone.
- Most of the growth promotion effects of growth hormone are actually due to IGF-I acting on its target cells.
Taking into account this distinction, we can analyze two main functions of growth hormone and its subaltern IGF-I in physiology.
Effects on growth
Growth is a very complex process and requires the coordinated action of several hormones.
The main role of growth hormone in stimulating body growth is to stimulate the liver and other tissues to secrete IGF-I. IGF-I stimulates the proliferation of chondrocytes (cartilage cells), resulting in bone growth.
Growth hormone seems to have a direct effect on bone growth by stimulating the differentiation of chondrocytes.
IGF-I also seems to be the key player in muscle growth. It stimulates both the differentiation and the proliferation of myoblasts. It also stimulates the absorption of amino acids and the synthesis of proteins in muscles and other tissues.
Metabolic effects of somatotropin
Growth hormone has important effects on the metabolism of proteins , lipids and carbohydrates.
In some cases, a direct effect of growth hormone has been clearly demonstrated, in others, IGF-I is thought to be the critical mediator, and in some cases direct and indirect effects appear to be at stake.
- Protein metabolism : in general, growth hormone stimulates protein anabolism in many tissues. This effect reflects a greater absorption of amino acids, a greater synthesis of proteins and a lower oxidation of proteins.
- Metabolism of fats : growth hormone improves the utilization of fats by stimulating the degradation and oxidation of triglycerides in adipocytes.
- Carbohydrate metabolism : Growth hormone is one of a battery of hormones that serves to keep blood glucose within a normal range.
Growth hormone is often said to have anti-insulin activity, because it suppresses insulin’s ability to stimulate glucose absorption in peripheral tissues and improve the synthesis of glucose in the liver.
In a somewhat paradoxical manner, the administration of growth hormone stimulates insulin secretion, which leads to hyperinsulinemia.
Control of growth hormone secretion
The production of growth hormone is modulated by many factors, including stress, exercise, nutrition, sleep and growth hormone itself. However, its primary controllers are two hypothalamic hormones and one stomach hormone:
- Growth hormone-releasing hormone (GHRH): is a hypothalamic peptide that stimulates both the synthesis and the secretion of growth hormone.
- Somatostatin (SS): is a peptide produced by various tissues of the body, including the hypothalamus. Somatostatin inhibits the release of growth hormone in response to GHRH and other stimulating factors such as low blood glucose concentration.
- Ghrelin: is a peptide hormone secreted by the stomach. Ghrelin binds to the somatotroph receptors and potently stimulates the secretion of growth hormone.
The secretion of growth hormone is also part of a negative feedback loop that involves IGF-I. Elevated levels of IGF-I in the blood lead to a decrease in the secretion of growth hormone not only by directly suppressing the somatotroph, but also by stimulating the release of somatostatin from the hypothalamus.
Growth hormone is also fed back to inhibit the secretion of GHRH and probably has a direct (autocrine) inhibitory effect on the secretion of the somatotroph.
The integration of all factors that affect the synthesis and secretion of growth hormone leads to a pulsatile pattern of release. The basal concentrations of the growth hormone in the blood are very low.
In children and young adults, the most intense period of growth hormone release is shortly after the onset of deep sleep.
The states of deficiency and excess of growth hormone provide very visible testimonies of the role of this hormone in normal physiology.
Such disorders may reflect lesions in the hypothalamus, pituitary, or target cells. A deficiency state can result not only from a deficiency in the production of the hormone, but in the response of the target cell to the hormone.
Clinically, deficiency in growth hormone or defects in its binding to the recipient are considered stunted or dwarfed.
The manifestation of the growth hormone deficiency depends on the age of onset of the disorder and may be the result of a hereditary or acquired disease.
The effect of excessive secretion of growth hormone also depends a lot on the age of onset and is considered as two distinctive disorders:
Giantism: is the result of excessive secretion of growth hormone that begins in young children or adolescents.
It is a very rare disorder, which is usually the result of a somatotropic tumor. One of the most famous giants was a man named Robert Wadlow. He weighed 8.5 pounds at birth, but at 5 years old he weighed 105 pounds and was 5 feet 4 inches tall.
Robert reached an adult weight of 490 pounds and 8 feet 11 inches tall. He died at 22 years old.
Acromegaly: is the result of excessive secretion of growth hormone in adults, usually the result of benign pituitary tumors. The onset of this disorder is usually internal, and occurs over several years.
The clinical signs of acromegaly include overgrowth of the extremities, swelling of the soft tissues, abnormalities in the structure of the jaw and heart disease.
Excessive growth hormone and IGF-I also lead to a series of metabolic disorders, including hyperglycemia.
Pharmaceutical and biotechnological applications of growth hormone
In past years, purified growth hormone from human cadaver pituitaries was used to treat children with severe growth retardation.
More recently, the virtually unlimited supply of growth hormone produced by recombinant DNA technology has led to several other applications for human and animal populations.
Human growth hormone is commonly used to treat children with pathologically low stature.
There is concern that this practice extends to the treatment of essentially normal children, the so-called “improvement therapy” or growth hormone on demand. Similarly, growth hormone has been used by some to improve athletic performance.
Although growth hormone therapy is generally safe, it is not as safe as any therapy and carries unpredictable health risks. Parents who request growth hormone therapy for children of essentially normal height are clearly wrong.
The role of growth hormone in normal aging remains poorly understood, but some of the cosmetic symptoms of aging appear to be susceptible to growth hormone therapy.
This is an active area of research, and additional information and recommendations about the risks and benefits will undoubtedly arise in the near future.
The somatotropin in animals
Growth hormone is currently approved and marketed to improve milk production in dairy cattle.
There is no doubt that the administration of bovine somatotropin to lactating cows results in an increase in milk production and, depending on the way cows are handled, can be an economically viable therapy.
However, this treatment breeds great controversy, even among dairy producers.
One thing that seems clear is that drinking milk from cattle treated with bovine growth hormone does not pose a risk to human health.
Another application of growth hormone in animal husbandry is the treatment of growing pigs with porcine growth hormone. It has been shown that such treatment significantly stimulates muscle growth and reduces fat deposition.
How it Works
The increase in HGH during fasting helps to preserve your muscle tissue and glycogen stores while using your fat stores instead. This breakdown of fat, which is called lipolysis, releases free fatty acids and glycerol, which are then metabolized to produce energy. According to Madelon Buijs, researcher at Leiden University Medical Center in the Netherlands, levels of HGH, which is produced by the pituitary gland, rise noticeably within 13 hours after starting a fast.
Biology 202 Exam 1 Endocrine & Reproductive
Hormones are transported to their target cells via the blood.
Hormones initiate responses by binding to receptors on their target cells.
Release hormones into the surrounding tissue fluid
The pancreas, gonads, placenta have other functions in addition to endocrine function.
Other organs have small clusters of cells that have endocrine function, i.e. the whole organ does not function as an endocrine gland.
Male sex hormone released by testis
Secreted by the pituitary, parathyroid, heart, stomach, liver, and kidneys
Synthesized as precursor molecules
Precursor molecules are processed by the ER
And are stored in the Golgi in secretory granules
**synthesized by removing a molecule of C02
Stored as granules in the cytoplasm until needed
Vertebrate endocrine system consist of glands (pituitary, thyroid, adrenal) and groups of scattered cells in epithelial tissue
Endocrine glands develop ---> All 3 germ layers
Cycles of secretion can maintain physiological and homeostatic control that lasts from hours to months. Ex: monthly menstrual cycle
Target cell membranes bind only to one type of hormone b/c they have receptors that only bind that specific hormone.
All human hormones act by binding to receptor molecules.
2.Hormone binding causes
The receptor to change shape
Binds to a nearby
inactive G-protein molecule
4.H-C binding causes the
replacement of a bound GDP
By a high energy GTP molecule
Moves along the membrane
Binds & activates a nearby
Inactive adenylate cyclase
6.Activated adenylate cyclase
Then converts ATP to cyclic AMP
(cAMP)----> 2nd messenger
Phosphorylation can activate or inhibit enzyme function
1 adenylate cyclase molecule can activate many cAMP molecules
1 PKA molecule can catalyze hundreds of reactions
As the cascade of activated intermediate enzymes form millions of products are also formed
(Figure 11.16) Cytoplasmic response to a signal: the stimulation of glycogen breakdown by epinephrine.
Many steps - ampliphication
Mutated phosphodiesterase = glucogon is gone, fat is constantly being broken down,
Hormone ---->PM receptor (plasma membrane -------> Gq --------------> Phospholipase C
DAG Releases PKC (protein kinase) *kinase add phosphate groups to other molecules
gonadotropin-releasing hormone (GnRH)
Others are removed from the blood by the kidneys or liver and their byproducts are excreted in urine or feces
Half life of hormone = amount of time necc to result in half the blood levels of the hormone
Water soluble hormones have the shortest half lives
It has two parts, anterior and posterior.
1. Posterior lobe is neural tissue that receives, stores, and releases hormones (oxytocin and antidiuretic hormone) made in the hypothalamus and is transported to the posterior pituitary via axons.
is connected to the hypothalamus via a nerve bundle called the hypothalamic- hypophyseal tract that runs through the infundiulum
The tract is made of neurons in the supraoptic and paraventricular nuclei of the hypothalamus
2. No direct connection b/t the anterior lobe and hypothalamus
3. There is a vascular connection
Stimulates most cells, but target bone and skeletal muscle
Stimulates the liver and other tissues to secrete insulin-like growth factor I (IGF-I or somatomedin)
IGF-I stimulates proliferation of chondrocytes (cartilage cells), resulting in bone growth.
Antagonistic hypothalamic hormones regulate GH
Thyrotropin releasing hormone (TRH) from the hypothalamus promotes the release of TSH
Corticotropin-releasing hormone (CRH) from the hypothalamus promotes the release of ACTH in a daily rhythm
In males LH travels to the testes (target cells) to stimulate secretion of testosterone.
In males scientists think prolactin influences the sensitivity of cells in the testes (interstitial cells) to the effects of luteinizing hormone (LH)
Prolactin-releasing hormone (PRH) from the hypothalamus stimulates the release of prolactin
Prolactin-inhibiting hormone (PIH) from the hypothalamus inhibits the release of prolactin
Tropin = hromones that regulate the secretion of other endo glands
Stimulates the smooth muscle of the uterus to contract, inducing labor
Stimulates the myoepithelial cells of the breasts to contract which releases milk from breasts when nursing.
Signals the collecting ducts of the kidneys to reabsorb more water and constrict blood vessels, which leads to higher blood pressure and thus counters the blood pressure drop caused by dehydration or other reasons
Diuretic - water uptake from kidney tubules
Thyroid hormones are held in storage but eventually attach to thyroid binding globulins (TBG) some are attached to transthyretin or albumin
Makes and secretes Corticosteroids (collection of over 30 hormones)
Stimulates the kidneys to reabsorb sodium if blood pressure drops - brings water
It also secretes (eliminates) potassium
secretes the hormones epinephrine and norepinephrine when
stimulated by sympathetic neurons of the autonomic nervous system (ANS)
2-stimulates many protein activation
3-translocation of Glut 4
to the plasma membrane causing
influx of glucose
4-glucose used to synthesis glycogen
5- glucose enters glycolysis of cellular
Respiration to form ATP
The number of chromosomes remains exactly the same after the division.
Prophase - chromosomes duplicate and condense, nuclear membrane breaks down
Metaphase - sister chromatids line up in the equatorial midline
Anaphase - sister chromatids are separated and moved to the opposite poles A (apart)
Telophase - chromosomes uncondense and nuclear envelope forms, and a new nucleus is formed this stage ends mitosis
There are two parts, I and II
Prophase I (nuclear envelope breaks down and chromosomes divide and chromatids condense)
Metaphase I This stage is different from Mitosis b/c here the HOMOLOGUS CHROMOSOMES line up at the equatorial midline **NOTE:Mitosis: in metaphase the SISTER CHROMATIDS line up
Anaphase I - homologous chromosomes move to the opposite poles of the cell
Telophase I -the chromosomes uncondense and new nuclear envelopes form, however there is no cytokinesis
The cell will enter the 2nd phase of meiosis if the it gets cues from the environment
Prophase II: The chromosomes condense again, following a brief interphase in which DNA does NOT replicate
Metaphase II: kinetochores of the paired chromatids line up across the equator of each cell
Anaphase II: The chromatids of the chromosomes finally separate, becoming chromosomes in their own right, and are pulled to opposite poles
Telophase II: the chromosomes gather into nuclei, and the cells divide. Each of the four cells has a nucleus with a haploid number of chromosomes.
III. EFFICACY OF SOMATOTROPIN
Somatotropin has been shown to have impressive effects on nutrient partitioning between muscle and adipose tissue that leads to a dramatic alteration in the growth of these tissues. Daily administration of maximally effective doses of pST (≥100 μg⋅kg body wt −1 ⋅day −1 ) to growing pigs for 30–77 days can increase average daily gain ∼10–20%, improve feed efficiency (i.e., the ratio of feed consumed to body weight gain) 13–33%, decrease lipid accretion rates by as much as 70%, and stimulate protein deposition (muscle growth) by as much as 62% (reviewed in Refs. 6668137). In general, responses in lean tissue accretion to ST treatment have been less for growing ruminants than observed for pigs. However, this species difference appears to relate to the difficulty in ensuring an amino acid supply that is adequate in balance and quantity. When the supply of rumen microbial protein is complemented with additional amino acids that escape rumen fermentation, the dramatic increase in protein accretion with bST treatment of ruminants is comparable to that observed with pST treatment of growing pigs (reviewed in Refs. 27137).
It is evident that pST administration has dramatic effects on protein accretion even in pigs highly selected for rapid growth and high rates of protein accretion (34). This is vividly illustrated by the results in Table 1, which show the effects of pST on rate of protein accretion in pigs that are considered to be “genetically elite” for rapid protein accretion. In this study, boars (intact males) treated with pST gained 273 g protein/day. This is the highest rate of protein deposition observed in pigs to date and corresponds to a muscle growth rate of ∼1.4 kg/day. When this rate of protein accretion rate is compared with that observed for elite pigs not treated with pST (162 g/day), it is apparent that the biological capacity or “ceiling” (as estimated by maximally effective doses of pST) for protein accretion is still considerably greater than rates presently attained despite the impressive improvements that have occurred with genetic selection over the last several decades in protein accretion rate. This suggests that considerable progress in increasing protein accretion rate can still be made with genetic selection programs that use protein accretion rate as a selection criterion.
Table 1. Effect of pST on accretion rates of protein and lipid in growing pigs (60–90 kg)
Dose of porcine somatotropin (pST) represents daily dose. Adapted from Campbell et al. (34).
The early studies evaluating the effects of pST on growth and carcass composition (407173) suggested that responsiveness was age dependent. This has been verified in subsequent studies (Table 2) that have shown the increase in growth rate and effects on protein and lipid deposition with pST treatment are significantly greater in the latter phase of the growth cycle. The mechanisms that account for this remain unclear.
Table 2. Summary of levels of performance and accretion rates of protein and lipid and responses to exogenous pST across different phases of growth in pigs
Dose of pST represents daily dose. Values in parentheses are response to pST treatment (in %). [* Data from Harrell et al. (89).
There is a good understanding of how changes in the pST dose affect various parameters of growth, productive efficiency, and carcass composition (2873137). Collectively, these studies have established that the dose relationship varies considerably among the different parameters (see Fig. 1). For example, body weight growth and rate of protein accretion are maximally stimulated at a daily dose of pST of ∼100 μg/kg body wt. In contrast, lipid accretion rate and the ratio of feed consumed to body weight decrease in a more linear manner over a range of pST up to 200 μg/kg body wt (see Fig. 1). The fact that there are differences in the shape of the dose-response curves is important because it illustrates that pST affects growth and nutrient metabolism of adipose tissue and muscle by different mechanisms. This is further illustrated by how dietary protein restriction affects lipid and protein accretion in pST-supplemented pigs (Fig. 2). The stimulatory effects of pST on protein accretion and circulating insulin-like growth factor (IGF)-I are progressively decreased until they are completely blunted as dietary protein levels decline (Fig. 2). In contrast, the ability of pST to reduce lipid accretion occurs across the range of dietary protein, even with the diets that contain the lowest protein levels. Collectively, the results depicted in Figs. 1 and 2 also provide valuable insight about nutrient requirements of pigs treated with pST. The marked changes that occur in compositional growth and growth rate in pigs treated with pST clearly underscore the importance of making adjustments in the dietary amino acid-calorie relationship to ensure an adequate availability of essential amino acids to accommodate the enhanced rate of protein accretion. This is particularly important because this dose of pST decreases feed intake.
Fig. 1.Relationship between porcine somatotropin (pST) dose and different parameters of growth performance (68). BW, body weight. [Adapted from Boyd and Bauman (26) and Boyd et al. (27).]
Fig. 2.Effect of dietary protein level on circulating insulin-like growth factor (IGF)-I and rates of lipid and protein accretion in growing pigs treated with pST (90 μg/day from 30 to 60 kg body wt ○) or excipient (•). Dietary protein levels were 8.9, 11.4, 14.5, 17.6, 20.7, and 23.8%. [Constructed using data of Campbell et al. (33).]
The precipitous decrease in lipid deposition (see Fig. 1) observed when pigs are treated with a daily dose of 30–200 μg pST/kg body wt illustrates the magnitude to which pST can alter nutrient utilization by adipose tissue and subsequent adipocyte hypertrophy. The effect of pST to decrease glucose (the primary substrate for lipogenesis in pig adipose tissue) utilization in adipose tissue results in a situation where glucose that is normally used for lipogenesis is redirected to other tissues, primarily muscle. This metabolic adaptation is important because it 1) decreases the rate of adipocyte hypertrophy and, hence, the rate of adipose tissue accretion and 2) accounts for the effects that ST has on productive efficiency as well as contributes to the increase in muscle growth.
Anabolic Steroid Hormones
Anabolic steroid hormones are synthetic substances that are related to the male sex hormones. They have the same mechanism of action within the body. Anabolic steroid hormones stimulate the production of protein, which is used to build muscle. They also lead to an increase in the production of testosterone. In addition to its role in the development of reproductive system organs and sex characteristics, testosterone is also critical in the development of lean muscle mass. Additionally, anabolic steroid hormones promote the release of growth hormone, which stimulates skeletal growth.
Anabolic steroids have therapeutic use and may be prescribed to treat problems such as muscle degeneration associated with disease, male hormone issues, and late onset of puberty. However, some individuals use anabolic steroids illegally to improve athletic performance and build muscle mass. Abuse of anabolic steroid hormones disrupts the normal production of hormones in the body. There are several negative health consequences associated with anabolic steroid abuse. Some of these include infertility, hair loss, breast development in males, heart attacks, and liver tumors. Anabolic steroids also effect the brain causing mood swings and depression.
Anterior and posterior pituitary hormones
The two sections of the pituitary gland produce a number of different hormones which act on different target glands or cells.
The anterior pituitary hormones:
- ( ACTH ) ( TSH ) ( LH )
- Follicle-stimulating hormone ( FSH ) ( PRL ) ( GH ) ( MSH )
The posterior pituitary hormones:
The anterior pituitary hormones
The anterior pituitary gland produces the four tropic hormones - the adrenocorticotropic hormone (ACTH), the thyroid-stimulating hormone, the follicle stimulating hormone (FSH), and the luteinizing hormone (LH).
ACTH and cortisol
Adrenocorticotropic hormone stimulates the adrenal gland to produce a hormone called cortisol. ACTH is also known as corticotropin.
Thyroid function of TSH
Thyroid-stimulating hormone stimulates the thyroid gland to secrete its own hormone, which is called thyroxine. TSH is also known as thyrotropin.
LH and FSH function
Luteinising and follicle-stimulating hormones control reproductive functioning and sexual characteristics. Stimulates the ovaries to produce oestrogen and progesterone and the testes to produce testosterone and sperm.
LH and FSH are known collectively as gonadotropins.
Luteinising hormone is also referred to as interstitial cell stimulating hormone (ICSH) in males.
Exact role of melanocyte-stimulating hormone in humans is unknown.
Functions and effects of the human growth hormone (somatotropin, HGH)
Human growth hormone spurs body growth by increasing:
- intestinal absorption of calcium
- cell division and development (especially in bone and cartilage)
- protein synthesis and lipid metabolism
- the release of fatty acids from fat cells, and prompts the conversion of fatty acids into fragments that can then form acetyl CoA for use as an energy source for the body.
Human growth hormone also suppresses glycolysis and increases glycogen production in the liver.
In summary, HGH spares proteins and carbohydrates by enhancing the use of lipids as an energy source for cell functions.
Somatotropin has a half-life of about 20 hours after secretion, after which it is no longer chemically active.
HGH, acting as a tropic hormone, triggers the production of growth factors in the liver and other tissues. These growth factors (composed of protein molecules) prolong the effects of somatotropin on bone and cartilage tissues.
Levels of human growth hormone tend to decrease with age. The resulting decline in protein synthesis may be responsible for some of the characteristic signs of aging, such as diminished muscle mass and wrinkles.
Insufficient HGH production during childhood results in a condition called pituitary dwarfism.
An excess of HGH production prior to puberty causes a disorder known as gigantism.
Excess somatotropin production during adult years produces acromegaly, symptoms of which include excessive thickening of bone tissue.
Function and secretion of prolactin hormone
Prolactin - a non-steroid hormone produced by the anterior pituitary and, in smaller quantities, by the immune system, the brain, and the pregnant uterus.
Prolactin stimulates the development of mammary gland tissue and milk production (lactogenesis).
The hypothalamic regulation of prolactin production is unusual.
The hypothalamus secretes the neurotransmitter dopamine, which inhibits rather than stimulates the production and secretion of prolactin by the pituitary. Severing the connection between the hypothalamus and the pituitary gland results in an increase in prolactin production.
After birth, however, the stimulation of nerve endings in the nipples during infant feeding will trigger the release of prolactin-secreting hormones by the hypothalamus. This spinal reflex (known as a neuroendocrine reflex) stimulates the production of prolactin.
Increasing estrogen levels also stimulate prolactin production in late pregnancy to prepare the mammary glands for lactation after the birth of a baby. Increased prolactin levels in pregnancy also inhibit ovulation by suppressing the production of Luteinising hormone.
Glands and hormones of the human endocrine system
The secretory organs that make up the human endocrine system, such as the anterior pituitary gland, the adrenal glands, and the pancreas, synthesize and secrete specific hormones. In addition, many endocrine glands, such as the thyroid gland, ovaries, and testes, are discrete, readily recognizable organs with defined borders and endocrine functions. Other glands are embedded within structures for example, the islets of Langerhans are embedded within the pancreas and may be seen clearly only under the microscope.
|Glands and hormones of the human endocrine system|
|*Intermediate lobe hormones referred to collectively as melanotropin or intermedin.|
|gland or tissue||principal hormone||function|
|testis||testosterone||stimulates development of male sex organs and secondary sex characteristics, including facial hair growth and increased muscle mass|
|ovary||estrogens (estradiol, estrone, estriol)||stimulate development of female sex organs and secondary sex characteristics, maturation of ovarian follicles, formation and maintenance of bone tissue, and contraction of the uterine muscles|
|inhibin (folliculostin)||inhibits secretion of follicle-stimulating hormone from the pituitary gland|
|progesterone||stimulates secretion of substances from the lining of the uterus (endometrium) in preparation for egg implantation in the uterine wall|
|relaxin||induces relaxation of pubic ligaments during childbirth to facilitate infant delivery|
|thyroid gland||thyroxine||stimulates cellular metabolism, lipid production, carbohydrate utilization, and central and autonomic nervous system activation|
|triiodothyronine||stimulates cellular metabolism, lipid production, carbohydrate utilization, and central and autonomic nervous system activation|
|adrenal gland, medulla||epinephrine (adrenaline)||stimulates "fight or flight" response, increases heart rate, dilates blood vessels in skeletal muscles and liver, increases oxygen delivery to muscle and brain tissues, increases blood glucose concentrations, and suppresses digestion|
|norepinephrine (noradrenaline)||stimulates "fight or flight" response, increases heart rate, constricts blood vessels, increases blood glucose concentrations, and suppresses digestion|
|adrenal gland, cortex||cortisol||activates physiological stress responses to maintain blood glucose concentrations, augments constriction of blood vessels to maintain blood pressure, and stimulates anti-inflammatory pathways|
|aldosterone||regulates balance of salt and water in the body|
|androgens||contribute to growth and development of the male reproductive system and serve as precursors to testosterone and estrogen|
|pituitary gland, anterior lobe||corticotropin (adrenocorticotropin, ACTH)||stimulates growth and secretion of cells of the adrenal cortex increases skin pigmentation|
|growth hormone (GH somatotropin)||stimulates growth of essentially all tissues in the body|
|thyrotropin (thyroid-stimulating hormone)||stimulates secretion of thyroid hormone and growth of thyroid cells|
|follicle-stimulating hormone (FSH)||stimulates maturation of egg follicles in females and development of spermatozoa in males|
|luteinizing hormone (LH interstitial cell stimulating hormone, ICSH)||stimulates rupture of mature egg follicles and production of progesterone and androgens in females and secretion of androgens in males|
|prolactin (PRL luteotropic hormone, LTH lactogenic hormone mammotropin)||stimulates and maintains lactation in breast-feeding mothers|
|pituitary gland, posterior lobe||oxytocin||stimulates milk ejection during breast-feeding and uterine muscle contraction during childbirth|
|vasopressin (antidiuretic hormone, ADH)||regulates fluid volume by increasing or decreasing fluid excretion in response to changes in blood pressure|
|pituitary gland, intermediate lobe||melanocyte-stimulating hormones (MSH)*||stimulate melanin synthesis in skin cells to increase skin pigmentation may also suppress appetite|
|hypothalamus||corticotropin-releasing hormone (CRH)||stimulates synthesis and secretion of corticotropin from the anterior pituitary gland|
|growth hormone-releasing hormone (GHRH)||stimulates synthesis and secretion of growth hormone from the anterior pituitary gland|
|thyrotropin-releasing hormone (TRH)||stimulates and regulates secretion of thyrotropin from the anterior pituitary gland and may modulate neuronal activity in the brain and spinal cord|
|gonadotropin-releasing hormone (GnRH)||stimulates synthesis and secretion of follicle-stimulating hormone and luteinizing hormone from the anterior pituitary gland|
|prolactin-inhibiting factor (PIF dopamine)||inhibits secretion of prolactin from the anterior pituitary gland|
|somatostatin||inhibits secretion of growth hormone from the anterior pituitary gland, inhibits secretion of insulin and glucagon in the pancreas, and inhibits secretion of gastrointestinal hormones and secretion of acid in the stomach|
|gastrointestinal neuropeptides||hormones secreted from the stomach and pancreas that stimulate hypothalamic secretion of neuropeptides, such as neuropeptide Y, gastrin-releasing peptide, and somatostatin, that regulate appetite, fat storage, and metabolism|
|pancreatic islets of Langerhans||glucagon||maintains blood glucose concentrations by stimulating release of glucose from the liver and production of glucose from amino acids and glycerol|
|insulin||stimulates glucose uptake and storage in adipose, muscle, and liver tissues|
|somatostatin||inhibits glucagon and insulin secretion from the pancreas and inhibits secretion of gastrointestinal hormones and secretion of acid in the stomach|
|pancreatic polypeptide||inhibits contraction of the gallbladder and secretion of exocrine substances from the pancreas|
|parathyroid gland||parathyroid hormone (parathormone)||increases serum calcium concentrations by stimulating release of calcium from bone tissue, reabsorption of calcium in the kidneys, and production of vitamin D in the kidneys inhibits reabsorption of phosphate in the kidneys|
|calcitonin||decreases serum calcium concentrations by promoting uptake of calcium into bone tissue and excretion of calcium in the urine|
|skin, liver, kidneys||calciferols (vitamin D)||maintain serum calcium concentrations by increasing absorption of calcium and phosphate in the intestines and reabsorption of calcium and phosphate in the kidneys mobilizes calcium from bone in response to parathyroid hormone activity|
|stomach||gastrin||stimulates secretion of acid and pepsin in the stomach and contraction of the pyloric region of the stomach near the small intestine to increase motility during digestion|
|duodenum||cholecystokinin (CCK pancreozymin)||stimulates release of bile from the gallbladder into the intestine and stimulates secretion of pancreatic juices into the intestine may induce satiety|
|secretin||stimulates secretion of water and bicarbonate from the pancreas into the duodenum inhibits secretion of gastrin in the stomach, delaying gastric emptying|
|gastric-inhibitory polypeptide (GIP)||inhibits secretion of acid into the stomach stimulates secretion of insulin from the pancreas|
|vasoactive intestinal peptide (VIP)||stimulates dilation of blood vessels and secretion of water and electrolytes from the intestine modulates immune functions|
|pineal gland||melatonin||regulates circadian rhythm (primarily in response to light and dark cycles) and release of gonadotropin-releasing hormone from the hypothalamus and gonadotropins from the pituitary gland|
|kidneys||renin||regulates blood pressure and blood flow by catalyzing conversion of angiotensinogen to angiotensin I in the kidneys|
|multiple tissues||insulin-like growth factors (somatomedins)||stimulate growth by mediating secretion of growth hormone from the pituitary gland|
|prostaglandins||regulate many physiological processes, including dilation and constriction of blood vessels, aggregation of platelets, and inflammation|
Other body tissues may also function as endocrine organs. Examples include the lungs, the heart, the skeletal muscles, the kidneys, the lining of the gastrointestinal tract, and the bundles of nerve cells called nuclei. While all nerve cells are capable of secreting neurotransmitters into the synapses (small gaps) between adjacent nerves, nerve cells that regulate certain endocrine functions—for example, the nerve cells of the posterior pituitary gland (neurohypophysis)—secrete neurohormones directly into the bloodstream.
Sometimes, endocrine cells of different embryological origins that secrete different hormones reside side by side within a gland. The most obvious example of this is the existence of the parafollicular cells that reside among the thyroid follicular cells within the thyroid gland. Endocrine glands with mixed cell populations have not evolved by chance. The hormonal secretions of one type of cell may regulate the activity of adjacent cells that have different characteristics. This direct action on contiguous cells, in which a hormone diffuses from its cell of origin directly to target cells without entering the circulation, is known as paracrine function. Excellent examples of the paracrine actions of hormones are provided by the ovaries and testes. Estrogens produced in the ovaries are crucial for the maturation of ovarian follicles before ovulation. Similarly, testosterone produced by the Leydig cells of the testes acts on adjacent seminiferous tubules to stimulate spermatogenesis. In these instances, very high local concentrations of hormones stimulate the target organs. A hormone also may act on its own cell, a phenomenon known as autocrine function.
37.3: Regulation of Body Processes
Hormones have a wide range of effects and modulate many different body processes. The key regulatory processes that will be examined here are those affecting the excretory system, the reproductive system, metabolism, blood calcium concentrations, growth, and the stress response.
Drinking alcoholic beverages causes an increase in urine output. This most likely occurs because alcohol:
- inhibits ADH release
- stimulates ADH release
- inhibits TSH release
- stimulates TSH release
FSH and LH release from the anterior pituitary is stimulated by ________.
What hormone is produced by beta cells of the pancreas?
When blood calcium levels are low, PTH stimulates:
- excretion of calcium from the kidneys
- excretion of calcium from the intestines
Name and describe a function of one hormone produced by the anterior pituitary and one hormone produced by the posterior pituitary.
In addition to producing FSH and LH, the anterior pituitary also produces the hormone prolactin (PRL) in females. Prolactin stimulates the production of milk by the mammary glands following childbirth. Prolactin levels are regulated by the hypothalamic hormones prolactin-releasing hormone (PRH) and prolactin-inhibiting hormone (PIH) which is now known to be dopamine. PRH stimulates the release of prolactin and PIH inhibits it. The posterior pituitary releases the hormone oxytocin, which stimulates contractions during childbirth. The uterine smooth muscles are not very sensitive to oxytocin until late in pregnancy when the number of oxytocin receptors in the uterus peaks. Stretching of tissues in the uterus and vagina stimulates oxytocin release in childbirth. Contractions increase in intensity as blood levels of oxytocin rise until the birth is complete.
Describe one direct action of growth hormone (GH).
Hormonal regulation is required for the growth and replication of most cells in the body. Growth hormone (GH), produced by the anterior pituitary, accelerates the rate of protein synthesis, particularly in skeletal muscles and bones. Growth hormone has direct and indirect mechanisms of action. The direct actions of GH include: 1) stimulation of fat breakdown (lipolysis) and release into the blood by adipocytes. This results in a switch by most tissues from utilizing glucose as an energy source to utilizing fatty acids. This process is called a glucose-sparing effect. 2) In the liver, GH stimulates glycogen breakdown, which is then released into the blood as glucose. Blood glucose levels increase as most tissues are utilizing fatty acids instead of glucose for their energy needs. The GH mediated increase in blood glucose levels is called a diabetogenic effect because it is similar to the high blood glucose levels seen in diabetes mellitus.
HGH as a doping agent
GH has been considered as an ergogenic drug since the late 1980s. Since that time, official and non‐official sources have reported that misuse in sport has steadily increased. The attractiveness of the product is based on popular knowledge that it is efficient, hard to detect, and without major side effects if well dosed. GH misusers primarily try to benefit from the known anabolic action of the drug, to increase their muscle mass and power.
The frequency of use and the dosage are hard to evaluate, but underground information suggests that the athletes misusing hGH take 10 IU/days three to four times a week to increase their lean body mass. We think that the mean dose is about 4 IU/day in combination with other doping agents, such as anabolic steroids in power sports or EPO in endurance sport. GH is often taken in cycles of four to six weeks, as is the case for anabolic steroids in bodybuilding. In endurance sport, little is known about the optimum utilisation of hGH doping in combination with other products. It is highly individual and empirical.
The effectiveness of rhGH in the improvement of sport performance is still under debate among users. The positive effects described in hGH deficient adults are not that clear among athletes. Although many of these underground reports indicate some positive effect on muscle mass, it is difficult to differentiate benefits obtained when hGH is taken in combination with anabolic steroids or even if the hGH used was a less effective product. The use of hGH as an anabolic agent still seems to be widespread, but it is difficult to investigate the extent of the phenomenon. It has been reported that 5% of male American high‐school students used or have used hGH as an anabolic agent. 22 It is unknown how popular hGH is among female athletes, but some use has been reported because of the low risk of androgenic side effects that are seen with anabolic steroids. Not only is the anabolic effect of hGH favored by high power output athletes, but its use is also gaining acceptance in endurance sport in combination with methods for enhancing oxygen transport. Although there are anecdotal reports on the solled dramatic increases in muscle mass and strength after large doses of hGH (especially among bodybuilders) their effectiveness under controlled conditions is generally less impressive.
As the results of controlled studies are generally not in agreement with subjective underground reports by misusers, it is difficult to draw any definite conclusions regarding the effects of excessive hGH administration on skeletal muscle function. It must be stressed that the regimen of hGH use in sport is designed to fulfil purposes other than just an increase in athletes' muscle mass. The doses involved are certainly specific to a discipline, its training model, and tailored to the regimen of other ergogenic substances being used concurrently.
GH misuse is still expensive and the high costs and difficulty in finding the “right” clean drug have certainly pushed some athletes to use products claimed to enhance GH production. Among these are the amino supplements such as arginine, ornithine, lysine, and tryptophan, but there are no clearly established results. The effectiveness of rhGH is also widely discussed among its users in the underground literature or in internet chat rooms without a clear positive position. Several aspects can be debated, but because of its price, some proportionality in the effects is to be expected by the users. Certainly disappointments are due to bad dosing, not combining with anabolic steroids, or a too‐short duration of use.
There are few controlled studies on the effectiveness of GH on the performance of top level athletes. In general these studies have been performed with supraphysiological dosages but not with the large amounts claimed to be effective, for instance, by bodybuilders. The results of most of these controlled studies are generally less impressive than the claims of those who misuse the substance. A study of volunteers under heavy resistance training found decrease of free fatty mass but no difference in the muscle strength. 23 With weight lifters, it has been shown that short term GH treatment does not increase muscle protein synthesis more than placebo 24 or other factors such as maximal voluntary strength (biceps or quadriceps). 25
These results conflict with reality, which is that rhGH misuse seems to exist in top‐level sport, because the compound is often found in police raids related to doping affairs. We believe that most of the time misusers will take rhGH as a part of their cocktail of specific preparations, rather than considering rhGH as a unique pharmaceutical preparation. The effects of GH on the metabolism are so widespread that one can be certain that this is taken in combination with other products. And the final effect generally occurs elsewhere, rather than in what is tested in the laboratories.
Overview of the Cross-Talk Between Hormones and Mitochondria
Béatrice Morio , . Luc Pénicaud , in Mitochondria in Obesity and Type 2 Diabetes , 2019
4.3.2 Growth Hormone
GH infusion induced mitochondrial ATP production and citrate synthase activity in skeletal muscle. 70 GH also induced gene expression of IGF-I, Tfam, and nuclear (cytochrome c oxidase subunit IV) and mitochondrial (cytochrome c oxidase subunit III) subunits of mitochondrial proteins. No changes in mitochondrial protein synthesis, however, were observed. 70 Because GH infusion stimulates plasma concentrations of IGF-1 and insulin, it is questionable whether the effects of GH on muscle mitochondrial activity are direct or indirect. Contrasting with these findings, results obtained in GH mutant mice evidenced upregulated mitochondrial metabolism in the liver during aging compared to wild-type animals or mutants treated with GH. 71 In particular, dwarf mice treated with GH evidenced a 45% decrease in complex II-driven mitochondrial respiration in the liver compared to dwarf mice treated with saline. GH treatment also decreased by 25% COX activity as well as gene expression and/or protein content of mitochondrial OXPHOS components, suggesting that GH could decrease mitochondrial functions. 71