Section 3, Chapter 13

The Peripheral Endocrine Glands

Thyroid GlandLocation: The thyroid gland is located just inferior to the larynx.

Structure:

• It consists of two lateral lobes connected by an isthmus

• Contains several follicles.

Thyroid Gland Follicles

Follicles consists of simple cuboidal epithelium & a colloid

center

Follicular Cells: produce T3 & T4

Coloid: contains Thyroglobulin,

which is a storage form of thyroid

hormones.

Follicular Cells take up thyroglobulin by endocytosis, then release

the thyroid hormones into the bloodstream.

Extrafollicular Cells: produce Calcitonin

Thyroid Hormones

Target Cells: T3 & T4 affect many cells throughout the body.

Actions of T3 & T4: Raise Metabolic Rate

• Increase rate of carbohydrate catabolism

• Enhance protein synthesis

• Promotes the breakdown and use of lipids

T3 & T4 are major factors in determining the basal metabolic rate T3 & T4 are major factors in determining the basal metabolic rate

(BMR)

BMR = calories required to sustain life

Thyroid Hormones

Follicular cells require iodine salts

(iodide) to produce T3 and T4.

• Nearly 75% of thyroid hormones are attached to thyroid binding

globulins.

• Only the small amounts of the unbound hormones act on target cells.

T3 & T4 are hydrophobic molecules (insoluble in water)

T4 accounts for 95% of circulating Thyroid Hormone, But$

Transport of Thyroid Hormones

T3 is physiologically more active.

• T3 is 5 times as potent as T4

• T3 also has a 50-fold higher “free” concentration in the plasma (see figure

below).

Thyroid Disorders

Hypothyroidism – insufficient T3 & T4

• During infancy – results in intellectual disability,

stunted growth, abnormal bone formation (cretinism)

• During adulthood – low metabolic weight,

sluggishness, poor appetite, and sensitivity to cold

Infantile

hypothyroidism

Hyperthyroidism – excess T3 & T4

• Results in high metabolic rate, hyperactivity, weight

loss, sensitivity to heat, and exophthamia (protruding

eyes)• Grave’s Disease

• Autoimmune Disorder: Antibodies target the

thyroid gland and mimic TSH. Thyroid antibodies

overstimulate thyroid gland, resulting in

hyperthyroidism.

Grave’s disease may

cause exophthalmia

hypothyroidism

Calcitonin

Extrafollicular cells (C-cells) secrete Calcitonin

Calcitonin lowers blood calcium concentrations.

• Stimulates Osteoblast activity – increases bone deposition

Actions of Calcitonin

• Stimulates Osteoblast activity – increases bone deposition

Major Source of Control: elevated blood calcium ion concentration

• Inhibits osteoclast activity – reduces bone resorption

• Promotes the excreting of calcium from the

kidneys

Parathyroid Glands• Location:

4 small parathyroid glands are located

on the posterior aspect of the thyroid gland

•Hormone: PTH (parathyroid hormone)

One parathyroid gland surrounded by thyroid

follicles.

Parathyroid Hormone elevates blood calcium levels.

Parathyroid Hormone (PTH)

• Stimulates Osteoclast activity – increases bone resorption

• Inhibits osteoblast activity – reduces bone

Actions of PTH:

• PTH also promotes the activation of Vitamin D, which

enhances calcium absorption from the small intestine.

• Inhibits osteoblast activity – reduces bone

deposition• Promotes calcium reabsorption from the kidneys.

Major Source of Control: Inadequate blood calcium ion concentration

Figure 13.27 Parathyroid Hormone (PTH) stimulates bone to release Calcium

(Ca2+) and the kidneys to conserve calcium. It indirectly stimulates the intestine to

absorb calcium. The resulting increase in blood calcium concentration inhibits

secretion of PTH by negative feedback.

Calcitonin and PTH have opposing effects on the levels of calcium

ions in circulation. Both work together to maintain calcium

homeostasis.

Adrenal Glands

Location: The adrenal glands are located on the superior aspect of the

kidneys.

Structure:

• Adrenal glands are pyramid shaped organs that consist of two parts

• Adrenal Medulla = secretions controlled by sympathetic nerve fibers

Adrenal Cortex = Under hormonal control

Hormones of the Adrenal Medulla

Hormones: Norepinephrine (noradrenalin) & Epinephrine (adrenalin)

• Both are classified as catecholamines.

Nerve fibers control secretions: Hormones of the adrenal medulla are

under control by the sympathetic division (fight or flight) of the ANS.

Actions: Effects are similar to sympathetic nerve fibers, but longer lasting.

• Increases heart rate and force of contraction

• Increases blood pressure

• Increases metabolic rate

• Increases blood glucose levels (primarily epinephrine)

• Decreases digestion

Beta Blockers• Epinephrine & Norepinephrine exert their effects by binding to Beta

(ß) adrenergic receptors in heart and walls of the blood vessels.

• Beta blockers bind to ß-receptors, thus obstructing the binding of catecholamines.

• Hence beta blockers reduce sympathetic influences of the heart and blood vessels.

• Therefore, beta blockers decrease heart rate, contractility, and reduce blood pressure.

Hormones of the Adrenal Cortex

3 Layers of the adrenal cortex secrete over 30 types of steroid hormones.

Hormones

Aldosterone – produced in zona glomerulosa

Cortisol – produced in zona fasciculata

Androgens – produced in zona reticularis

Hormones of the Adrenal Cortex

1. Aldosterone (mineralocorticoid)

• regulates Na+ and K+ concentrations

• regulates blood pressure

Actions

• Aldosterone causes the kidneys to reabsorb Na+ and to excrete K+

• Aldosterone indirectly raises blood pressure:

Increased Na+ reabsorption increases water reabsorption by osmosis. Increased Na+ reabsorption increases water reabsorption by osmosis.

Controls of Aldosterone Secretion

• Low blood pressure stimulates aldosterone secretion

(renin-angiotensin-aldosterone pathway)

• Elevated blood K+ concentration promotes aldosterone secretion

• Low Na+ has only a slight effect on aldosterone secretion.

Renin-Angiontensin-Aldosterone System

ACE Inhibitors block

the actions of ACE, the actions of ACE,

and thus lower blood

pressure.

Hormones of the Adrenal Cortex

2. Cortisol (glucocorticoid)

• Its primary effect is to build up and conserve blood glucose supplies

• Its actions keep blood glucose levels constant between meals.

Actions

• Promotes gluconeogenesis in the liver

gluconeogenesis = glucose synthesis from non-carbohydrates

• Inhibits protein synthesis: amino acids used in gluconeogenesis

• Promotes the release and used of fatty acids from adipose for energy.

Using fatty acids for energy allows glucose to be conserved.

Hormones of the Adrenal Cortex

3. Androgens

• Supplement the sex hormones secreted from the gonads.

• Androgens may be converted into testosterone and estrogens.

The Pancreas

Structure & Location: The pancreas is located posterior to the stomach,

attached to the duodenum.

The pancreas has both digestive and endocrine functions.

• Pancreatic Islets (Islets of Langerhans) = endocrine cells

• Digestion cells

(we’ll discuss these with the digestive system)

Cells of the Pancreatic Islets

3 distinct type of cells secrete 3 hormones:

• Alpha Cells – secrete glucagon

• Beta Cells – secrete insulin

• Delta Cells – secrete somatostatin

Pancreatic hormones regulate

the storage, use, and release of the storage, use, and release of

fuels (glucose).

Pancreatic Hormones

1. Glucagon

Overall Effect: During fasting, when blood glucose levels drop,

glucagon elevates blood glucose levels

Actions of Glucagon:

• Stimulates glycogenolysis in the liver (breakdown of glycogen into glucose)• Stimulates glycogenolysis in the liver (breakdown of glycogen into glucose)

• Glucagon also promotes gluconeogenesis

• Glucagon also stimulates the breakdown of fats into glycerol and fatty acids.

• Glycerol is used in gluconeogenesis

• Fatty Acids are metabolized for energy

glycogen

Gluconeogenesis

Amino acids glycerol

Glycogenolysis

Liver

glucose

glucose

Glucagon secretions elevates blood glucose concentrations.

• Gluconeogenesis converts noncarbohydrates, such as amino acids

and glycerol, into glucose.

• Glycogenolysis breaks down large glycogen molecules into glucose.

2. Insulin

Pancreatic Hormones

Overall Effect: Following a meal, when blood carbohydrate levels

are high, insulin removes excess glucose from the blood.

Actions of Insulin:

• Stimulates glycogenesis in the liver (formation of glycogen from glucose). • Stimulates glycogenesis in the liver (formation of glycogen from glucose).

• It inhibits gluconeogenesis.

• Insulin promotes glucose uptake in adipose tissue, skeletal muscles, and

cardiac muscle.

3. Somatostatin

Overall Effect: Helps regulate glucose metabolism by inhibiting the

secretion of glucagon and insulin.

Hormonal Control of Glucose

Insulin and glucagon function together to stabilize

blood glucose concentration. Negative feedback

responding to blood glucose concentration controls

the levels of both hormones.

Diabetes Mellitus

Type I Diabetes Mellitus (juvenile)

• Autoimmune disease – immune system destroys beta cells, resulting in the

loss of insulin production.

• Without insulin, blood glucose cannot be taken up and used for energy.

• Glucose accumulates in the blood and urine = hyperglycemia.

Type II Diabetes Mellitus (adult onset)

• Receptors on target cells wear down and become insensitive to insulin.

• Target cells resist glucose uptake, even in the presence of insulin.

• Insulin levels must be higher than normal just to maintain

normal glucose concentrations.

Other Endocrine Glands

Pineal Gland

• The pineal gland secretes melatonin, which

regulates circadian rhythms (sleep/wake cycle)

• Located posterior to thalamus.

• Melatonin secretions are greatest in dark. Light

inhibits secretions.

Thymus Gland

• Secretes thymosins

• Promotes development of certain lymphocytes

• Important in role of immunity

Reproductive Organs

• Ovaries produce estrogens and progesterone

• Testes produce testosterone

• Placenta produces estrogens, progesterone, and gonadotropin

Other organs: digestive glands, heart, and kidney

Other Endocrine Glands

End of Section 3, Chapter 13