General endocrinology

Last updated: December 16, 2023

Summary

Endocrinology is the study of the endocrine system (i.e., the hypothalamus, pituitary gland, thyroid gland, adrenals, and gonads), metabolic diseases, and certain aspects of nutritional medicine. The endocrine glands are responsible for producing and secreting hormones, which influence the function of cells in certain tissues of the body. Hormone secretion is controlled by highly regulated pathways, the most important of which is the hypothalamic-pituitary axis. The hypothalamus secretes and stores nontropic hormones (e.g., ADH, oxytocin) and releasing hormones (e.g., TRH, CRH, GnRH). The pituitary gland is composed of the anterior pituitary, which secretes tropic hormones (e.g., ACTH, TSH, FSH, LH) and whose function is controlled by hypothalamic releasing hormones, and the posterior pituitary, which stores ADH and oxytocin. The gonads are the ovaries in female individuals and testicles in male individuals. Their function is controlled via the hypothalamic-pituitary-gonadal axis, as well as the secretion of sex hormone-binding globulin (SHBG). Disruption of the hypothalamic-pituitary axis can result in the development of various endocrine disorders, which are classified according to the level of pathway disruption: primary (disorders of the peripheral endocrine gland), secondary (pituitary dysfunctions), and tertiary (hypothalamic disorders). An understanding of these hormone pathways is important for the diagnosis and management of endocrine disorders, particularly when interpreting changes in hormone levels and the results of suppression and/or stimulation tests.

For more information, see the articles "Thyroid gland and parathyroid glands" and “Adrenal gland.”

Chalk Talk: The neuroendocrine system

Overview of endocrinological diseases

This article focuses on the hypothalamic-pituitary axis. Other important structures, hormones, and metabolic diseases are discussed in their respective articles.

Types of endocrinological diseases
- Primary disease: caused by disorders of the endocrine gland (e.g., Addison disease)
- Secondary disease: caused by disorders of the pituitary (e.g., Cushing disease)
- Tertiary disease: caused by disorders of the hypothalamus (e.g., hypothalamic trauma, hemorrhage)
Metabolic diseases
- Diabetes mellitus
- Metabolic syndrome
- Osteoporosis (See “Calcium homeostasis” in “Hypocalcemia”)
Diseases of the endocrine glands of the hypothalamic-pituitary axis

Basics of endocrinology

Hormones

Definition
- Hormones are endogenous messengers produced by endocrine glands or single cells that are responsible for signal transduction.
- They influence the function and metabolic rate of other organs and cells in the body.
- Complex regulatory circuits (e.g., the hypothalamic-pituitary axis) control their secretion.
Types of hormones

Overview of the most important types of hormones
Type of hormone	Description	Example
Based on signaling pathways
Paracrine hormones	Affect the neighboring cells via diffusion	D cells of the stomach produce somatostatin to inhibit neighboring G cells from secreting gastrin.
Autocrine hormones	Affect the secreting cell itself	Autocrine signaling is particularly important for the self-renewal of embryonic stem cells. ^[1]
Endocrine hormones	Secreted into the bloodstream to reach their targets	Pancreatic β cells secrete insulin directly into the bloodstream to stimulate the uptake of glucose by the hepatic, muscle, and adipose tissue cells.
Based on chemical nature
Steroid hormones	Derived from cholesterol	Testosterone Progesterone Estrogen Glucocorticoids Mineralocorticoids
Amine hormones	Derived from a single amino acid such as phenylalanine, tyrosine, or tryptophan	Catecholamines Thyroid hormones (T₃ and T₄)
Peptide hormones	Derived from a few or many amino acids	Oxytocin Vasopressin Prolactin Glucagon Insulin
Based on solubility
Lipophilic hormones	Diffuse through the lipid plasma membrane of cells, bind to intracellular receptors, and affect transcription Usually have long-term effects with delayed onset (e.g., sex hormones)	Steroid hormones Thyroid hormones
Hydrophilic hormones	Water-soluble Bind to receptor proteins on the cellular membrane	Amine and peptide hormones (except for thyroid hormones, which are lipophilic)

Hydrophilic hormones (e.g., catecholamines) are stored in secretory granules and released when needed. Lipophilic hormones (e.g., adrenocortical steroid hormones) pass into the bloodstream once synthesized without being stored in cells.

Degradation of hormones
- Steroid hormones and thyroid hormones: inactivation and conjugation in the liver and excretion in bile
- Catecholamines: enzymatic degradation and excretion in urine (e.g., vanillylmandelic acid)
- Peptide/protein hormones: proteolytic degradation mainly in the liver and kidneys

Feedback control mechanisms

Hormone secretion is controlled by the following feedback mechanisms: ^[2]

Negative feedback
- Hormone secretion by the endocrine gland suppresses the release of hypothalamic and pituitary hormones.
- Negative feedback loop types include:
  - Ultrashort feedback loop: Hypothalamic hormones inhibit their own secretion via autocrine effects.
  - Short feedback loop: Pituitary hormones inhibit the release of hypothalamic hormones.
  - Long feedback loop: Hormones from peripheral endocrine glands inhibit the release of hypothalamic and pituitary hormones.
- Example: Thyroid hormone signaling decreases the production of thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH).
Positive feedback
- Hormone secretion enhances its own production.
- Example: Uterine stretching during labor contractions under the influence of oxytocin triggers the release of more oxytocin from the posterior pituitary.

Negative feedback (inhibition) of the hypothalamus-pituitary axis

Diagnosis of endocrine diseases

Direct measurement of hormone blood levels (e.g., measuring prolactin blood level upon suspicion of prolactinoma)
Stimulation of glands to detect underactivity (e.g., ACTH stimulation test for Addison disease)
Inhibition of glands to detect hyperactivity (e.g., dexamethasone suppression test for Cushing syndrome)
Imaging of glands to determine:
- Morphological abnormalities (e.g., thyroid ultrasound)
- Functional abnormalities (e.g., thyroid scintigraphy)
Specific laboratory studies (e.g., determination of thyrotropin receptor antibodies; HbA_1c for diabetes mellitus)

Hypothalamus and pituitary gland

Hypothalamus

Anatomy
- Ventral part of the diencephalon (see “Diencephalon”)
- Composed of multiple nuclei (e.g., lateral nucleus, preoptic nucleus)
Function
- Regulation of hormonal secretion by the anterior pituitary gland via the hypothalamic-pituitary axis
- Secretion/storage of ADH and oxytocin
  - ADH and oxytocin are produced in the supraoptic nucleus and paraventricular nucleus of the hypothalamus.
  - Both hormones are transported to the posterior pituitary via neurophysins (a group of carrier proteins) and released into the circulation as needed.
- Reception and integration of sensory inputs (e.g., from area postrema, OVLT)
- Thirst and hunger regulation
- Autonomic function control
- Thermoregulation
Hormones
- Inhibiting hormones
  - Function: decrease hormonal secretion from the pituitary gland
  - Examples: somatostatin, dopamine
- Releasing hormones
  - Function: increase hormonal secretion from the pituitary gland
  - Examples: thyrotropin-releasing hormone (TRH), corticotropin-releasing hormone (CRH), gonadotropin-releasing hormone (GnRH), growth hormone-releasing hormone (GHRH)

Functional anatomy of the hypothalamic-pituitary axis

Pituitary gland (hypophysis)

Anatomy
- Located in the sella turcica (midline depression of the sphenoid bone) of the middle cranial fossa
- Connected to the hypothalamus via the pituitary stalk (a tube-like structure between the median eminence of the hypothalamus and the posterior pituitary that contains the axons of the posterior pituitary neurons)
- Consists of two major parts:
  - Anterior pituitary gland (adenohypophysis): develops from oral ectoderm (Rathke pouch)
  - Posterior pituitary gland (neurohypophysis): develops from neural ectoderm
- The three major types of pituitary cells are:
  - Acidophil cells
    - Secrete prolactin and growth hormone (GH)
    - Stain well with acidic dyes such as eosin
  - Basophilic cells
    - Secrete adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH)
    - Stain well with basic dyes (e.g., hematoxylin)
  - Chromophobe cells
    - Do not secrete hormones ^[3]
    - Stain poorly with both acidic and basic dyes
Function
- Anterior pituitary gland
  - Regulation of endocrine gland function via the release of tropic hormones
  - Secretion of nontropic hormones with direct peripheral effects
- Posterior pituitary gland: storage/release of ADH and oxytocin in pituicytes (glial cells)
- Intermediate pituitary gland: secretion of melanocyte-stimulating hormone (MSH)
Hormones
- Tropic hormones: act on endocrine glands to mediate their effects
  - All pituitary glycoprotein hormones (e.g., FSH, LH, TSH) have a common alpha subunit.
  - Each hormone has a unique beta subunit.
- Nontropic hormones: act directly on target-tissue cells

Adenohypophysis

“B-FLAT”: Basophils secrete FSH, LH, ACTH, and TSH.

“PiG on Acid”: Prolactin and GH are secreted by Acidophils.

Hypothalamic-pituitary axis

Hypothalamus and anterior pituitary

Tropic hormones

Tropic hypothalamic hormones and their effects
Axis	Hypothalamus	Pituitary gland	Endocrine target organ
Hypothalamic-pituitary-adrenal axis	CRH Stimulates ACTH, MSH, and β-endorphin secretion from proopiomelanocortin (POMC) precursor CRH levels decrease after long-term steroid treatment via negative feedback.	ACTH Stimulates adrenal glucocorticoid and androgen production Cleaved in the corticotropic cells of the anterior pituitary ACTH and MSH share the common precursor POMC, which explains the hyperpigmentation seen in Cushing disease.	Adrenal cortex
Hypothalamic-pituitary-thyroid axis	TRH Stimulates TSH and prolactin secretion An increase in TRH levels (e.g., in primary/secondary hypothyroidism) may result in the development of galactorrhea because it stimulates prolactin secretion.	TSH Stimulates thyroid hormone production TSH secretion is inhibited by dopamine, somatostatin, and glucocorticoids. ^[4] TSH levels are the best initial test in the workup of hypothyroidism.	Thyroid gland
Hypothalamic-pituitary-gonadal axis	GnRH Stimulates FSH and LH secretion During breastfeeding, high prolactin levels cause supressed GnRH secretion, which results in the development of lactational amenorrhea. Pulsatile GnRH secretion is responsible for puberty and reproductive function.	Gonadotropins LH Female individuals: triggers ovulation Male individuals: stimulates testosterone synthesis in Leydig cells FSH: stimulates the maturation of germ cells in both male and female individuals	Gonads Female individuals: ovaries Male individuals: testicles

Overview of the hypothalamic-pituitary-target organ axes Regulation of the hypothalamic-pituitary-adrenal axis Regulation of thyroid hormone synthesis Hypothalamic-pituitary-gonadal axis (male)

Nontropic hormones

Nontropic hypothalamic hormones and their effects
Axis	Hypothalamus	Pituitary gland
Hypothalamic-pituitary-somatotropic axis	GHRH Stimulates GH secretion Synthetic forms of GHRH (tesamorelin) can be used for abdominal fat reduction in HIV-associated lipodystrophy.	GH (growth hormone, somatotropin) Direct effects ↓ Glucose uptake into cells (↑ insulin resistance) ↑ Lipolysis ↑ Protein synthesis in muscle ↑ Amino acid uptake Indirect effects: mediated by IGF-1 (insulin-like growth factor 1; originally called somatomedin C) Growth stimulation Anabolic effect on body GH regulation ^[5]^[6] ↑ GH secretion: exercise, deep sleep, puberty, hypoglycemia, CKD, thyroid hormone, estrogen, testosterone, and short-term glucocorticoid exposure ↓ GH secretion: glucose, somatostatin, somatomedin, free fatty acids, and chronic glucocorticoid therapy ^[6]^[7]
Hypothalamic-pituitary-somatotropic axis	Somatostatin Inhibits GH and TSH secretion Synthetic forms of somatostatin are used in the treatment of acromegaly (e.g., octreotide).
Hypothalamic-pituitary-prolactin axis	Dopamine (prolactin-inhibiting hormone): inhibits secretion of prolactin in the pituitary gland and has a higher influence on prolactin regulation than TRH	Prolactin (secreted by lactotropic cells) ↑ Breast tissue growth and lactation Inhibits GnRH secretion Female individuals Inhibition of ovulation Amenorrhea Galactorrhea Decreased libido Male individuals Inhibition of spermatogenesis Decreased libido
Hypothalamic-pituitary-prolactin axis	TRH: stimulates the secretion of prolactin (but is not part of the hypothalamic-pituitary-prolactin axis)
Hypothalamic-melanocortin system	Melanocyte-inhibiting hormone: inhibits release of MSH	α-MSH Cleaved in the arcuate nucleus Regulation of appetite and metabolism: promotes satiety ^[8] Stimulates melanogenesis → melanocyte stimulation → hyperpigmentation β-MSH

“No PRO-BLAM:” Derivatives of PROopiomelanocortin are Beta-endorphin, ACTH, and MSH.

Hypothalamic-pituitary-somatotropic axis Hormonal feedback control of nontropic hormones

Hypothalamus and posterior pituitary

Hormones of the posterior pituitary gland
Hormone	Regulation ^[9]	Main effects	Clinical relevance
Antidiuretic hormone	Plasma osmolality: sensed by hypothalamic osmoreceptors Hypovolemia: sensed by the atrial stretch receptors Hypotension: sensed by the peripheral baroreceptors Angiotensin II: sensed by hypothalamic receptors	Regulation of plasma osmolality Mediated by V2 receptors Insertion of aquaporin channels in the principal cells of the renal collecting duct and DCT ^[10] Results in increased water reabsorption Regulation of blood pressure Mediated by V1 receptors Vasoconstrictive effects at higher levels Increase of urea reabsorption in the collecting duct: increases the corticomedullary gradient and facilitates urine concentration ACTH release ^[11]	Elevated in SIADH despite plasma hypoosmolality ADH deficiency or resistance can lead to diabetes insipidus. Second-line therapy for septic shock (increases organ perfusion) Alcohol inhibits ADH release and causes diuresis. ^[12]
Oxytocin	Nipple stimulation Stretching of the vagina or cervix	Promotes uterine contractions during labor Facilitates milk ejection reflex via myoepithelial cell contraction	Involved in the neuromodulation of social and reproductive behavior, fear, anxiety, and depression

Hormonal feedback control of ADH secretion Effect of ADH on the kidney Hypothalamic-pituitary axis: oxytocin Stimulation of milk production and ejection

Hypothalamic and pituitary drugs

Overview of hypothalamic and pituitary drugs
Drug class	Examples	Mechanism of action	Indications	Side effects
GnRH agonists	Goserelin Leuprolide Nafarelin Histrelin	Excessive pituitary stimulation → ↓ GnRH receptors → ↓ LH and FSH secretion → ↓ estradiol production in ovaries, ↓ testosterone in male individuals ^[13] Transient agonist effects are followed by the suppression of the hypothalamic-pituitary-gonadal axis.	Cancer (continuous administration) Breast cancer Prostate cancer Uterine leiomyoma Infertility (pulsatile administration) Endometriosis Precocious puberty	Hypogonadism Decreased libido Vaginal dryness Hot flashes Nausea, vomiting Decreased bone mineral density
GnRH antagonists	Degarelix	Block GnRH receptors on pituitary to decrease FSH and LH secretion	Prostate cancer In vitro fertilization ^[14]	Hypogonadism Hot flashes Elevated liver enzymes Nausea, vomiting
Somatostatin analogs	Octreotide Lanreotide	Inhibit GH secretion Inhibit the release of splanchnic vasodilatory hormones (e.g., gastrin, glucagon, insulin, VIP)	Acromegaly Carcinoid tumor VIPoma Acute esophageal variceal bleeding Glucagonoma Gastrinoma Insulinoma	General Fatigue, weakness Depressed mood Gastrointestinal Steatorrhea Nausea, vomiting Abdominal pain, cramps Cholelithiasis (due to inhibition of cholecystokinin)
GHRH analogs ^[15]	Tesamorelin	Stimulate GH receptors	Growth hormone deficiency Turner syndrome HIV-associated lipodystrophy Short stature (e.g., in children with CKD) ^[16]	Idiopathic intracranial hypertension Increased insulin resistance Prepubertal gynecomastia Slipped capital femoral epiphysis Progression of scoliosis
GH receptor antagonists	Pegvisomant	Block GH receptor	Acromegaly	Hepatotoxicity
Dopamine agonists	Bromocriptine Cabergoline	Stimulate dopamine receptors	Prolactinoma Parkinson disease Neuroleptic malignant syndrome Malignant hyperthermia	Nausea, vomiting Orthostatic hypotension Confusion, hallucination Dyskinesia
ADH antagonists ^[17]^[18]	Conivaptan Tolvaptan Demeclocycline (a tetracycline)	Block V2 receptors and decrease water reabsorption in the renal collecting duct Tolvaptan: selective V2 receptor antagonism Conivaptan: dual V1A and V2 receptor antagonism Demeclocycline seems to disrupt the intracellular second messenger cascade that follows after the binding of vasopressin to the V2 receptor in renal collecting ducts → ↓ ADH effect	Euvolemic hyponatremia (e.g., SIADH) Hypervolemic hyponatremia (e.g., congestive heart failure, liver cirrhosis) Demeclocycline: bacterial infections	Hypernatremia Nephrogenic DI (specific to demeclocycline) Hypotension Dry mouth Liver failure ^[19] Nausea, vomiting, stomach pain Increased thirst, hunger, urination Weight loss CYP3A (including CYP3A4) inhibition and CYP3A induction Demeclocycline Azotemia and nephrotoxicity Hepatotoxicity Skin reactions
ADH analogs	Desmopressin Terlipressin	Act on the V1 and V2 receptors Release vWF stored in the endothelium	Central DI Von Willebrand disease Hemophilia A Nocturnal enuresis	Hyponatremia
Oxytocin	Oxytocin	Mediates calcium influx → uterine contraction	Induction of labor Augmentation of labor Postpartum hemorrhage	Hyponatremia Tachysystole Hypotension

Adrenal cortex

The adrenal cortex consists of three distinct layers:
- Zona glomerulosa: produces mineralocorticoids (i.e., aldosterone)
- Zona fasciculata: produces glucocorticoids (i.e., cortisol)
- Zona reticularis: produces androgens (i.e., dehydroepiandrosterone)
Feedback control mechanism
- ↑ Hypothalamic secretion of CRH → ↑ ACTH secretion from the pituitary → ↑ synthesis of glucocorticoids and androgens from the adrenal cortex
- Mineralocorticoids are secreted as a result of renin-angiotensin-aldosterone system activation.
See “Hormones of the adrenal cortex” in “Adrenal gland.”

Regulation of the hypothalamic-pituitary-adrenal axis Renin-angiotensin-aldosterone system

Thyroid gland

The thyroid gland cells produce the following hormones: ^[20]
- Follicular cells: the thyroid hormones T₃ (triiodothyronine) and T₄ (tetraiodothyronine)
- Parafollicular cells: calcitonin
The main function of the thyroid hormones is the regulation of basal metabolism and growth, while calcitonin is involved in calcium and phosphate homeostasis.
Feedback control mechanism
- ↑ Hypothalamic secretion of TRH → ↑ TSH secretion from the pituitary → ↑ thyroid hormone production
- Calcitonin is not controlled by the hypothalamic-pituitary-thyroid axis. It is released in response to increased serum Ca²⁺ levels.
See “Thyroid gland and parathyroid glands.”

Regulation of thyroid hormone synthesis

Gonads

Overview

Definition
- Gonads are reproductive organs that produce gametes and sex hormones.
- The male gonad is the testicle and the female gonad is the ovary.
Sex hormones
- Male individuals: testosterone, dihydrotestosterone
- Female individuals: estrogen, progesterone
Regulation: The secretion of sex hormones is controlled by the pituitary and hypothalamic hormones.
- LH
- FSH
- GnRH

Physiological effects of LH and FSH

Hormone	Target gonad
Hormone	Ovary	Testicle
FSH	Maturation of follicles Estrogen production Inhibin B secretion by granulosa cells Inhibin B suppresses the release of FSH (in both male and female individuals). Involved in the regulation of ovarian follicles Can be used to measure ovarian reserve A marker of granulosa cell tumors	Spermatogenesis Inhibin B secretion by sertoli cells: can be used as a marker of sertoli cell function and spermatogenesis ^[21]
LH	Ovulation Estrogen production Progesterone production	Testosterone production by Leydig cells

Physiological effects of sex hormones

See “Female sex hormones” and “Male sex hormones.”

Feedback control mechanisms

Hypothalamus
- Central regulation
  - Pulsatile release of GnRH during puberty stimulates secretion of FSH, LH, and sex hormones.
  - GnRH secretion may be influenced by competitive sports, malnutrition, or stress, any of which can lead to amenorrhea in women.
- Peripheral regulation via feedback inhibition of GnRH, FSH, and LH secretion by the following hormones:
Sex hormone-binding globulins (SHBGs): a group of transporter proteins required for the transport of lipophilic sex hormones
- Hyperestrogenism (e.g., pregnancy, OCP use) causes increased SHBG levels.
- Female individuals with low levels of SHBG (e.g., PCOS) have higher levels of free testosterone, which is responsible for the development of hirsutism in these patients.
- Male individuals with high estrogen levels (e.g., in liver cirrhosis) are at risk of developing gynecomastia because of increased SHBG levels and decreased free testosterone levels.

Regulation of appetite and satiety

Overview ^[22]^[23]^[24]

Input
- Gastrointestinal system
  - Endocrine hormones: released into the circulation in response to feeding/fasting state
  - Vagal afferents: relay signals from intestinal mechanoreceptors to the nucleus tractus solitarius
- Fat tissue: leptin hormone released into the circulation
Integrating center: arcuate nucleus (hypothalamus)
Projection: The arcuate nucleus relays signals to other hypothalamic nuclei via orexigenic and anorexigenic neurons.
- Orexigenic neurons
  - Stimulate appetite
  - Release neuropeptide Y and agouti-related peptide
- Anorexigenic neurons
  - Suppress appetite
  - Release POMC
Output
- Lateral nucleus of the hypothalamus (hunger center): appetite stimulation
- Ventromedial nucleus of the hypothalamus (satiety center): appetite suppression
Clinical relevance
- Polyphagia: excessive hunger (e.g., in hyperthyroidism, Prader-Willi syndrome)
- Anorexia: a loss of appetite (e.g., in cancer, HIV)

Regulation of appetite and satiety

Regulation of appetite

Neuroendocrine regulation of appetite
Neurotransmitter/hormone	Regulation	Site of production	Effects
Ghrelin ^[22]^[24]	↑ Levels during: Fasting states Sleep deprivation Prader-Willi syndrome ↓ Levels after: Food intake Gastric bypass surgery	Stomach	↑ Appetite GH release (via GH secretagogue receptor)
Endocannabinoid	Hunger ^[25] Intake of fatty and sweet food	Unclear ^[26]	↑ Appetite ↑ Dopamine release from nucleus accumbens (reward pathway) ^[27] Exogenous cannabinoids are responsible for “the munchies” effect.
Neuropeptide Y	Hunger	Hypothalamus	↑ Appetite Regulation of anxiety-related behavior Increased neuronal excitability

Regulation of satiety ^[22]^[24]

Neuroendocrine regulation of satiety
Hormone	Regulation	Source	Effects
Leptin	↓ Levels during: Starvation Sleep deprivation ↑ Levels in: Obesity (due to leptin resistance) Fed state	Adipose tissue	↓ Appetite (long term) ↓ Neuropeptide Y release Leptin gene mutation causes obesity.
Cholecystokinin	Lipid-rich chyme Protein-rich chyme	I cells of the small intestine	↓ Appetite (short term) ↓ Gastric emptying
GLP-1	Carbohydrate-rich chyme Lipid-rich chyme	L cells of the small and large intestine	↓ Appetite (short term) ↓ Gastric emptying ↑ Insulin ↓ Glucagon
Peptide YY	Protein-rich chyme	L cells of the small and large intestine	↓ Appetite (short term) ↓ Gastric emptying
Amylin ^[28]	Glucose (cosecreted with insulin)	β cells of the pancreas	↓ Appetite (short term) ↓ Gastric emptying ↓ Glucagon release

Ghrelin makes you Gain weight. Leptin makes you Lose weight.

Appetite regulators

Appetite-regulating drugs
Drug class	Example	Mechanism of action	Indication	Side effects
Cannabinoid receptor agonist ^[29]^[30]	Dronabinol	Activation of CB1 and CB2 receptors	Appetite stimulation (e.g., in HIV patients) Chemotherapy-induced emesis	Sedation Euphoria/dysphoria Hallucinations Dry mouth Autonomic effects Tachycardia Orthostatic hypotension
Synthetic progestin	Megestrol acetate	Unclear ^[31]	Appetite stimulation ^[32] Cancer cachexia AIDS	Thromboembolism risk Edema Adrenal suppression and Cushing syndrome ^[33]
GLP-1 agonist ^[34]	Liraglutide	Activation of GLP-1 receptor	Weight loss (↑ satiety) Diabetes	Nausea and vomiting Pancreatitis

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General endocrinology

Summary

Overview of endocrinological diseases

Basics of endocrinology

Hormones

Feedback control mechanisms

Diagnosis of endocrine diseases

Hypothalamus and pituitary gland

Hypothalamus

Pituitary gland (hypophysis)

Hypothalamic-pituitary axis

Hypothalamus and anterior pituitary

Tropic hormones

Nontropic hormones

Hypothalamus and posterior pituitary

Hypothalamic and pituitary drugs

Adrenal cortex

Thyroid gland

Gonads

Overview

Physiological effects of LH and FSH

Physiological effects of sex hormones

Feedback control mechanisms

Regulation of appetite and satiety

Overview [22][23][24]

Regulation of appetite

Regulation of satiety [22][24]

Appetite regulators

References

3 free articles remaining

Overview ^[22]^[23]^[24]

Regulation of satiety ^[22]^[24]