Locomotion and Movement

CHEMICAL COORDINATION AND INTEGRATION

**Definition:** Chemical coordination refers to the regulation of physiological functions through hormones—non-nutrient chemicals produced by endocrine glands and transported via blood to distant target tissues. This system works alongside the neural system to maintain homeostasis and coordinate body functions.

**Key Difference from Neural Coordination:**

Neural coordination: Fast, short-lived, point-to-point

Hormonal coordination: Slower onset, long-lasting effects, wide-spread action on multiple tissues

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ENDOCRINE GLANDS AND HORMONES

**Classical Definition of Hormones:** Chemicals produced by endocrine glands, released into blood, transported to distantly located target organs.

**Modern/Current Definition:** Hormones are **non-nutrient chemicals that act as intercellular messengers and are produced in trace amounts**. This definition encompasses molecules from non-endocrine tissues as well.

**Key Characteristics of Hormones:**

Produced in trace amounts but have potent effects

Released directly into bloodstream (ductless glands)

Act on specific target tissues possessing receptors

Effect is slower but longer-lasting than nerves

Can be stored and released on demand

**Invertebrate vs. Vertebrate Endocrine Systems:** Invertebrates possess simple endocrine systems with few hormones, while vertebrates (especially humans) have complex endocrine systems with numerous chemical messengers providing detailed regulation.

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HUMAN ENDOCRINE SYSTEM: OVERVIEW

The human endocrine system consists of:

**Organized Endocrine Glands:**

Pituitary gland

Pineal gland

Thyroid gland

Parathyroid glands (4 pairs)

Adrenal glands (1 pair)

Pancreas

Thymus

Gonads (testis in males; ovary in females)

**Hormone-Producing Non-Endocrine Tissues:**

Heart (atrial wall)

Kidney (juxtaglomerular cells)

Gastrointestinal tract

Liver

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THE HYPOTHALAMUS

**Location:** Basal part of diencephalon (forebrain)

**Structure and Function:**

Contains neurosecretory cells organized into nuclei (functional groups)

Produces two types of hormones:

**Releasing hormones:** Stimulate pituitary hormone secretion (e.g., GnRH—Gonadotrophin Releasing Hormone)

**Inhibiting hormones:** Suppress pituitary hormone secretion (e.g., somatostatin inhibits GH release)

**Mechanism of Action:**

Hypothalamic hormones originate in neurosecretory neurons

Travel through axons to nerve endings in pituitary stalk

Released into portal circulatory system (special blood vessels connecting hypothalamus to anterior pituitary)

Regulate anterior pituitary function (via hormonal control)

Regulate posterior pituitary function (via direct neural connection)

**Clinical Significance:** Damage to hypothalamus disrupts pituitary function and causes metabolic disturbances.

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THE PITUITARY GLAND

**Location:** Sella tursica (small bony cavity in sphenoid bone)

**Attachment:** Connected to hypothalamus via pituitary stalk (infundibulum)

**Anatomical Divisions:**

ADENOHYPOPHYSIS (Anterior Pituitary)

Consists of two regions:

**1. Pars Distalis (Anterior Pituitary Proper)**

Produces six hormones:

**Growth Hormone (GH/Somatotropin):**

Stimulates linear growth and protein synthesis

Hypersecretion in childhood → Gigantism (abnormally tall stature)

Hyposecretion in childhood → Pituitary Dwarfism (stunted growth)

Hypersecretion in adults → Acromegaly (enlargement of facial bones, hands, feet; severe disfigurement; can be life-threatening)

**Prolactin (PRL):**

Stimulates mammary gland growth

Promotes milk production (lactation)

Functions during and after pregnancy

**Thyroid Stimulating Hormone (TSH/Thyrotropin):**

Stimulates thyroid gland to synthesize and secrete T3 and T4

Follows negative feedback regulation

Deficiency leads to hypothyroidism

**Adrenocorticotrophic Hormone (ACTH):**

Stimulates adrenal cortex to secrete glucocorticoids (mainly cortisol)

Follows circadian rhythm

Regulated by negative feedback

**Luteinizing Hormone (LH) [Gonadotrophin]:**

**In males:** Stimulates Leydig cells of testis to produce testosterone and other androgens

**In females:** Triggers ovulation of mature Graafian follicles; maintains corpus luteum

**Follicle Stimulating Hormone (FSH) [Gonadotrophin]:**

**In males:** Works with androgens to regulate spermatogenesis

**In females:** Stimulates growth and development of ovarian follicles; triggers estrogen secretion

**2. Pars Intermedia**

Secretes **Melanocyte Stimulating Hormone (MSH)**

Acts on melanocytes (pigment cells) to regulate skin pigmentation

In humans, pars intermedia is vestigial/merged with pars distalis

MSH also regulates fat mobilization and metabolism

NEUROHYPOPHYSIS (Posterior Pituitary)

**Structure:** Composed of axonal endings of hypothalamic neurons; stores and releases hormones synthesized by hypothalamus

**Hormones Released:**

**Oxytocin:**

Stimulates smooth muscle contraction

Functions in females: Uterine contraction during labor; milk ejection reflex (mammary gland contractions during breastfeeding)

Functions in males: Aids sperm transport and ejaculation

Also promotes emotional bonding and trust (social behavior)

**Vasopressin (Antidiuretic Hormone/ADH):**

Stimulates reabsorption of water and electrolytes by distal tubules and collecting ducts of kidney

Reduces urine volume (antidiuresis)

Increases blood osmotic pressure indirectly

**Diabetes Insipidus:** Impaired ADH production or kidney response → excessive water loss, severe dehydration, polydipsia (excessive thirst), polyuria (excessive urination)

**Exam Point:** Remember posterior pituitary stores and releases hormones; it does not synthesize them. Synthesis occurs in hypothalamic neurons.

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THE PINEAL GLAND

**Location:** Dorsal surface of forebrain (behind thalamus)

**Hormone:** **Melatonin**

**Functions of Melatonin:**

Regulates 24-hour (circadian/diurnal) biological rhythms

Controls sleep-wake cycle (secreted more during darkness; suppressed by light)

Maintains body temperature rhythm

Influences metabolism and metabolic rate

Regulates skin pigmentation

Influences menstrual cycle in females

Enhances immune defense capability (immunomodulatory role)

Protects against oxidative stress (antioxidant)

**Clinical Significance:** Melatonin dysfunction affects sleep disorders; melatonin supplements used for jet lag and shift-work disorders.

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THYROID GLAND

**Anatomy:**

Bilobed structure located on either side of trachea (windpipe)

Two lobes connected by isthmus (thin connective tissue band)

Composed of follicles (spherical structures containing colloid) and stromal tissue

**Follicular Structure:**

Follicular cells (thyroid epithelial cells) synthesize and secrete hormones

Enclose cavity filled with colloid (protein matrix containing thyroglobulin)

Iodine incorporated into thyroglobulin; stored in colloid

**Hormones Produced:**

**Thyroxine (T4/Tetraiodothyronine):** Contains 4 iodine atoms

**Triiodothyronine (T3):** Contains 3 iodine atoms

**Thyrocalcitonin (TCT/Calcitonin):** Protein hormone; produced by parafollicular cells (C cells)

**Functions of Thyroid Hormones (T3 and T4):**

Regulate basal metabolic rate (BMR) — increased metabolic activity

Control carbohydrate, protein, and fat metabolism

Promote oxidative phosphorylation in mitochondria

Support red blood cell (RBC) formation (erythropoiesis)

Maintain water and electrolyte balance

Regulate heat production (thermogenesis)

Essential for normal growth and development

Control cardiovascular activity

**Thyrocalcitonin (TCT) Functions:**

Decreases blood calcium levels (hypocalcemic)

Stimulates calcium uptake by bones

Inhibits osteoclastic activity (bone resorption)

Antagonistic to parathyroid hormone

**Iodine Requirement:** Essential cofactor for thyroid hormone synthesis. Iodine deficiency leads to reduced hormone production.

**Thyroid Disorders:**

**Hypothyroidism (Low Thyroid Hormone):**

Decreased metabolic rate, weight gain, fatigue, cold intolerance

Goitre: Thyroid gland enlargement (compensatory growth) due to iodine deficiency

**Cretinism:** Hypothyroidism during pregnancy and childhood → stunted growth, mental retardation, low IQ, abnormal skin, deaf-mutism, irregular facial features

In adult females: Irregular/heavy menstrual cycles

**Hyperthyroidism (Excess Thyroid Hormone):**

Increased metabolic rate, weight loss, excessive sweating, heat intolerance

Increased heart rate and palpitations

Anxiety, nervousness, tremor

**Exophthalmic Goitre (Graves' Disease):** Autoimmune hyperthyroidism characterized by:

Thyroid enlargement

Protrusion of eyeballs (exophthalmos) due to inflammation and swelling behind eyes

Increased basal metabolic rate

Weight loss despite increased appetite

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PARATHYROID GLANDS

**Anatomy:**

Four small glands (4-6 mm diameter) embedded in dorsal/posterior surface of thyroid gland

One pair in each thyroid lobe

Composed of chief cells (secrete PTH) and oxyphil cells (function unclear)

**Hormone:** **Parathyroid Hormone (PTH/Parathormone)**

Peptide hormone

Secretion regulated by blood calcium ion (Ca²⁺) concentration (negative feedback)

**Functions of PTH:**

**Increases blood Ca²⁺ levels (Hypercalcemic hormone)** through three mechanisms:

1. **Bone Resorption:** Stimulates osteoclasts to break down bone matrix, releasing Ca²⁺ into blood

2. **Kidney:** Stimulates reabsorption of Ca²⁺ by renal tubules (distal convoluted tubule and collecting duct), reducing urinary calcium loss

3. **Intestine:** Increases absorption of Ca²⁺ from digested food by activating vitamin D (calcitriol)

**Regulation:**

**Low blood Ca²⁺** → Stimulates PTH secretion

**High blood Ca²⁺** → Inhibits PTH secretion

Works antagonistically with thyrocalcitonin to maintain calcium homeostasis

**Calcium Homeostasis:** PTH and TCT maintain blood Ca²⁺ at 8.5-10.5 mg/dL, essential for:

Muscle contraction

Nerve impulse transmission

Blood clotting

Bone mineralization

**Clinical Significance:** Hypoparathyroidism (low PTH) → hypocalcemia, tetany, muscle spasms; Hyperparathyroidism → hypercalcemia, bone loss, kidney stones.

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THYMUS GLAND

**Location:** Lobular structure located:

Between the two lungs

Behind sternum

On ventral side of aorta

In thoracic cavity

**Structure:** Divided into lobes and lobules; composed of lymphoid tissue

**Hormones:** **Thymosins** (group of peptide hormones)

**Functions:**

Major role in immune system development

**Differentiation of T-lymphocytes:** Thymosins promote maturation and differentiation of T cells from bone marrow precursors

T cells provide **cell-mediated immunity** (cellular immune response against intracellular pathogens and cancer cells)

Promotes production of antibodies → **Humoral immunity** (antibody-mediated immune response)

**Age-Related Changes:**

Thymus reaches maximum size at puberty

Gradually degenerates (involutes) with age

Elderly individuals produce less thymosins

Result: Weakened immune responses in aging, increased susceptibility to infections and diseases

**Exam Point:** Thymus is largest and most active in children and adolescents; its involution explains age-related immunosenescence.

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ADRENAL GLAND

**Anatomy:**

Pair of glands located: one above each kidney (retroperitoneal)

Each adrenal gland is 4-5 cm long

Composed of two distinct tissue types:

**Outer layer:** Adrenal cortex (yellow; derived from mesoderm)

**Inner layer:** Adrenal medulla (reddish; derived from ectoderm)

ADRENAL MEDULLA

**Embryological Origin:** Neural crest cells (ectodermal)

**Hormones:** **Catecholamines**

Adrenaline (Epinephrine)

Noradrenaline (Norepinephrine)

**Secretion Trigger:**

Sympathetic nervous system stimulation (direct nerve innervation)

Stress, fear, pain, excitement, exercise, danger

Rapidly secreted during emergency situations

**Functions (Emergency/Fight-or-Flight Response):**

**Cardiovascular effects:**

Increased heart rate (tachycardia) and force of contraction

Increased cardiac output

Increased blood pressure

**Respiratory effects:**

Increased rate and depth of respiration

Bronchodilation (widening of airways)

**Metabolic effects:**

Glycogenolysis (breakdown of glycogen) → increased blood glucose (hyperglycemia)

Lipolysis (breakdown of fats) → increased blood fatty acids

Proteolysis (breakdown of proteins) → amino acid release

Increased metabolic rate

**Behavioral/Sensory effects:**

Increased alertness and arousal

Pupilary dilation (mydriasis) — enlarged pupils for better vision

Piloerection (hair standing on end)

Increased sweating (diaphoresis)

**Blood redistribution:**

Blood diverted from skin and GI tract to muscles and brain

Pale skin appearance

**Clinical Significance:** Prolonged or excessive catecholamine secretion causes hypertension, cardiac arrhythmias, anxiety disorders.

ADRENAL CORTEX

**Embryological Origin:** Mesoderm (coelomic epithelium)

**Histological Zones (3 layers from outer to inner):**

1. **Zona Glomerulosa (Outer):** Produces mineralocorticoids

2. **Zona Fasciculata (Middle):** Produces glucocorticoids

3. **Zona Reticularis (Inner):** Produces androgens and glucocorticoids

**Hormones Produced:**

**1. Glucocorticoids** (mainly Cortisol/Hydrocortisone)

Produced in zona fasciculata and reticularis

Secretion regulated by ACTH (negative feedback)

Follows circadian rhythm (peak in early morning, lowest at night)

**Functions:**

**Carbohydrate metabolism:**

Stimulate gluconeogenesis (glucose synthesis from non-carbohydrates)

Increase hepatic glucose output

Decrease glucose uptake by peripheral tissues

Result: Hyperglycemia

**Protein metabolism:**

Stimulate protein breakdown (proteolysis)

Decrease amino acid uptake and utilization by cells

Negative nitrogen balance

**Fat metabolism:**

Stimulate lipolysis (fat breakdown)

Increase blood fatty acids

**Cardiovascular function:**

Maintain vascular tone and blood pressure

Permissive action on catecholamines (needed for catecholamine effectiveness)

**Immune and inflammatory response:**

Anti-inflammatory effects (reduce inflammation)

Immunosuppression (suppress immune response)

Reduce antibody production

Prevent excessive inflammatory damage

**Kidney function:**

Essential for normal kidney function

Maintain glomerular filtration rate

**RBC production:**

Stimulate erythropoiesis

Increase RBC count

**Stress response:**

Produced during stress (emergency hormone)

Helps body cope with physical and psychological stress

**2. Mineralocorticoids** (mainly Aldosterone)

Produced in zona glomerulosa

Secretion regulated by:

Plasma K⁺ levels (high K⁺ stimulates; low K⁺ inhibits)

Angiotensin II (part of renin-angiotensin system)

ACTH (minor effect)

**Functions:**

**Renal effects:**

Stimulates reabsorption of Na⁺ in distal convoluted tubule and collecting duct

Stimulates excretion of K⁺ and PO₄³⁻

Result: Increased Na⁺ and water retention in blood

**Electrolyte and fluid balance:**

Maintains Na⁺ homeostasis (normal serum Na⁺: 135-145 mEq/L)

Maintains K⁺ homeostasis (normal serum K⁺: 3.5-5 mEq/L)

**Osmotic pressure:**

Maintains blood osmotic pressure

Prevents excessive water loss

**Blood pressure:**

Increases blood volume (via Na⁺ and water retention)

Increases blood pressure

**3. Androgens** (small amounts)

Produced in zona reticularis and fasciculata

Mainly DHEA and testosterone precursors

**Functions:**

Growth of axillary (underarm) hair

Growth of pubic hair

Growth of facial hair (during puberty)

Minor contribution to anabolic effects

**Adrenal Cortex Disorders:**

**Addison's Disease (Primary Adrenal Insufficiency):**

Underproduction of adrenal cortex hormones

Causes acute weakness, fatigue, hypotension, hypoglycemia

Altered carbohydrate metabolism

Hyperpigmentation of skin (due to elevated ACTH stimulating MSH)

Can be life-threatening (adrenal crisis)

**Cushing's Syndrome (Excess Glucocorticoids):**

Caused by excessive cortisol production

Moon facies (round face), buffalo hump, central obesity

Muscle weakness, hypertension, diabetes

Osteoporosis (bone loss)

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PANCREAS

**Anatomy:**

Composite gland located in retroperitoneal space (behind stomach)

Dual function: Exocrine (secretes digestive enzymes) and endocrine (secretes hormones)

Size: 15-20 cm long

**Endocrine Portion:** **Islets of Langerhans**

**Structure:**

Scattered throughout pancreatic tissue

Number: 1-2 million islets in normal pancreas

Represent: 1-2% of pancreatic tissue

Main cell types:

**α-cells (Alpha cells):** 20% of islet cells; produce glucagon

**β-cells (Beta cells):** 70% of islet cells; produce insulin

δ-cells (Delta cells): Produce somatostatin

PP cells: Produce pancreatic polypeptide

**Hormones:**

GLUCAGON

**Source:** α-cells

**Type:** Peptide hormone (29 amino acids)

**Secretion Trigger:**

Low blood glucose (hypoglycemia)

Stress, exercise

High amino acid levels

**Mechanism of Action:**

Binds to glucagon receptors on hepatocytes and other cells

Activates adenylyl cyclase → increases cAMP (second messenger)

**Functions (Hyperglycemic Hormone — Raises Blood Glucose):**

**Glycogenolysis (primary effect):**

Stimulates breakdown of liver glycogen to glucose

Glucose released into blood

Rapidly increases blood glucose levels

**Gluconeogenesis (secondary effect):**

Stimulates synthesis of glucose from non-carbohydrate sources:

Amino acids (from proteolysis)

Glycerol (from lipolysis)

Lactate (from anaerobic glycolysis)

Increases blood glucose further

**Decreased glucose utilization:**

Reduces cellular glucose uptake

Inhibits glycolysis

Inhibits glycogenesis

**Metabolic effects:**

Stimulates lipolysis (fat breakdown)

Increases blood fatty acids

Stimulates proteolysis

Increases blood amino acids

**Regulation:**

**Low glucose** (< 70 mg/dL) → Stimulates glucagon secretion

**High glucose** → Inhibits glucagon secretion (negative feedback)

**Exam Point:** Glucagon is catabolic hormone; breaks down stores to raise glucose.

INSULIN

**Source:** β-cells

**Type:** Peptide hormone (51 amino acids)

**Secretion Trigger:**

High blood glucose (hyperglycemia)

Amino acids, fatty acids

Gastrointestinal hormones (GIP, GLP-1)

Parasympathetic stimulation

**Mechanism of Action:**

Binds to insulin receptors (tyrosine kinase receptors) on target cells

Activates intracellular signaling cascades

Promotes glucose uptake via GLUT4 translocation to cell membrane

**Functions (Hypoglycemic Hormone — Lowers Blood Glucose):**

**Glucose uptake and utilization (primary effect):**

Stimulates cellular glucose uptake by facilitating GLUT4 transporter movement

Increases glucose utilization in hepatocytes, adipocytes, and muscle cells

Rapid movement of glucose from blood into cells

**Glycogenesis:**

Stimulates conversion of glucose to glycogen (glycogen synthesis)

Glycogen stored in liver and muscle

Decreases blood glucose

**Glucose oxidation:**

Promotes glycolysis (breakdown of glucose)

Increases ATP production

**Lipogenesis (anabolic):**

Stimulates fatty acid synthesis from acetyl-CoA

Promotes triglyceride synthesis

Promotes fat storage

**Protein synthesis (anabolic):**

Stimulates amino acid uptake by cells

Promotes protein synthesis

Reduces protein breakdown

**Inhibits catabolic processes:**

Inhibits gluconeogenesis

Inhibits glycogenolysis

Inhibits lipolysis

Inhibits proteolysis

**Regulation:**

**High glucose** (> 100 mg/dL) → Stimulates insulin secretion

**Low glucose** → Inhibits insulin secretion (negative feedback)

**Exam Point:** Insulin is anabolic hormone; promotes storage and synthesis; builds up reserves.

GLUCOSE HOMEOSTASIS

**Maintaining Normal Blood Glucose (70-100 mg/dL fasting):**

| Condition | Hormonal Response | Mechanism |

|-----------|-------------------|-----------|

| **High blood glucose (> 100 mg/dL)** | ↑ Insulin ↓ Glucagon | Glucose uptake, glycogenesis, lipogenesis, protein synthesis |

| **Low blood glucose (< 70 mg/dL)** | ↑ Glucagon ↑ Adrenaline ↑ Cortisol | Glycogenolysis, gluconeogenesis, lipolysis |

**Synergistic Action:** While insulin lowers glucose, glucagon, adrenaline, and cortisol raise it. This antagonistic regulation maintains glucose within narrow range essential for:

Brain function (glucose-dependent organ)

Red blood cell metabolism

Renal medulla function

DIABETES MELLITUS

**Definition:** Complex metabolic disorder due to absolute or relative insulin deficiency; characterized by persistent hyperglycemia.

**Types:**

**Type 1 (IDDM):** Autoimmune destruction of β-cells; absolute insulin deficiency; early onset

**Type 2 (NIDDM):** Insulin resistance and relative deficiency; late onset; associated with obesity

**Pathophysiology of Hyperglycemia:**

Glucose accumulates in blood (cannot enter cells efficiently)

Blood glucose exceeds renal threshold (> 180 mg/dL)

Glucose filtered into urine (glycosuria) — **loss of glucose through urine**

Osmotic diuresis (excessive urination)

**Complications of Prolonged Hyperglycemia:**

**Ketone Body Formation (Ketosis):**

Uncontrolled lipolysis releases fatty acids

Excessive fatty acid oxidation produces ketone bodies (acetoacetate, β-hydroxybutyrate, acetone)

Ketone bodies are harmful compounds

Accumulation causes metabolic acidosis (diabetic ketoacidosis)

Acidosis affects CNS, respiratory system; can cause coma and death

**Acute complications:**

Hyperglycemic hyperosmolar state

Diabetic ketoacidosis (DKA)

**Chronic complications:**

Retinopathy (eye damage; blindness)

Nephropathy (kidney damage; renal failure)

Neuropathy (nerve damage; loss of sensation)

Cardiovascular disease, stroke

Poor wound healing

**Treatment:** Insulin therapy; oral hypoglycemic agents; diet and exercise.

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TESTIS

**Location:** Scrotal sac (external pouch) outside abdomen

**Structure:**

Pair of oval glands (4-5 cm length)

Composed of:

**Seminiferous tubules:** Site of spermatogenesis; produce sperm

**Stromal/Interstitial tissue:** Contains Leydig cells (interstitial cells)

**Dual Function:**

1. Primary sex organ (gametogenic function)

2. Endocrine gland (hormonal function)

**Hormone:** **Androgens** (mainly Testosterone)

**Source:** Leydig cells (interstitial cells) in intertubular spaces

**Regulation of Testosterone Secretion:**

**GnRH** from hypothalamus → **LH** from anterior pituitary → Leydig cells produce testosterone

Negative feedback: High testosterone inhibits GnRH and LH

**FSH** stimulates spermatogenesis (indirectly)

**Functions of Androgens (Testosterone):**

**Development and maintenance of male reproductive system:**

Development of epididymis, vas deferens, seminal vesicles, prostate gland, urethra

Maintains structure and function of these organs

**Spermatogenesis:**

Essential for initiation and maintenance of sperm production

Works with FSH to stimulate seminiferous tubule activity

Major stimulatory role

**Secondary sexual characteristics (male):**

Growth of facial hair (beard, mustache)

Growth of axillary (underarm) hair

Growth of pubic hair

Hair growth on chest and limbs

Growth of larynx (Adam's apple)

Deepening of voice (low pitch)

**Muscular development:**

Stimulates muscle protein synthesis

Increases muscle mass and strength

Increases bone density and strength

**Behavioral effects:**

Influences male sexual behavior (libido/sex drive)

Acts on central nervous system

Increases aggression, dominance behavior

**Metabolic effects (Anabolic):**

Promotes protein synthesis (anabolic effect)

Increases nitrogen retention

Increases metabolic rate

Promotes carbohydrate metabolism

**Erythropoiesis:**

Stimulates red blood cell production

**Age-Related Changes:**

Testosterone levels peak in young adulthood

Gradual decline with age (andropause)

Results in decreased muscle mass, bone density, sexual function

**Exam Point:** Androgens are anabolic hormones; responsible for male masculinity.

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OVARY

**Location:** Abdominal cavity (one on each side)

**Structure:**

Pair of almond-shaped glands (3-4 cm)

Composed of:

**Ovarian follicles:** Contain oocytes (egg cells) surrounded by follicular cells

**Stromal tissue:** Connective tissue

**Corpus luteum:** Formed after ovulation from ruptured follicle

**Dual Function:**

1. Primary sex organ (gametogenic function) — produces ovum

2. Endocrine gland (hormonal function) — produces estrogen and progesterone

**Hormones:**

ESTROGEN (Estradiol and Estriol)

**Source:** Growing ovarian follicles (follicular cells)

**Regulation:**

**GnRH** from hypothalamus → **FSH** from anterior pituitary → stimulates follicle growth and estrogen secretion

Negative feedback: High estrogen inhibits GnRH and FSH (negative feedback at follicular phase)

Positive feedback: Surge of estrogen triggers LH surge → ovulation (at mid-cycle)

**Functions:**

**Female reproductive system development:**

Stimulates growth and activity of uterus, uterine tubes, vagina

Develops endometrial tissue (uterine lining)

Increases uterine blood supply

**Secondary sexual characteristics (female):**

Breast development (mammary gland growth)

Development of subcutaneous fat (wider hips, thighs, buttocks)

Growth of pubic and axillary hair (finer than males)

Higher pitched voice (compared to males)

Female body shape and distribution of body hair

**Follicular development:**

Stimulates growth of ovarian follicles

Positive feedback for its own synthesis in early follicular phase

**Sexual behavior:**

Influences female sexual behavior

Increases sexual receptivity (estrus)

**Metabolic effects:**

Increases metabolic rate

Affects bone metabolism

Increases calcium absorption

**Cardiovascular effects:**

Protective effects on cardiovascular system

Improves lipid profiles (raises HDL, lowers LDL)

**Endometrial changes:**

Stimulates endometrial proliferation during follicular phase

Increases endometrial thickness

PROGESTERONE

**Source:** Corpus luteum (formed after ovulation from ruptured Graafian follicle)

**Timing:** Secreted during luteal phase of menstrual cycle (after ovulation)

**Regulation:**

**LH** maintains corpus luteum

Corpus luteum produces progesterone for ~14 days

If no pregnancy, corpus luteum degenerates → progesterone drops → menstruation

**Functions:**

**Pregnancy support (major function):**

Prepares and maintains uterine lining (endometrium) for implantation

Maintains uterine quiescence (prevents contractions that would expel embryo)

Prevents further ovulation during pregnancy (inhibits GnRH and LH)

Maintains pregnancy by suppressing immune rejection of fetus

**Mammary gland development:**

Acts on mammary glands primed by estrogen

Stimulates development of alveoli (milk-secreting sacs)

Promotes milk secretion capacity

Prepares for lactation

**Endometrial changes:**

Converts proliferated endometrium to secretory endometrium

Increases endometrial secretions (nutrients for embryo)

Increases endometrial blood vessels

Establishes favorable environment for embryo

**Metabolic effects:**

Slightly increases metabolic