HORMONES

 

INTRODUCTION

HORMONE

These are organic substance secreted by plants and animals that functions in the regulation of physiological activities and in maintaining homeostasis. Hormones carry out their functions by evoking responses from specific organs or tissues that are adapted to react to minute quantities of them. The classical view of hormones is that they are transmitted to their targets in the bloodstream after discharge from the glands that secrete them. This mode of discharge (directly into the bloodstream) is called endocrine secretion. The meaning of the term hormone has been extended beyond the original definition of a blood-borne secretion, however, to include similar regulatory substances that are distributed by diffusion across cell membranes instead of by a blood system

AUXINS

These are a powerful growth hormone produced naturally by plants. They are found in shoot and root tips and promote cell division, stem and root growth. They can also drastically affect plant orientation by promoting cell division to one side of the plant in response to sunlight and gravity.

Auxins Have Four Key Effects on Plant Growth:

ü  Stimulating shoot elongation – Auxins positively influence gibberlins that promote cell elongation. This increases plant length. Essentially, gibberlins and thereby auxins, increase the distance between nodes, spacing the branch points further apart.
Controlling seedling orientation – It was the infamous Charles Darwin and his son Francis who first noticed that seedlings bend toward the light. However, whether a new shoot grows into the soil or towards light, depends on where auxins are located and how they influence cells within the plant. Auxins will move downward due to gravity and laterally, away from light. Cells grow more in areas of the plant where auxins are highly concentrated.

ü  Stimulating root branching – When an auxin is applied to a cut stem, the stem will initiate roots at the cut.

ü  Promoting fruit development – Auxins in the flower promote maturation of the ovary wall and promote steps in the full development of the fruit.

Fast growth of shoot: auxins is known to cause the shoot of plants to grow fast

ü  It causes epical dominace   

ü  Retention of fruits

ü  It induces flowering

ü  It induce root formation

ü  It breaks dominance in seeds

ü  It induce pathenocarpy

ü  Delay of abscission of seed formed and seed ripening

Auxins can be produced naturally (by the plant) or synthetically (in a lab). When produced synthetically, they can be used in high concentrations as a pesticide, causing drastic growth. The herbicide, 2-4-D, is an example of an auxin-based pesticide, specifically engineered to cause dicots (plants like dandelions) to grow quickly and uncontrollably, ultimately killing the plant.

GIBBERELLINS DEFINITION

“Gibberellins are any group of plant hormones that stimulate elongation of the stem, flowering and germination.”

Gibberellins (GAs) are plant hormones that regulate various developmental processes, including stem elongation, germination, dormancy, flowering, flower development, and leaf and fruit senescence. GAs are one of the longest-known classes of plant hormone

As, we humans have different types of hormones, a chemical messenger produced by the endocrine glands to perform several metabolic activities within the body.

Like humans, plants also have five major types of plant hormones which are collectively called as plant growth regulators, promoters, inhibitors, and phytohormones.

Gibberellins are the plant growth regulators involved in regulating the growth and influencing different developmental processes which include stem elongation, germination, flowering, enzyme induction, etc.

Gibberellins have different effects on plant growth and the stem elongation is the most dramatic amongst all.  The stem starts to grow when it is applied in low concentration to a bush. The internodes grow so long that the plants become indistinguishable from climbing. The Gibberellins overcome the genetic limitations in different dwarf varieties.

There are more than 70 gibberellins isolated. They are GA1, GA2, GA3 and so on. GA3 Gibberellic acid is the most widely studied plant growth regulators.

Gibberellin is a diterpenoid. It forms the basis of molecules such as vitamins A and E. The figure above shows the structure of the Gibberellin A1, the first identified gibberellin.

The structure of all the gibberellins is the same with several side groups attached. These groups determine the unique functions of gibberellins in different tissues.

FUNCTION OF GIBBERELLINS

Gibberellin function in plants

The important gibberellins function are mentioned below:

ü  Seed Germination

Some seeds that are sensitive to light such as tobacco and lettuce exhibit poor germination in the absence of sunlight. Germination begins rapidly if the seeds are exposed to the sunlight. If the seeds are treated with gibberellic acid, the light requirement can be overcome.

ü  Dormancy of Buds

The buds that are formed in autumn stay dormant until next spring. This dormancy can be overcome by treating them with gibberellin.

ü  Root Growth

Gibberellins have almost no effect on the growth of roots. However, some inhibition of growth can occur at a higher concentration in a few plants.

ü  Elongation of the Internodes

Internodes elongation is the most pronounced effects of gibberellins on plant growth. In many plants such as dwarf pea and maize, the genetic dwarfism can be overcome.

For example, the dwarf pea plants have expanded leaves and short internodes. But the internodes expand and look like tall plants when treated with gibberellin.

Gibberellins exhibit their impact by altering gene transcription.

The steps of gibberellin functions are mentioned below:

The GA enters the cell and binds to a soluble protein receptor.

This binds to a protein complex (SCF) that attaches ubiquitin to one or the other DELLA proteins.

This activates the destruction of DELLA proteins through proteasomes.

The destruction of DELLA proteins releases the inhibition and gene transcription starts.

This procedure is amongst different cases in biology where the pathway is turned on by inhibiting the pathway. However, most of the proteins that are involved differ according to circumstances, both auxin and gibberellins influence gene expression by a common mechanism of repression relief.

IT also promote the development of flowers

USES OF GIBBERELLINS

Gibberellin is commercially obtained from fungi. It is used to facilitate the germination of seeds.

It is sprayed on the grapevines and used to enlarge them.

It is used on cucumber plants to produce all-male flowers. This helps the farmers to obtain pollen of desired characteristics to be used for hybridization.

Biennial plants produce flowers only during low temperatures. When gibberellin is applied, these plants will flower irrespective of the low temperatures.

The dwarf varieties of plants which are genetic mutants can be made to grow by applying gibberellins to them.

KINETIN

Is a cytokinin. Cytokinins are compounds that stimulate plants to grow. Kinetin occurs naturally in humans and is sometimes used to make medicine.
People use kinetin most often for aging skin, skinwrinkles from sun damage, and a skin condition that causes redness on the face (rosacea), but there is no good scientific evidence to support these uses.

How does it work ?

Kinetin prevents green plant leaves from turning brown. There is some information that suggests kinetin might prevent age-related changes in human skin by protecting the DNA in skin cells from damage (antioxidant effects) and decreasing skin water loss

Uses & Effectiveness 

1.      Insufficient Evidence for

A skin condition that causes redness on the face (rosacea). Early research shows that applying a lotion containing kinetin helps to reduce most symptoms of rosacea, like roughness and redness, in most people. But it doesn't seem to help everyone.

Skin wrinkles from sun damage. Early research shows that applying a lotion containing kinetin to the face helps to reduce wrinkles and to improve the feeling of the skin in people who have wrinkled skin from the sun.

Aging skin.

2.      An inner ear disorder marked by dizziness, hearing loss, and ringing in the ear (Meniere disease).

3.      Skin imperfections.

Other conditions.

More evidence is needed to rate the effectiveness of kinetin for these uses

When taken by mouth: There isn't enough reliable information to know if kinetin is safe. It might cause side effects such as nausea, headache, diarrhea, rash, and ringing in the ears.
When applied to the skin: Kinetin is POSSIBLY SAFE when used in a cream or lotion containing kinetin 0.1% for up to 12 weeks. It might cause side effects such as redness, dryness, peeling, burning, stinging, and itching in some people. But it isn't clear if these symptoms are from kinetin or another ingredient in the products used.
When applied into the ear: There isn't enough reliable information to know if kinetin is safe or what the side effects might be.

Special Precautions and Warnings

Pregnancy and breast-feeding: There isn't enough reliable information to know if kinetin is safe to use when pregnant or breast-feeding. Stay on the safe side and avoid use.
Bleeding disorders: There is some concern that kinetin might prolong bleeding time and increase the risk of bruising and bleeding in some people with bleeding disorders. If you have a bleeding disorder, use kinetin with caution.
Surgery: Kinetin might increase the risk of bleeding during and after surgery. Stop taking kinetin at least 2 weeks before a scheduled surgery.

FUNCTION OF KINETINS

1.      It control cell division

2.      It can stimulate the development of roots

3.      It slow down aging of plant part

4.      It can break dormancy of buds leading to bud growth

5.      Kit stimulate mitosis in meristems and in embryos during germination

6.      It increase the reisitance of some plant to harmful effects scuh as viral infection, radiation and low temperature

7.      It promote axilary bud growth in plant

ETHYLENE is a group of plant growth regulators which are widely used for ripening fruits and for the production of more flowers and fruits. Ethylene is a small hydrocarbon, the colourless flammable gas which is denoted by a formula C₂H₄ or H₂C=CH₂. Ethene is the IUPAC name for ethylene.

FUNCTION OF ETHYLEN OR ETHENE GAS

It rtards lateral bud development

It hastens the ripening of fruits

It inhibit stem enlongation

It accelerate abscission of leaves, flowers and fruits

It accelerate aging of plant organs

 

 

DIFFERENCES BETWEEN VITAMINS AND HOMONES

One vitamin, Vitamin D, or cholecalciferol, is a hormone: it is made in the skin on exposure to sun and then interacts with a receptor in intestinal cells to induce synthesis of calcium binding protein. But the other vitamins are enzyme cofactors. The main difference is that vitamins participate chemically in specific enzymatic reactions whereas hormones are simply signals that are either bound to a receptor or not. Both vitamins and hormones are effective in very small amounts and do not supply calories.”

Maybe some elaboration would help, using a simple example. Vitamin B3, nicotinamide, is converted to the enzyme cofactor, NAD+. It binds to enzymes and participate in chemical reactions called hydride transfers. It is changed to NADH in the process. Example:

lactate + NAD+ <=> pyruvate + NADH.

From a chemist’s point of view, NAD+ is an oxidizing reagent, and NADH is reducing reagent.

NADH is recycled by the electron transport chain back to NAD+, which why we only need small amounts of the vitamin.

A hormone such as insulin does not undergo any chemical changes. It would be classified as a signalling molecule. It binds to a receptor, causing a conformation change that initiates a signalling cascade. The result is numerous chemical reactions downstream, but insulin itself never changes. It binds to a receptor and dissociates again, in dynamic equilibrium, able to bind to another receptor.

Hormones and vitamins differ in many other ways, but this is the key difference in terms of how they function.

Unlike plant hormones, animal hormones are often (though not always) produced in specialized hormone-synthesizing glands (shown below). The hormones are then secreted from the glands into the blood stream, where they are transported throughout the body. Some other differences include:

1.      Vitamins are synthesized in plants and taken by animals while hormones secreted mostly by endocrine glands and some by neurosecretory cells of animals

2.      Vitamins include esters, organic acids, etc. while hormones include water soluble amino acids and polypeptide or fat solublesteroids.

3.      Vitamins have ctatalytic properties and act as coenzyme while hormones excitatory and sometimes inhibitory but never act as coenzyme.

4.      Vitamins deficiency causes specific deficiency disease while hormones directly influence gene expressions.

ANIMAL HORMONES

Hormones which are sometimes called chemical messengers or organic substance are produced by duckless glands (endocrine glands)

There are many glands and hormones in different animal species, and we will focus on just a small collection of them.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Locations of endocrine glands in the human body. Image credit: OpenStax Anatomy and Physiology (2021).

In vertebrates, glands and hormones they produce include (note that the following list is not complete):

 

hypothalamus: integrates the endocrine and nervous systems; receives input from the body and other brain areas and initiates endocrine responses to environmental changes; synthesizes hormones which are stored in the posterior pituitary gland; also synthesizes and secretes regulatory hormones that control the endocrine cells in the anterior pituitary gland. Hormones produced include

1.      growth-hormone releasing hormone: stimulates release of growth hormone (GH) from the anterior pituitary

2.      corticotropin-releasing hormone: stimulates release of adrenocorticotropic hormone (ACTH) from the anterior pituitary

3.      thyrotropin-releasing hormone: stimulates release of thyroid-stimulating hormone (TSH) from the anterior pituitary

4.      gonadotropin-releasing hormone: stimulates release of follicle -stimulating hormone and luteinizing hormone from the anterior pituitary

5.      antidiuretic hormone (vasopressin): promotes reabsorption of water by kidneys; stored in posterior pituitary

6.      oxytocin: induces uterine contractions labor and milk release from mammary glands; stored in posterior pituitary

pituitary gland: the body’s master gland; located at the base of the brain and attached to the hypothalamus via a stalk called the pituitary stalk; has two distinct regions: the anterior portion of the pituitary gland is regulated by releasing or release-inhibiting hormones produced by the hypothalamus, and the posterior pituitary receives signals via neurosecretory cells to release hormones produced by the hypothalamus. Hormones produced (or secreted) by the gland include:

anterior pituitary: the following hormones are produced by the anterior pituitary and released in response to hormone signals from the hypothalamus

§  growth hormone: stimulates growth factors

§  adrenocorticotropic hormone (ACTH): simulates adrenal glands to secrete glucocorticoids such as cortisol

§  thyroid-stimulating hormone: stimulates thyroid gland to secrete thyroid hormones

§  follicle-stimulating hormone (FSH) and luteinizing hormone (LH): stimulates production of gametes and sex steroid hormones

§  prolactin: stimulates mammary gland growth and milk production

posterior pituitary: the following hormones are produced by the hypothalamus and stored in    the posterior pituitary

v  antidiuretic hormone: promotes reabsorption of water by kidneys; stored in posterior pituitary

v  oxytocin: induces uterine contractions during labor and milk release from mammary glands during suckling; stored in posterior pituitary

v  thyroid gland: butterfly-shaped gland located in the neck; regulated by the hypothalamus-pituitary axis; produces hormones involved in regulating metabolism and growth:

v  thyroxine (T₄) and triiodothyronine (T3): increase the basal metabolic rate, affect protein synthesis and other metabolic processes, help regulate long bone growth (synergy with growth hormone)

adrenal glands: two glands, each located on one kidney; consist of adrenal cortex (outer layer) and adrenal medulla (inner layer), which each produce different sets of hormones:

adrenal cortex:

mineralocorticoids, such as aldosterone: increases reabsorption of sodium by kidneys to regulate water balance

glucocorticoids, such as cortisol and related hormones: long-term stress response hormones that increase blood glucose levels by stimulating synthesis of glucose and gluconeogenesis (converting a non-carbohydrate to glucose) by liver cells; promote the release of fatty acids from adipose tissue

 

 

adrenal medulla:

epinephrine (adrenaline) and norepinephrine (noradrenaline): short-term stress response (“fight-or-flight”) hormones that increase heart rate, breathing rate, cardiac muscle contractions, blood pressure, and blood glucose levels; accelerate the breakdown of glucose in skeletal muscles and stored fats in adipose tissue; release of epinephrine and norepinephrine is stimulated directly by neural impulses from the sympathetic nervous system

pancreas: located between the stomach and the proximal portion of the small intestine; regulates blood glucose levels via the hormones:

insulin: decreases blood glucose levels by promoting uptake of glucose by liver and muscle cells and conversion to glycogen (a sugar storage molecule)

glucagon: increases blood glucose levels by promoting breakdown of glycogen and release of glucose from the liver and muscle

gonads: produce sex steroid hormones that promote development of secondary sex characteristics and regulation of gonad function:

ovaries (in females):

estradiol: regulates development and maintenance of ovarian and menstrual cycles

progesterone: prepares uterus for pregnancy

testes (in males): regulates development and maintenance of sperm production

The hormones produced and/or stored by the pituitary gland are summarized here:

Hormonal Regulation of Body Processes in Animals

The information below was adapted from OpenStax Biology 37.3

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 blood glucose, hunger, metamorphosis, stress, and sex. We will primarily focus on these processes in vertebrates, but will also consider invertebrates in some cases.

Blood Glucose

Glucose is the primary energy source for most animal cells, and it is distributed throughout the body via the blood stream. The ideal, or target, blood glucose concentration is about 90 mg/100 mL of blood, which equates to about 1 tsp of glucose per 6 quarts of blood. After a meal, carbohydrates are broken down during digestion and absorbed into the blood stream. The amount present following a meal is typically more than what the body needs at that moment, and so the extra glucose must be removed and stored for later use. The opposite phenomenon occurs following a period of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining appropriate blood glucose levels.

Insulin is produced by the beta cells of the pancreas, which are stimulated to release insulin as blood glucose levels rise (for example, after a meal is consumed). Insulin lowers blood glucose levels through several processes:

Ø  enhances the rate of glucose uptake and utilization by target cells, which use glucose for ATP production

Ø  stimulates the liver to convert glucose to glycogen, which is then stored by cells for later use

Ø  increases glucose transport into certain cells, such as muscle cells and the liver

Ø  stimulates the conversion of glucose to fat in adipocytes and the synthesis of proteins.

These actions together cause cause blood glucose concentrations to fall, called a hypoglycemic ‘low sugar’ effect, which inhibits further insulin release from beta cells through a negative feedback loop.

When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized rapidly during exercise, the hormone glucagon is released from the alpha cells of the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect through several mechanisms:

Ø  stimulates the breakdown and release of glucose from glycogen in skeletal muscle cells and liver cells

Ø  stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose

Ø  stimulates adipose cells to release fatty acids into the blood

Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells. These actions mediated by glucagon result in an increase in blood glucose levels to normal homeostatic levels. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in below. Growth and Metamorphosis

In vertebrate species that undergo metamorphosis, such as amphibians, surges of T₃ are responsible for initiating development of new structures, reorganization of  internal organ systems, and other processes that occur during metamorphosis. In insects, metamorphosis is controlled by a set of hormones that determine whether the animal grows into the next larval stage or changes into an adult as it gets larger. The corpus allatum, an endocrine gland in the brain, secretes a hormone called juvenile hormone during all larval stages, which maintains the larval status of the animal. As the larvae grows, another endocrine gland in the brain releases prothoracicotropic hormone, which signals to the prothoracic gland to release the hormone ecdysone. Ecdysone promotes either molting (shedding the exoskeleton) or metamorphosis, depending on the level of juvenile hormone. Ecdysone in combination with high juvenile hormone results in molting into the next larval stage; ecdysone in combination with low juvenile hormone results in metamorphosis into an adult.

Stress: Short vs Long Term Responses

One of the main functions of endocrine hormones is to ensure the body’s internal environment remains stable (homeostasis). Stressors are stimuli that disrupt homeostasis. Some stressors require immediate attention and activate the short term, “fight-or-flight” stress response, which stimulates an increase in energy levels through increased blood glucose levels. This prepares the body for physical activity that may be required to respond to stress: to either fight for survival or to flee from danger. The fight-or-flight response exists in some form in all vertebrates.

In contrast, some stresses, such as illness or injury, can last for a long time. Glycogen reserves, which provide energy in the short-term response to stress, are exhausted after several hours and cannot meet long-term energy needs. If glycogen reserves were the only energy source available, neural functioning could not be maintained once the reserves became depleted due to the nervous system’s high requirement for glucose. In this situation, the body has evolved a response to counter long-term stress through the actions of the glucocorticoids, which ensure that long-term energy requirements can be met. The glucocorticoids mobilize lipid and protein reserves, stimulate gluconeogenesis, conserve glucose for use by neural tissue, and stimulate the conservation of salts and water.

The sympathetic nervous system regulates the stress response via the hypothalamus. Stressful stimuli cause the hypothalamus to signal the adrenal medulla (which mediates short-term stress responses) via nerve impulses, and the adrenal cortex, which mediates long-term stress responses, via the hormone adrenocorticotropic hormone (ACTH), which is produced by the anterior pituitary.

Short-term Stress Response

When presented with a stressful situation, the body responds by calling for the release of hormones that provide a burst of energy. The hormones epinephrine (also known as adrenaline) and norepinephrine (also known as noradrenaline) are released by the adrenal medulla. These two hormones prepare the body for a burst of energy in the following ways:

cause glycogen to be broken down into glucose and released from liver and muscle cells

increase blood pressure

increase breathing rate

increase metabolic rate

change blood flow patterns, leading to increased blood flow to skeletal muscles, heart, and brain; and decreased blood flow to digestive system, skin, and kidneys

Long-term stress response differs substantially from short-term stress response. The body cannot sustain the bursts of energy mediated by epinephrine and norepinephrine for long times. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. The adrenal cortex is stimulated by ACTH to release steroid hormones called corticosteroids. The two main corticosteroids are glucocorticoids such as cortisol, and mineralocorticoids such as aldosterone. These hormones mediate the long-term stress response in the following ways:

glucocorticoids:

promote breakdown of fat into fatty acids in the adipose tissue and release into bloodstream for ATP production

stimulate glucose synthesis from fats and proteins to increase blood glucose levels

inhibit immune function to conserve energy

mineralcorticoids:

promote retention of sodium ions and water by kidneys

increase blood pressure and volume (via sodium/water retention)

Coticosteriods are under control of a negative feedback loop (illustrated below), which can become mis-regulated in cases of chronic long-term stress.

 

CONCLUSION

Hormones olays vital roles in the development of both plants and animals. Over secretion and under secretion of these hormone can lead to abnormalities

 

 

 

 

 

 

 

 

 

 

 

 

REFERENCES

American College of Obstetricians and Gynecologists Women’s Health Care Physicians. Executive Summary: hormone therapy. Obstet Gynecol. 2004;104(4 Suppl):1S–4. 

American Academy of Family Physicians. Hormone Replacement Therapy. Leawood, KS: American Academy of Family Physicians; 2005. [4 May 2012]. Accessed at http://www​.aafp.org/online​/en/home/clinical​/exam/hormonereplacement.html

American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 420, November 2008: hormone therapy and heart disease. Obstet Gynecol. 2008;112(5):1189–92. 

American College of Physicians. ACP Clinical Practice Guidelines. Philadelphia: American College of Physicians; 2012. [4 May 2012]. Accessed at http://www​.acponline​.org/clinical_information​/guidelines/guideline

Anderson GL, Judd HL, Kaunitz AM, et al. Effects of estrogen plus progestin on gynecologic cancers and associated diagnostic procedures: the Women’s Health Initiative randomized trial. JAMA. 2003;290(13):1739–48. 

Britainiaacademy.com/plants and animal hormones 2020.

Canadian Task Force on Preventive Health Care. Hormone Replacement Therapy for the Primary Prevention of Chronic Diseases. Ottowa, Canada: Canadian Task Force on Preventive Health Care; 2004. [4 May 2012]. Accessed at http://www​.canadiantaskforce​.ca/recommendations/2003_01_eng​.html

Cauley JA, Robbins J, Chen Z, et al. Effects of estrogen plus progestin on risk of fracture and bone mineral density: the Women’s Health Initiative randomized trial. JAMA. 2003;290(13)

Chlebowski RT, Anderson GL, Gass M, et al. Estrogen plus progestin and breast cancer incidence and mortality in postmenopausal women. JAMA. 2010;304(15):1684–92.

Chlebowski RT, Hendrix SL, Langer RD, et al. Influence of estrogen plus progestin on breast cancer and mammography in healthy postmenopausal women: the Women’s Health Initiative randomized trial. JAMA. 2003;289(24):3243–53. 

Chlebowski RT, Schwartz AG, Wakelee H, et al. Oestrogen plus progestin and lung cancer in postmenopausal women (Women’s Health Initiative trial): a post-hoc analysis of a randomised controlled trial. Lancet. 2009;374(9697):1243–51. 

Chlebowski RT, Wactawski-Wende J, Ritenbaugh C, et al. Estrogen plus progestin and colorectal cancer in postmenopausal women. N Engl J Med. 2004;350(10):991–1004. 

Cirillo DJ, Wallace RB, Rodabough RJ, et al. Effect of estrogen therapy on gallbladder disease. JAMA. 2005;293:330–9. 

Cushman M, Kuller LH, Prentice R, et al. Estrogen plus progestin and risk of venous thrombosis. JAMA. 2004;292(13):1573–80. 

Gramling R, Eaton CB, Rothman KJ, et al. Hormone replacement therapy, family history, and breast cancer risk among postmenopausal women. Epidemiology. 2009;20(5):752–6.

Homones (functions and uses) by Ernest J.W. Barrington 2007

Humphrey LL, Takano LM, Chan BK. Postmenopausal Hormone Replacement Therapy and Cardiovascular Disease, Systematic Evidence Review No. 10. Rockville, MD: Agency for Healthcare Research and Quality; 2002. [4 May 2012]. Accessed at http://www​.ncbi.nlm.nih​.gov/books/NBK42645/

Harris RP, Helfand M, Woolf SH, et al. Current methods of the third U.S. Preventive Services Task Force. Am J Prev Med. 2001;20(3S):21–35.

Hays J, Ockene JK, Brunner RL, et al. Effects of estrogen plus progestin on health-related quality of life. N Engl J Med. 2003;348(19):1839–54.

Heiss G, Wallace R, Anderson GL, et al. Health risks and benefits 3 years after stopping randomized treatment with estrogen and progestin. JAMA. 2008;299(9):1036–45. 

Hendrix SL. The Women’s Health Initiative estrogen plus progestin trial: the study and how it changes our practice. J Am Osteopath Assoc. 2003;103(2 Suppl 2):S3–5. 

Hendrix SL, Cochrane BB, Nygaard IE, et al. Effects of estrogen with and without progestin on urinary incontinence. JAMA. 2005;293(8):935–48.

Hsia J, Criqui MH, Rodabough RJ, et al. Estrogen plus progestin and the risk of peripheral aerterial disease. Circulation. 2004;109(5):620–6. 

Humphrey LL. Hormone Replacement Therapy and Breast Cancer, Systematic Evidence Review No. 14. Rockville, MD: Agency for Healthcare Research and Quality; 2002. [4 May 2012]. Accessed at http://www​.ncbi.nlm.nih​.gov/books/NBK42718/

LeBlanc ES, Chan BK, Nelson HD. Hormone Replacement Therapy and Cognition, Systematic Evidence Review No. 13. Rockville, MD: Agency for Healthcare Research and Quality; 2002. [4 May 2012]. Accessed at http://www​.ncbi.nlm.nih​.gov/books/NBK42704/

LeBlanc ES, Janowsky J, Chan BK, Nelson HD. Hormone replacement therapy and cognition: systematic review and meta-analysis. JAMA. 2001;285(11):1489–99. 

Miller J, Chan BK, Nelson HD. Postmenopausal estrogen replacement and risk for venous thromboembolism: a systematic review and meta-analysis for the U.S. Preventive Services Task Force. Ann Intern Med. 2002;136(9):680–90. 

Miller J, Chan BK, Nelson HD. Hormone Replacement Therapy and Risk of Venous Thromboembolism, Systematic Evidence Review No. 11. Rockville, MD: Agency for Healthcare Research and Quality; 2002. [4 May 2012]. Accessed at http://www​.ncbi.nlm.nih​.gov/books/NBK42678/

Management of osteoporosis in postmenopausal women: 2010 position statement of the North American Menopause Society. Menopause. 2010;17(1):25–54. 

Mosca L, Benjamin E, Berra K, et al. Effectiveness-based guidelines for the prevention of cardiovascular disease in women—2011 update: a guideline from the American Heart Association. Circulation. 2011;123(11):1243–62.

Manson JE, Hsia J, Johnson KC, et al. Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. 2003;349(6):523–34. 

Margolis KL, Bonds DE, Rodabough RJ, et al. Effect of oestrogen plus progestin on the incidence of diabetes in postmenopausal women: results from the Women’s Health Initiative hormone trial. Diabetologia. 2004;47(7):1175–87. 

 

Nelson HD, Humphrey LL, Nygren P, et al. Postmenopausal hormone replacement therapy: scientific review. JAMA. 2002;288(7):872–81. 

Nelson HD. Assessing benefits and harms of hormone replacement therapy: clinical applications. JAMA. 2002;288(7):882–4. 

Nelson HD. Hormone Replacement Therapy and Osteoporosis, Systematic Evidence Review No. 12. Rockville, MD: Agency for Healthcare Research and Quality; 2002. [4 May 2012]. Accessed at http://www​.ncbi.nlm.nih​.gov/books/NBK42693/

North American Menopause Society. Gass ML, Manson JE, et al. The 2012 hormone therapy position statement of the North American Menopause Society. Menopause. 2012;19(3):257–271. 

OpenStax Biology 37.3 2016

OpenStax Anatomy and Physiology, 2020.

Professor of Zoology, University of Nottingham, England, 1949–74. Author of Introduction to     General and Comparative Endocrinology.

Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial. JAMA. 2002;288(3):321–33. 

Rossouw JE, Prentice RL, Manson JE, et al. Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause. JAMA. 2007;297(13):1465–77.

Toh S, Hernandez-Diaz S, Logan R, et al. Coronary heart disease in postmenopausal recipients of estrogen plus progestin therapy: does the increased risk ever disappear? A randomized trial. Ann Intern Med. 2010;152(4):211–7.

U.S. Preventive Services Task Force. Hormone therapy for the prevention of chronic conditions in postmenopausal women: recommendations from the U.S. Preventive Services Task Force. Ann Intern Med. 2005;142(10):855–60. 

US Food and Drug Administration. Estrogen and Estrogen With Progestin Therapies for Postmenopausal Women. Silver Spring, MD: U.S. Food and Drug Administration; 2010. [4 May 2012]. Accessed at http://www​.fda.gov/Drugs​/DrugSafety/InformationbyDrugClass​/ucm135318.htm.

U.S. Preventive Services Task Force. Postmenopausal hormone replacement therapy for primary prevention of chronic conditions: recommendations and rationale. Ann Intern Med. 2002;137(10):834–9. 

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