endocrinology ii
TRANSCRIPT
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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