endocrinology ii

Endocrinology II: Axis Endocrinology II: Axis and systemsand systems

Advanced Physiology of AnimalsAdvanced Physiology of AnimalsANSC 3405ANSC 3405

• Endocrine glands/organs

• Hormones of hypothalamus and pituitary

• HPA axis and adrenals

• Hypothalamic Pituitary Gonadals axis

• Thyroid axis

• Growth axis

• Calcium homeostasis

Outline

Endocrine Tissues

Located at base of brain

(Testis in Male)

Adrenal Gland Ovary

KidneyPituitary

Hypothalamus

ThyroidParathyroid

Endocrine Tissue

Tissue 1

Tissue 2

Tissue 3

+

+

-

-

+

Long Loop

Short Loop

Open Loop

(Figure 9-12)

Hypothalamus-pituitary

Pituitary Stalk

Hypophyseal Portal Vessels Posterior Pituitary(Neurohypophysis)

Hypothalamus

Anterior Pituitary(Adenohypohysis)

(STUDY Figure 9-15)

Hypothalamo-hypophyseal portal system

• Carries hypothalamic hormones specifically to the anterior pituitary without dilution in the systemic blood.

1. Allows rapid response2. Little dilution of peptide hormones3. Peptides have short 1/2 life

• Specific hypothalamic nuclei secrete releasing or release

• Receptors to inhibit/control release of pituitary hormones.

Neurosecretory cells of Posterior Pituitary

• Posterior pituitary gland does NOT have cells that produce/store hormones

• Neurosecretory cells of hypothalamus release hormones– Directly into Posterior pituitary– Which is rapidly released into systemic

bloodstream– Rapid response

• Corticotropin releasing hormone (CRH)

• Gonadotropin Releasing Hormone (GnRH)

• Thyroid Releasing Hormone (TRH)

• Growth Hormone Releasing Hormone (GHRH)

• Oxytocin

• Vasopressin (VP, AVP)

Hypothalamic Hormones

Pituitary Gland

Anterior Pituitary

Posterior Pituitary

Anterior Pituitary Cell Types and Hormones

• Corticotrophs - Adrenalcorticotrophic (ACTH)

• Gonadotrophs– Release Leutinizing Hormone (LH) and Follicle

stimulating hormone (FSH)• Thyrotrophs

– Thyroid Stimulating Hormone (TSH)• Lactotrophs

– Release Prolactin• Somatotrophs

– Release Growth Hormone (GH)

Adrenals

Kidney

Posterior Pituitary Gland

Hypothalamus

AnteriorPituitary Gland

ACTH

Stress Circadian

rhythm

CRH

(-)

Glucocorticoids, Catecholamines, etc..

Glucocorticoids, Catecholamines, etc..

Muscle: Net loss of aminoAcids (glucose)

Liver: Deamination of

proteins into amino acids,

gluconeogenesis (glucose)

Fat Cells: Free fatty

acid mobilization

Heart rate: Increased

Immune system: altered

Hypothalamopituitary adrenal (HPA) axis

(Figure 9-40)

Adrenal Glands

Adrenals

Zona ReticularisSex steroids (androgens)

Zona FasciculataGlucocorticoids (Cortisol)

Glucose homeostasis and many others

Zona Glomerulosa

Mineralocorticoids (Aldosterone)

Na+, K+ and water homeostasis

Medulla: “Catecholamines”Epinephrine, Norepinephrine, dopamine

CORTEX

Sertoli cells

Leydig cells

Hypothalamic-Pituitary-Gonadal Axis (HPG):

Males

Hypothalamus

AnteriorPituitary

GnRH

Inhibin

-

-

-

Seminferous tubules:(Spermatogenisis)

Male characteristicsGrowthBehavior: Libido, aggression

+

+

Testosterone

Testosterone

LHFSH

+

(Figure 9-46)

Hypothalamus

AP

GnRH

Hypothalamic-Pituitary-Gonadal Axis (HPG):

Females

LH surgeTonic LH

Progesterone

PGF2a

Estrogens

+

FSH

Estrogen

LH

(Figure 9-47)

Estrous cycle

Menstrual cycle

(STUDY Figure 9-48)

Female Hormones

• Estrogens– Somatic growth– Mammary growth (after puberty)– Reproductive organs

• Progesterones– Mammary tissue growth (after fertilization)– Reproductive organs: Uterus lining– Maintain corpus luteum– PGF2α from uterus causes regression of corpous

luteum

Mammary Function

• Oxytocin– Smooth Muscle contraction– During birth– Causes contraction of myoepithelial cells, allowing

milk ejection– Increases after cervical distention and suckling– High progesterone inhibits

• Prolactin– Synthesis of milk proteins– Growth of mammary glands– Dopamine and PIH inhibits– Increased estrogen and low PIH causes increase

Oxytocin

Calf Stimulationof Mammary Gland

SpinalCord

Neural Pathwayto Hypothalamus

Hypothalamus

Posterior Pituitary

Capillaries

OxytocinReleasein Blood

Gender Developmental Hormones

• Testosterone – Testosterone does not make the brain masculine– Testosterone is converted into estrogen (aromatase)

in the brain, and estrogen makes the brain masculine

• Alpha Feto Protein– In females, AFP binds to the estrogen, preventing

estrogen from entering the brain– If a female animal lacks this AFP, or if estrogen levels

are synthetically too high, then a female may develop a masculine brain

• AVP in males– male aggression, mating persistence,

territoriality, jealousy

• Oxytocin in females– sexual arousal/receptivity and satiety,

bonding, nurturing behaviors, social memories–  males and females release oxytocin and

opioids during copulation which reduces aggression and facilitates social bonding

Gender and Hormones

Hypothalamothyroid axis

• Tissues become sensitive to epinephrine

• Increase cellular respiration, O2 use and metabolism

• Heat is generated• Thermoregulation• Growth and

developement(Figure 9-42)

Thyroid Hormones• Thyroxine (T4) and 3,5,3-triiodothyronine (T3)

– Formed from 2 iodinnated tyrosines precursers– Lipd soluble

Thyroid diseases

• Hypothyroidism – From low iodine during

development causes severe retardation in growth (cretinism)

– TSH increases, causing hypertrophy of gland (goiter)

– Other forms cause obesity, thinning of hair and skin and lethargy, and feeling coldness

Thyroid Diseases• Hyperthyroidism

– Overactive thyroid (ex. Graves disease)

– T3 and T4 over secretion

– Propotosis, weight loss, hair loss, hot flashes, mood swings

• Insulin – β cells secrete due

to high blood glucose levels

– Glucose uptake into tissues increases

• Glucagon– α cells secrete when

blood glucose is low– Glucose is released

from tissues back into blood

Pancreatic axis

(Figure 9-43)

Diabetes mellitus

• Type I– “Childhood” diabetes– Loss of pancreatic β cells– Decreased insulin

• Type II– “Adult” diabetes– Defective signal reception in insulin pathway– Decreased insulin

• Both cause hyperglycemia, glycosuria, lipid breakdown because tissues are deficient in glucose, ketone bodies

Growth hormone

• Control of GH– Stress, exercise nutrition,

sleep– Somatostatin (SS) inhibits– GH causes inhibition of

glucose uptake and utilization, increased a.a. uptake and protein synthesis

(Figure 9-44)

Growth HormonesAction of several hormones. • GH primary job is to stimulate the liver

– To secrete IGF-1 (Insulin Growth Factor)

• IGF-1 – stimulates proliferation of

chondrocytes (cartilage cells), resulting in bone growth.

– differentiation and proliferation of myoblasts

– Stimulates amino acid uptake and protein synthesis in muscle and other tissues.

Giantism

• Excessive GH durining childhood

• Growth plate stimulation

• Tumor of somatotrophs

Robert Wardlow 8’ 11”.

• GH late in life

• Causes excessive growth of flat bones

Acromegaly

Rondo Hatton

Calcium Homeostasis• Parathyroid

– most important endocrine regulator of calcium and phosphorus concentration in extracellular fluid (PTH)

– Targets receptors on bones and kidneys

• Calcitonin– C cells of Thymus– Decreases mobilization

and uptake of calciumStudy Figure 9.45

Calcium Homeostasis

(Figure 9-45)

Parathyroid “C” Cells

PTH Calcitonin

BoneKidney

Intestine

BoneKidney

[Ca++] [Ca++]

Stim

ulat

e Stim

ulate

Inhi

bit

Inhi

bit

In plasma In plasma

Calcium Homeostasis

More endocrine fun to come!

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