Endocrine glands & hormones — the overview
The body uses two parallel coordination systems. The neural system delivers point-to-point, electrical, short-lived signals; the endocrine system uses chemicals — hormones — carried by the blood, slower to act but capable of regulating every cell at once. NCERT defines hormones as non-nutrient chemicals which act as intercellular messengers and are produced in trace amounts. They are secreted by endocrine glands, which lack ducts and pour their products directly into the bloodstream — hence the older name "ductless glands."
The organised endocrine glands of the human body are the hypothalamus, pituitary, pineal, thyroid, parathyroid, thymus, adrenal, pancreas, and the gonads (testis or ovary). In addition, several organs that are not classically endocrine — the heart, the kidney, the gastrointestinal tract, the liver — also release hormones from specialised cells. NIOS adds the placenta to this list, which produces hCG to sustain the corpus luteum during pregnancy.
The endocrine roster — NCERT Chapter 19 in one table. Memorise the gland → main hormone(s) → headline action. Almost every NEET question on this chapter starts from this matrix.
Hypothalamus
Releasing & inhibitory
controls pituitary
GnRH, TRH, CRH, GHRH stimulate. Somatostatin and dopamine inhibit.
Pituitary
Master gland
9 hormones in 3 lobes
Anterior: GH, TSH, ACTH, FSH, LH, prolactin. Intermedia: MSH. Posterior: oxytocin, ADH.
Pineal
Melatonin
circadian rhythm
Sleep-wake cycle, body temperature, pigmentation, menstrual rhythm.
Thyroid
T3, T4, calcitonin
iodine-dependent
BMR, growth, RBC formation. Calcitonin lowers blood Ca²⁺.
Parathyroid
PTH
hypercalcaemic
Four glands on dorsal thyroid. Raises blood Ca²⁺ via bone, kidney, gut.
Thymus
Thymosins
T-cell maturation
Behind sternum. Atrophies after puberty. Cell-mediated + humoral immunity.
Adrenal
Cortex + medulla
stress + Na/K
Cortex: cortisol, aldosterone, sex steroids. Medulla: adrenaline, noradrenaline.
Pancreas (islets)
Insulin + glucagon
glucose homeostasis
β-cells: insulin. α-cells: glucagon. Antagonists.
Testis
Testosterone
Leydig cells
Secondary sex characters, spermatogenesis, anabolic effects.
Ovary
Oestrogen + progesterone
menstrual cycle
Follicle: oestrogen. Corpus luteum: progesterone. Female secondary sex characters.
Heart, kidney, GIT
ANF, EPO, gut peptides
non-endocrine organs
Heart: ANF lowers BP. Kidney: erythropoietin. Gut: gastrin, secretin, CCK, GIP.
Four chemical classes
Peptide · Steroid
Iodothyronine · Amino-acid
Peptide hormones use membrane receptors; steroids and thyroid hormones use intracellular receptors.
Hypothalamus & the pituitary gland
The hypothalamus is the basal part of the diencephalon and the true command-and-control centre of the endocrine system. It contains neurosecretory nuclei whose neurons produce two kinds of hormones — releasing hormones that stimulate the pituitary, and inhibitory hormones that shut pituitary secretion down. Gonadotrophin-releasing hormone (GnRH), thyrotrophin-releasing hormone (TRH), corticotrophin-releasing hormone (CRH) and growth hormone-releasing hormone (GHRH) are stimulatory. Somatostatin (GHIH) and dopamine (prolactin-inhibiting factor) are inhibitory. These hormones travel down the axons of the hypothalamic neurons and are released near the median eminence, from where they reach the anterior pituitary through the hypothalamic-hypophyseal portal circulation.
The pituitary sits in the bony cavity called sella turcica and hangs from the hypothalamus by a stalk. It has two anatomical divisions. The adenohypophysis is glandular and contains the pars distalis (anterior pituitary) and pars intermedia. The neurohypophysis is the pars nervosa (posterior pituitary) and is essentially a downward extension of the hypothalamus itself. This anatomy decides everything about how each hormone is controlled.
Anterior pituitary — six trophic hormones
The pars distalis manufactures and secretes six hormones. Growth hormone (GH) drives growth of bones and soft tissues; over-secretion in childhood causes gigantism, in adulthood causes acromegaly, under-secretion in childhood causes pituitary dwarfism. Prolactin (PRL) regulates mammary growth and milk synthesis. Thyroid-stimulating hormone (TSH) stimulates the thyroid. Adrenocorticotrophic hormone (ACTH) stimulates the adrenal cortex to secrete glucocorticoids. Luteinising hormone (LH) and follicle-stimulating hormone (FSH) are the gonadotrophins — in males LH drives Leydig cell androgen synthesis and FSH supports spermatogenesis; in females LH triggers ovulation and maintains the corpus luteum, while FSH drives follicular growth. The pars intermedia secretes a single hormone, melanocyte-stimulating hormone (MSH), which acts on melanocytes and regulates skin pigmentation. In humans the pars intermedia is almost fused with the pars distalis.
Posterior pituitary — two stored hormones
The pars nervosa does not make any hormone of its own. It stores and releases two hormones synthesised by the hypothalamus and transported down the axons. Oxytocin acts on the smooth muscle of the uterus to drive labour contractions and on the mammary gland myoepithelium to eject milk during nursing. Vasopressin, also called antidiuretic hormone (ADH), acts on the distal tubules of the kidney to promote reabsorption of water and electrolytes — preventing diuresis. Failure of ADH synthesis or release causes diabetes insipidus: profuse, dilute urine and dehydration.
Pituitary anatomy → hormone list. A classic NEET trap: students assume every pituitary hormone is made by the anterior lobe. The posterior pituitary releases two of them but synthesises neither.
Anterior pituitary (pars distalis)
6 hormones
trophic + somatic
GH — somatic growth (gigantism / acromegaly / dwarfism).
Prolactin — mammary growth, milk synthesis.
TSH — stimulates thyroid (T3, T4).
ACTH — stimulates adrenal cortex glucocorticoids.
LH — ovulation; Leydig androgens.
FSH — follicle growth; spermatogenesis.
NEET 2017, 2019 — both tested GH excessPars intermedia
1 hormone
almost fused in humans
MSH — melanocyte-stimulating hormone; acts on melanocytes; regulates skin pigmentation.
Often clubbed under anterior pituitary in MCQsPosterior pituitary (pars nervosa)
2 hormones
stored, not synthesised
Oxytocin — uterine contraction during childbirth, milk ejection.
Vasopressin / ADH — water reabsorption in distal tubules; deficiency = diabetes insipidus.
Trap: both are made by the hypothalamusPineal gland — the body clock
The pineal gland is a small conical structure on the dorsal aspect of the forebrain (epithalamus). It secretes a single hormone, melatonin, derived from the amino acid tryptophan via serotonin. Melatonin regulates the 24-hour (diurnal/circadian) rhythm of the body — most famously the sleep-wake cycle, but also body temperature, pigmentation, the menstrual cycle and the body's defence capability. Light striking the retina suppresses melatonin secretion via the suprachiasmatic nucleus; darkness releases the brake and melatonin rises through the night.
Thyroid gland
The thyroid sits in the front of the neck as two lobes on either side of the trachea, joined by a thin isthmus. Histologically it is built from follicles filled with colloid. The follicular cells synthesise two iodine-containing hormones — tetraiodothyronine (T4, thyroxine) and triiodothyronine (T3). Separately, the parafollicular C-cells secrete thyrocalcitonin (TCT), a protein hormone that lowers blood calcium.
Iodine is non-negotiable: without dietary iodine the follicles cannot synthesise T3 or T4. NCERT describes three clinical consequences of disturbed thyroid function. Hypothyroidism with iodine deficiency enlarges the gland into a visible neck swelling — goitre. Hypothyroidism during pregnancy impairs development of the foetus, producing cretinism: stunted growth, mental retardation, low IQ, abnormal skin, deaf-mutism. In adult women, hypothyroidism also makes menstrual cycles irregular. Hyperthyroidism — typically from a thyroid nodule or cancer — raises BMR, drives weight loss, and in its classic form (exophthalmic goitre / Graves' disease) produces protruding eyeballs alongside the enlarged gland.
Functionally, T3 and T4 regulate basal metabolic rate, support red blood cell formation, control the metabolism of carbohydrates, proteins and fats, and influence water-and-electrolyte balance. NEET 2023 (Q.188) tested precisely this scope: thyroid hormones do NOT control the sleep-wake cycle (that is melatonin) and do NOT develop the immune system (that is the thymus).
Parathyroid gland — calcium control
Four small parathyroid glands sit on the dorsal (back) surface of the thyroid, one pair embedded in each thyroid lobe. They secrete a peptide hormone called parathyroid hormone (PTH). PTH secretion is regulated directly by blood Ca²⁺ levels — falling calcium triggers PTH release; rising calcium switches it off.
PTH is a hypercalcaemic hormone — its job is to raise blood Ca²⁺ by three coordinated actions. It acts on bone to stimulate resorption (dissolution/demineralisation), releasing calcium and phosphate into the blood. It acts on the kidney to stimulate reabsorption of Ca²⁺ by the renal tubules. And it stimulates Ca²⁺ absorption from digested food in the gut. PTH and thyrocalcitonin (TCT) act as antagonists, between them setting blood calcium at its narrow homeostatic range.
Thymus — the immune coach
The thymus is a lobular gland behind the sternum on the ventral side of the aorta. It plays a major role in developing the immune system. Its secretions, the thymosins, are peptide hormones that drive the differentiation of T-lymphocytes — the cells that mediate cell-mediated immunity. Thymosins also promote production of antibodies, supporting humoral immunity. In old individuals the thymus atrophies, thymosin output drops, and immune responses weaken — one biological reason why elderly people are more susceptible to infection.
Adrenal gland — stress and salt
Each kidney wears a cap-like adrenal gland on its upper pole. The adrenal is two glands fused into one: a centrally placed adrenal medulla derived from neural crest, and a surrounding adrenal cortex derived from mesoderm. The two halves secrete entirely different families of hormones with different chemistry, different speeds, and different jobs.
Adrenal medulla — the fight-or-flight switch
The medulla secretes two catecholamines: adrenaline (epinephrine) and noradrenaline (norepinephrine). These are the emergency hormones — released in response to stress of any kind (fear, anger, injury, cold, low blood sugar). They prepare the body for fight or flight: heart rate rises, contraction force rises, respiration rate rises, blood glucose rises (via glycogenolysis), pupils dilate, hair stands erect (piloerection), sweating increases, alertness sharpens. Catecholamines also stimulate breakdown of lipids and proteins. Adrenaline and noradrenaline are amino-acid-derived hormones (from tyrosine) — NEET 2018 set the question on epinephrine as the amino-acid-derived hormone, contrasted against ecdysone and the oestrogens (steroids).
Adrenal cortex — three layers, three classes
The cortex has three zones — outer zona glomerulosa, middle zona fasciculata, inner zona reticularis — and secretes a family of steroid hormones collectively called corticoids. Three classes matter for NEET.
Glucocorticoids, dominated by cortisol, control carbohydrate metabolism. They stimulate gluconeogenesis, lipolysis and proteolysis, inhibit cellular amino-acid uptake, support cardiovascular and renal function, stimulate RBC production, and — crucially — produce anti-inflammatory reactions and suppress the immune response. Cortisol is the body's main glucocorticoid and the medicalised target of "steroid therapy."
Mineralocorticoids, dominated by aldosterone, regulate water and electrolyte balance. Aldosterone acts at the renal tubules, stimulating reabsorption of Na⁺ and water and excretion of K⁺ and phosphate. It is the body's main mediator of body-fluid volume, osmotic pressure and blood pressure.
Sex corticoids are androgenic steroids in small amounts — sufficient to drive the growth of axial, pubic and facial hair at puberty. Under-production of the cortex as a whole causes Addison's disease: weakness, fatigue, disturbed carbohydrate metabolism.
Pancreas — islets of Langerhans
The pancreas is a composite gland that lives a double life. The exocrine portion (lobules of acini) drains digestive enzymes into the duodenum through the pancreatic duct. The endocrine portion is a scatter of cell clusters called the islets of Langerhans — about one to two million islets in a normal pancreas, accounting for only 1–2% of pancreatic tissue. Two main cell types matter for NEET. α-cells secrete glucagon. β-cells secrete insulin.
Insulin is a peptide hormone that acts mainly on hepatocytes and adipocytes. It enhances cellular glucose uptake and utilisation — pulling glucose out of the blood into cells. It stimulates conversion of glucose to glycogen (glycogenesis) in the target cells. The net effect is hypoglycaemia — falling blood glucose. Glucagon, also a peptide hormone, acts mainly on hepatocytes. It stimulates glycogenolysis (breakdown of liver glycogen) and gluconeogenesis (synthesis of new glucose from non-carbohydrate precursors), and reduces cellular glucose uptake. The net effect is hyperglycaemia — rising blood glucose. The two hormones operate as antagonists, jointly maintaining glucose homeostasis. Prolonged hyperglycaemia, from insulin deficiency or insulin resistance, produces diabetes mellitus — glycosuria, polyuria, polydipsia, ketone-body formation. Insulin therapy is the established treatment.
Testis — androgens from Leydig cells
The paired testes live in the scrotal sac outside the abdominal cavity. They are dual-function organs: a primary sex organ (spermatogenesis) and an endocrine gland. Histologically, the testis is composed of seminiferous tubules (sperm production) and interstitial tissue (between tubules). The Leydig cells (interstitial cells) in this intertubular tissue secrete a group of male sex hormones called androgens, dominated by testosterone.
Androgens regulate the development, maturation and function of the male accessory sex organs — epididymis, vas deferens, seminal vesicles, prostate, urethra. They drive the male secondary sex characters: muscular development, facial and axillary hair, aggressiveness, low-pitched voice. They play a major stimulatory role in spermatogenesis (together with FSH from the pituitary). They act on the central nervous system to influence male sexual behaviour (libido). And they exert anabolic effects on protein and carbohydrate metabolism — the reason synthetic androgens are abused as anabolic steroids.
Ovary — oestrogen and progesterone
The paired ovaries lie in the abdominal cavity. Like the testis, the ovary is a dual-function organ — producing the gamete (one ovum per menstrual cycle) and two groups of steroid hormones, oestrogen and progesterone. Histologically the ovary contains ovarian follicles at various stages of development plus stromal tissue.
Oestrogens are synthesised and secreted mainly by the growing ovarian follicles. They stimulate growth and activity of the female accessory sex organs and follicular development; they produce the female secondary sex characters (high-pitched voice, breast development); they regulate female sexual behaviour. Progesterone is secreted mainly by the corpus luteum, the structure left behind after ovulation when the ruptured follicle reorganises itself into a temporary endocrine gland. Progesterone supports pregnancy and acts on the mammary gland to stimulate alveolar development and milk secretion. NEET 2017 set the question on corpus luteum as a temporary endocrine gland, and NEET 2021 tested relaxin, also secreted by the corpus luteum during the later phase of pregnancy.
Hormones from heart, kidney and GIT
Not every hormone comes from a "gland." Several non-endocrine organs run quiet, parallel chemistries that the NEET examiner loves to test as recall.
The atrial wall of the heart contains specialised cells that secrete a peptide hormone called atrial natriuretic factor (ANF). When blood pressure rises, atrial stretch triggers ANF release. ANF causes dilation of blood vessels and promotes Na⁺ and water excretion by the kidney, lowering blood pressure. ANF acts as a functional antagonist of aldosterone (NEET 2016 antagonist pair).
The juxtaglomerular cells of the kidney secrete two important hormones. Erythropoietin (EPO) is a peptide hormone that stimulates erythropoiesis — the formation of red blood cells in the bone marrow. Renin, although NCERT does not develop it in detail in this chapter, is also released by the JG cells. NEET 2021 explicitly tested erythropoietin as a JG-cell product.
The gastrointestinal tract houses endocrine cells in its epithelium that secrete four peptide hormones tested directly by NEET 2023.
Gastrin
Stomach
pyloric mucosa
Stimulates gastric glands to secrete HCl and pepsinogen.
Secretin
Duodenum
acid-triggered
Acts on exocrine pancreas; stimulates secretion of water and bicarbonate ions.
CCK (cholecystokinin)
Duodenum
fat-triggered
Acts on both pancreas and gall bladder; drives pancreatic enzyme secretion and bile release.
GIP (gastric inhibitory peptide)
Duodenum
post-meal brake
Inhibits gastric secretion and motility. Released when food has moved into the small intestine.
Mechanism of hormone action
Hormones do not enter every cell — they act only on target cells that express the right hormone receptor. Each receptor is specific for one hormone. Binding produces a hormone-receptor complex which triggers downstream biochemistry that ultimately changes metabolism, gene expression, or both. NCERT splits hormones into four chemical classes and two receptor pathways.
The four chemical classes are: peptide / polypeptide / protein hormones (insulin, glucagon, pituitary hormones, hypothalamic hormones); steroids (cortisol, testosterone, oestradiol, progesterone); iodothyronines (T3, T4); and amino-acid derivatives (epinephrine). This classification is a frequent NEET stem — NEET 2018 used "amino-acid-derived hormone" as the discriminator with options including ecdysone (steroid) and the oestrogens (steroids).
The two receptor pathways are decided by the hormone's solubility. Peptide and amine hormones are water-soluble; they cannot cross the lipid bilayer. They bind membrane-bound receptors on the outside of the target cell. Receptor activation generates second messengers inside the cell — cyclic AMP (cAMP), IP3, Ca²⁺ — which propagate the signal through enzyme cascades to regulate cellular metabolism. The hormone itself never enters the cell. Steroid and thyroid hormones are lipid-soluble. They cross the plasma membrane freely and bind intracellular receptors, mostly in the nucleus. The hormone-receptor complex binds DNA, altering gene expression. No second messenger is involved; the action is slower but durable.
"Hormone-receptor complex formation leads to certain biochemical changes in the target tissue."
— NCERT, Chapter 19, §19.4
NEET PYQ Snapshot
Five PYQs that cover the chapter's high-yield zones — match, mechanism, antagonist pairs.
Match List I with List II. (A) CCK — (B) GIP — (C) ANF — (D) ADH, with (I) Kidney (II) Heart (III) Gastric gland (IV) Pancreas. Choose the correct mapping.
Answer: (2) A-IV, B-III, C-II, D-IWhy: CCK acts on the pancreas (and gall bladder) — IV. GIP inhibits gastric secretion and motility — III. ANF is released by the atrial wall of the heart — II. ADH acts on the kidney's distal tubules — I.
Which of the following are NOT under the control of thyroid hormone? (A) Maintenance of water and electrolyte balance, (B) Regulation of basal metabolic rate, (C) Normal rhythm of sleep-wake cycle, (D) Development of immune system, (E) Support the process of RBCs formation.
Answer: (4) C and D onlyWhy: Thyroid hormones regulate BMR, water-and-electrolyte balance, and RBC formation. They do not regulate the sleep-wake cycle (that is melatonin from the pineal) or develop the immune system (that is thymosins from the thymus).
Erythropoietin hormone which stimulates RBC formation is produced by:
Answer: (1) Juxtaglomerular cells of the kidneyWhy: The juxtaglomerular cells of the kidney secrete erythropoietin, which drives erythropoiesis in the bone marrow. Alpha cells make glucagon; bone marrow cells are the target, not the source.
How does steroid hormone influence the cellular activities?
Answer: (2) Binding to DNA and forming a gene-hormone complexWhy: Steroid hormones, being lipid-soluble, cross the plasma membrane and bind intracellular (mostly nuclear) receptors. The hormone-receptor complex binds DNA — a gene-hormone complex — to alter gene expression. cAMP belongs to the peptide-hormone route.
Which of the following pairs of hormones are not antagonistic (having opposite effects) to each other?
Answer: (3) Relaxin — InhibinWhy: Insulin/glucagon (glucose), aldosterone/ANF (Na⁺ and BP), and parathormone/calcitonin (Ca²⁺) are textbook antagonists. Relaxin (corpus luteum, late pregnancy) and inhibin (gonadal feedback on FSH) act on different systems and are not antagonists.
Expert FAQs
Questions NEET has asked from this chapter, answered straight.
Which hormones are released by the posterior pituitary?
Why does iodine deficiency cause goitre?
What is the difference between insulin and glucagon?
How do steroid hormones act on target cells?
Why are adrenaline and noradrenaline called emergency hormones?
Which hormone is a hypercalcaemic hormone and which is hypocalcaemic?
What is the role of ANF and erythropoietin?
How does the hypothalamus control the anterior pituitary?
Go Deeper
Drill into the subtopics that NEET asks most often.