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Chapter 11

Endocrine Glands -

Secretion & Action of Hormones

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Endocrine Glands

Are ductless & secretehormones into

bloodstream

Hormones go to targetcells that containreceptor proteins for it

Neurohormones aresecreted into blood byspecialized neurons

Hormones affect

metabolism of targets

Fig 11.1

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Chemical Classification of Hormones

Amine hormones are derived from tyrosine or tryptophan

Include NE, Epi, thyroxine, melatonin

Polypeptide/protein hormones are chains of amino acids

Include ADH, GH, insulin, oxytocin, glucagon, ACTH, PTH

Glycoproteins

Long polypeptide bound to a carbohydrate group

Include LH, FSH, TSH

Steroids are lipids derived from cholesterol

Include testosterone, estrogen, progesterone & cortisol

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Common Aspects of Neural & Endocrine

Regulation

Both NS & endocrine system use chemicals tocommunicate

Difference between NTs & hormones is transport inblood & more diversity of effects in hormone targets

Some chemicals are used as hormones & NTs

Targets for both NTs & hormones must have

specific receptor proteins

Must be way to rapidly inactivate both

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A tissue usually responds to # of hormones 2 hormones are synergistic if work together to

produce an effect

Produce a larger effect together than individual effectsadded together

Effects of Epi and NE on heart rate

A hormone haspermissiveeffect if it enhances

responsiveness of a target organ to 2nd hormone

If action of 1 hormone inhibits effect of another, it isantagonistic

Hormone Interactions

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Hormone Levels & Tissue Responses

Half-life is time required for blood level to bereduced by half

Ranges from mins to hrs for most (days for thyroidhormones)

Normal tissue responses are produced only whenhormones are in physiological range

High (pharmacological) doses can cause # of sideeffects

Probably by binding to receptors of other hormones

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Priming effect (upregulation) occurs when a hormoneinduces more of its own receptors in target cells

Results in greater response in target cell

Desensitization (downregulation) occurs after long exposureto high levels of polypeptide hormone

Subsequent exposure to this hormone produces a lesser response

Due to decrease in # of receptors on targets

Most peptide hormones havepulsatilesecretion which preventsdownregulation

Hormone Levels & Tissue Responses continued

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Mechanisms of Hormone Action

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Mechanisms of Hormone Action

Target cell receptors show specificity, high affinity,& low capacity for a hormone

Lipid hormones have receptors in target's cytoplasm

&/or nucleus because can diffuse thru plasmamembrane

Receptors for water-solubles are on surface of targetcell

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Hormones That Bind to Nuclear Receptor

Proteins

Lipid hormones travelin blood attached tocarrier proteins

They dissociate from

carriers to pass thruplasma membrane oftarget

Receptors are callednuclear hormone receptors

Fig 11.4

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Nuclear Hormone Receptors

Serve as transcription factors when bound to hormone

ligands

Activate transcription

Constitute a "superfamily" composed of steroid family &thyroid hormone family (which includes vitamin D &retinoic acid)

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Nuclear Hormone Receptors

Have ligand (hormone)-binding & DNA-binding domains Binds hormone & translocates to nucleus

Binds to hormone-response element (HRE) on DNA located adjacent to targetgene

Fig 11.5

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Fig. 11.6

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Mechanism of Thyroid Hormone Action

continued

T3 & receptor bind to1 half-site

Other half-site bindsretinoic acid

Two partners formheterodimerthatactivates HRE

Stimulates

transcription of targetgene

Fig 11.7

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Hormones That Use 2nd Messengers

Water soluble hormones use cell surface receptorsbecause cannot pass through plasma membrane

Actions are mediated by 2nd messengersHormone is extracellular signal; 2nd messenger carries

signal from receptor to inside of cell

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Mediates effects of many polypeptide & glycoprotein hormones

Hormone binds to receptor causing dissociation of a G-protein subunit

Adenylate Cyclase-cAMP

Fig 11.8

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G-protein subunit binds to & activates adenylate cyclase Which converts ATP into cAMP cAMP attaches to inhibitory subunit ofprotein kinase

Adenylate Cyclase-cAMP continued

Fig 11.8

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Inhibitory subunit dissociates, activating protein kinase

Which phosphorylates enzymes that produce hormones effects

cAMP inactivated byphosphodiesterase

Adenylate Cyclase-cAMP continued

Fig 11.8

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Pituitary Gland

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Pituitary Gland

Pituitary gland is located beneath hypothalamus at base of forebrain

Fig 8.16

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Pituitary Gland continued

Is structurally &functionally divided intoanterior & posterior lobes

Hangs below hypothalamusby infundibulum

Anterior produces ownhormones Controlled by hypothalamus

Posterior stores & releaseshormones made inhypothalamus

Fig 11.1211-36

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Anterior Pituitary

Secretes 6 trophichormones that

maintain size oftargets

High blood levelscause target to

hypertrophy Low levels cause

atrophy

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Anterior Pituitary continued

Growth hormone (GH) promotes growth, protein synthesis, &movement of amino acids into cells

Thyroid stimulating hormone (TSH) stimulates thyroid to produce &

secrete T4 & T3 Adrenocorticotrophic hormone (ACTH) stimulates adrenal

cortex to secrete cortisol, aldosterone

Follicle stimulating hormone (FSH) stimulates growth ofovarian follicles & sperm production

Luteinizinghormone (LH) causes ovulation & secretion oftestosterone in testes

Prolactin (PRL) stimulates milk production by mammaryglands

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Anterior Pituitary continued

Release of Anterior Pituitary hormones is controlledby hypothalamic releasing & inhibitingfactors & byfeedbackfrom levels of target gland hormones

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Anterior Pituitary continued

Releasing & inhibitinghormones fromhypothalamus arereleased from axonendings into capillary

bed in median eminence

Carried by hypothalamo-hypophyseal portal systemdirectly to anothercapillary bed in A. Pit.

Diffuse into A. Pit. &regulate secretion of itshormones

Fig 11.15

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Feedback Control of Anterior Pituitary Involves short feedbackloop in which retrograde

flow of blood & hormonesfrom A. Pit. tohypothalamus inhibits

secretion of releasinghormone

Involves negative feedbackof target gland hormones

& during menstrual cycle,estrogen stimulates LHsurge bypositive feedback

Fig 11.17

11-41

Hi h B i F i & A i Pi i

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Higher Brain Function & Anterior Pituitary

Secretion

Hypothalamus receives input from higher braincenters that can affect A. Pit. secretion

E.g. psychological stress affects circadian rhythms,

menstrual cycle, & adrenal hormones

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Growth Hormone Secretion

Is from anterior pituitary; stimulated by GHRH, &inhibited by somatostatin, from hypothalamus

Follows a circadian pattern--is greater during sleep& lower during waking hours

Stimulates growth in children & adolescents

Has important metabolic effects in adults

Is stimulated by increased blood amino acids &decreased blood glucose

Is increased during fasting

Stimulates protein synthesis, fat breakdown, & decreases

glucose use by most tissues 19-61

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Growth Hormone (GH or somatotropin)

Stimulates uptake of amino acids; proteinsynthesis; growth in most tissues.

Stimulates breakdown of fats to be used as

an energy source but stimulates synthesis ofglycogen: glucose sparing (diabetogenic)

Promotes bone and cartilage growth

Regulates blood levels of nutrients after ameal and during periods of fasting

Stimulates glucose synthesis by liver

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Are similar to pro-insulin; produced by many tissues Are called somatomedins because mediate many of

GH's effects

Liver produces & secretes IGF-1 in response to GHIGF-1 in turn stimulates cell division & growth of

cartilage

These actions are supported by IGF-2 which has more insulin-

like actions Do not mediate effects of GH on lipolysis & glucose

sparing (i.e. metabolic effects)

Insulin-like Growth Factors (IGFs)

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Figure 16.6

Metabolic Action of Growth

Hormone

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Growth Hormone & Body Growth

Growth of skeleton occurs first as growth ofcartilage at epiphyseal discs which then becomeconverted to bone

Mediated by IGF-1 & 2 which stimulate chondrocytesto divide & secrete more cartilaginous matrix

Growth stops when epiphyseal discs are ossified

Gigantism produced by excess GH secretion in

children Dwarfism caused by inadequate secretion of GH

during childhood

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Growth Hormone & Body Growth

Excess GH secretion inadults, after epiphysealdiscs are ossified,results in acromegaly

There is no increase inheight

However soft tissue stillgrows

Causing elongation of

jaw, deformities in hands,feet, & bones of face

Fig 19.18 19-65

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Growth Hormone Stimulation:functions in

regulating growth, tissue maintenance, metabolismGHRHfrom hypothalamus causes release of

Growth hormonefrom anterior pituitary effects

Target tissues: most tissues of the body

Direct effect: GH binds to receptors on cells and causeschanges within the cells. Increased lipolysis and decreaseduse of glucose for energy

Indirect effect: causes liver and skeletal muscle to produce

somatomedins; e.g., insulinlike growth factors (IGFs) Insulinlike growth factors: bind to receptors on

membranes of target cells. Stimulate growth incartilage, bone; increased synthesis of proteins inskeletal muscle.

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Regulation of GH Secretion

1. Stress and decreased glucose

levels increase release ofGHRH and decreased re-

lease of GHIH.

2. GHRH and GHIN travel via

the hypothalamo-hypophyseal

portal system to ant. pituitary

3. Increased GHRH and reduced

GHIH act on AP and result in

increased GH secretion.

4. GH acts on target tissues.

5. Increasing GH levels have neg

feedback effect on hypothala.

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Growth Hormone: Inhibition

Hypothalamus produces growth hormone inhibitinghormone (GHIH = somatostatin)

Inhibits production of GH by anterior pituitary.

GHRH secretion in response to low blood glucose, stress,increase in certain a.a.

GHIH secretions in response to high blood glucose.

Peak GH levels during deep sleep; levels lower at other

times of day. Hyposecretion of GH may result in dwarfism

Hypersecretion may result ingiantism oracromegaly de-

pending on ossification of epiphyseal plates

P i Pi i

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Posterior Pituitary

Stores & releases 2 hormones produced inhypothalamus:

Antidiuretic hormone (ADH/vasopressin) whichpromotes H20 conservation by kidneys

Oxytocin which stimulates contractions of uterus duringparturition

& contractions of mammary gland alveoli for milk-ejectionreflex

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Hypothalamic Control of Posterior Pituitary

Supraoptic nuclei ofhypothalamus produceADH

Paraventricular nucleiproduce oxytocin

Both transported alonghypothalamo-hypophysealtract to posterior pituitary

Release controlled inhypothalamus byneuroendocrine reflexes

Fig 11.13 11-44

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Thyroid Gland

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Thyroid Gland

Is located just

below the larynx Secretes T4 & T3

which set BMR &

are needed forgrowth,

development

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Thyroid Gland Consists of microscopic thyroid follicles

Outer layer is follicle cells that synthesize T4

Interior filled with colloid, a protein-rich fluid

11-53

Production of Thyroid Hormones

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Production of Thyroid Hormones

Iodide (I-) in blood isactively transported intofollicles & secreted intocolloid

Where it is oxidized to

iodine (I2) & attached totyrosines ofthyroglobulin

A large storage molecule forT4 & T3

TSH stimulates hydrolysis

of T4 & T3s fromthyroglobulin & thensecretion

Fig 11.23

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Thyroid Hormones Produced by follicular cells

Triiodothyronine orT3-less produced Tetraiodothyronine orT4 orthyroxine-more

99.6% of thyroxine in the blood is bound to thyroxine-binding globulin (TBG) from the liver. Rest is free.

TBG has a higher affinity for T4

than for T3

; amt of freeunbound T3 in plasma is 10xs greater than free T4.

Only free thyroxine and T3 can enter cells; bound-thyroxine serves as a reservoir of this hormone

33-40% of T4 converted to T3 in cells: T3 more potent

Bind with intracellular receptormolecules and initiatenew protein synthesis

Increase rate of glucose, fat, protein metabolism inmany tissues thus increasing body temperature

Normal growth of many tissues dependent on presence

of thyroid hormones.

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Effects of T3 and T4

1. Maintain normal rate of metabolism.

2. Increase the rate at which glucose, fat, and protein are meta-bolized.

3. Increase the activity of Na+-K+ pump which increases body

temperature (calorigenic effect)

4. Can alter the number and activity of mitochondria resulting in

greater ATP synthesis and heat production.

5. Normal growth and maturation of bone, hair, teeth, c.t., and

nervous tissue require thyroid hormone.

6. Both T3 and T4 play a permissive role for GH and GH does not

have its normal effect on tissues if T3 and T4 are lacking.7. See Table 18.4 for effects of hypo- and hypersecretion

Diseases of the Thyroid Goiter

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Diseases of the Thyroid - Goiter

In absence of sufficient

dietary iodide, T4 & T3

cannot be made & levels

are low

Low T4 & T3dont providenegative feedback & TSH

levels go up

Because TSH is a trophic

hormone, thyroid gland

grows

Resulting in a goiter

Fig 11.2511-55

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People with inadequate T4 & T3 levels are

hypothyroid

Have low BMR, weight gain, lethargy, cold intolerance

& myxedema = puffy face, hands, feet

During fetal development hypothyroidism can cause

cretenism (severe mental retardation)

Diseases of the Thyroid - Hypothyroidism

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Goiters are also produced by Grave's disease

Autoimmune disease where antibodies act like TSH &

stimulate thyroid gland to grow & oversecrete =

hyperthyroidism Characterized by exopthalmos, weight loss, heat intolerance,

irritability, high BMR

Diseases of the Thyroid - Hyperthyroidism

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11-58

Calcitonin

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Calcitonin

Secreted by C cells of thyroid gland

Works with PTH & 1,25 Vit D3 to regulate bloodCa2+ levels

Stimulated by increased plasma Ca2+

Inhibits activity of osteoclasts

Stimulates urinary excretion of Ca2+ & P043- by

inhibiting reabsorption

Physiological significance in adults is notunderstood

19-72

Parathyroid Glands

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Parathyroid Glands

Are 4 glandsembedded in laterallobes of thyroid gland

Secrete Parathyroidhormone (PTH)

Most importanthormone for control of

blood Ca2+

levels

Fig 11.28

11-59

Parathyroid Hormone (PTH)

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Parathyroid Hormone (PTH)

Secreted by parathyroid glands

Is most important hormone in control of Ca2+ levels

Release is stimulated by low blood Ca2+ levels

Stimulates osteoclasts to reabsorb bone

Stimulates kidneys to reabsorb Ca2+ from filtrate, & inhibits

reabsorption of P043-

Promotes formation of 1,25 Vit D3 that stimulates Ca2+absorption by intestines

Many cancers secrete PTH-related protein that interacts

with PTH receptors producing hypercalcemia19-71

Parathyroid Hormone

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Parathyroid Hormone

Release stimulated bydecreased blood Ca2+

Acts on bones, kidney,& intestines to increase

blood Ca2+ levels

Fig 11.29

11-60

Effects of Parathyroid Hormone

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Figure 16.11

Effects of Parathyroid Hormone

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1 25 Vitamin D

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1,25 Vitamin D3

Synthesis begins in skin when cholesterol derivative is converted to

Vit D3 by sunlight

Fig 19.21

19-75

1 25 Vitamin D

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1,25 Vitamin D3continued

Directly stimulates intestinal absorption of Ca2+ &P04

3-

When Ca2+ intake is inadequate, directly stimulatesbone reabsorption

Stimulates kidney to reabsorb Ca2+ and P043

Simultaneously raising Ca2+ & P043- results in increased

tendency of these to precipitate as hydroxyapatite

Stimulated by PTH Inadequate Vit D in diet & body causes

osteomalacia & rickets (loss of bone calcification)

19-76

Overview of Hormonal Control of Ca2+

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Overview of Hormonal Control of Ca Fig 19.23 Fig 19.24

19-77

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Adrenal Gland

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Adrenal Glands

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Adrenal Glands

Sit on top ofkidneys

Each consists ofouter cortex &inner medulla

2 arise differentlyduring

development

Fig 11.18

11-46

Adrenal Glands

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Adrenal Glands

Medulla synthesizes & secretes 80% Epi & 20% NE Controlled by sympathetic

Cortex is controlled by ACTH & secretes:

Cortisol which inhibits glucose utilization & stimulates

gluconeogenesis Aldosterone which stimulate kidneys to reabsorb Na+ and

secrete K+

& some supplementary sex steroids

11-47

Adrenal Medulla

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Adrenal Medulla

Hormonal effects of Epi last 10X longer than NE

Innervated by preganglionic Symp fibers

Activated during "fight or flight" response

Causes:

Increased respiratory rate

Increased HR & cardiac output

General vasoconstriction which increases venous return Glycogenolysis & lipolysis

11-49

Effects of Epinephrine Secretion from

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Effects of Epinephrine Secretion from

Adrenal Medulla

Metabolic Effects of Epi & Norepi

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Metabolic Effects of Epi & Norepi

Are similar to glucagon, stimulating glycogenolysis &lipolysis

Fig 19.15

19-57

H f Ad l C t

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Hormones of Adrenal Cortex

Mineralocorticoids: Zona glomerulosa

Aldosterone produced in greatest amounts. Increasesrate of sodium reabsorption by kidneys increasingsodium blood levels

Glucocorticoids: Zona fasciculata

Cortisol is major hormone. Increases fat and proteinbreakdown, increases glucose synthesis, decreasesinflammatory response

Androgens: Zona reticularis

Weak androgens secreted then converted to testosteroneby peripheral tissues. Stimulate pubic and axillary hairgrowth and sexual drive in females

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Regulation of Cortisol Secretion

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Help the body resist stress by:

Keeping blood sugar levels relatively constant

Maintaining blood volume and preventing water shift into tissue

Cortisol provokes: Gluconeogenesis (formation of glucose from noncarbohydrates)

Rises in blood glucose, fatty acids, and amino acids

Glucocorticoids (Cortisol)

Metabolic Effects of Cortisol

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Metabolic Effects of Cortisol

Cortisol is secreted in response to ACTH

Which is often released in response to stress, including

fasting & exercise

Where it supports effects of glucagon

Promotes lipolysis, ketogenesis, & protein breakdown

Protein breakdown increases amino acid levels for use in

gluconeogenesis in liver

19-58

Metabolic Effects of Cortisol continued

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Fig 19.16

Metabolic Effects of Cortisol continued

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Figure 16.15

Stress and the Adrenal Gland

Stress & the Adrenal Gland

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Stress & the Adrenal Gland

Stress induces anon-specificresponse calledgeneral adaptation

syndrome (GAS) Causes ACTH &

cortisol release

Often affects

physiologynegatively

Fig 11.20

11-50

Pancreas

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Pancreas

Located along small intestine and

stomach; retroperitoneal Exocrine gland

Produces pancreatic digestive

juices

Endocrine gland

Consists of pancreatic islets

Composed of

Alpha cells; secrete glucagon

Beta cells; secrete insulin

Delta cells; secrete somatostatin

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A 29-amino-acid polypeptide hormone that is a potent

hyperglycemic agent

Its major target is the liver, where it promotes:

Glycogenolysis the breakdown of glycogen to glucose

Gluconeogenesissynthesis of glucose from lactic acid and

noncarbohydrates

Release of glucose to the blood from liver cells

Glucagon

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Target tissue is the liver, adipose tissue, muscle, andsatiety center of hypothalamus

A 51-amino-acid protein consisting of two amino acid

chains linked by disulfide bonds

Synthesized as part of proinsulin and then excised byenzymes, releasing functional insulin

Insulin:

Lowers blood glucose levels

Enhances transport of glucose into body cells

Counters metabolic activity that would enhance blood glucose

levels

Insulin

Islets of Langerhans continued

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Betas secrete insulin inresponse to low bloodglucose

Promotes entry ofglucose into cells

& conversion of glucoseinto glycogen & fat

Decreases blood glucose

Islets of Langerhans continued

Fig 11.31

11-64

Insulin & Glucagon Secretion

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g

Fig 19.7

Normal fastingglucose level is 65105 mg/dl

Insulin & glucagon

normally preventlevels from risingabove 170mg/dlafter meals or falling

below 50mg/dlbetween meals

19-40

Regulation of Blood Glucose Levels

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g

The

hyperglycemic

effects ofglucagon and

the

hypoglycemic

effects of

insulin

Figure 16.17

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Regulation of Insulin Secretion

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Fig 19.10 19-44

Effects of ANS on Insulin & Glucagon

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g

ANS innervates islets

Activation of Parasymp NS stimulates insulinsecretion

Activation of Symp NS stimulates glucagon &inhibits insulin

This can cause "stress hyperglycemia"

19-45

Diabetes Mellitus

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Characterized by chronic high blood glucose levels(hyperglycemia)

Type I (insulin dependent orIDDM) is due to

insufficient insulin secretion Type II (insulin independent orNIDDM) is due to

lack of effect of insulin

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Results from hyposecretion or hypoactivity of insulin

The three cardinal signs of DM are:

Polyuriahuge urine output

Polydipsiaexcessive thirst

Polyphagiaexcessive hunger and food consumption

Hyperinsulinismexcessive insulin secretion, resulting in

hypoglycemia

Diabetes Mellitus (DM)

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Figure 16.18

Diabetes Mellitus (DM)

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Type I Diabetes

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yp

b cells of islets are destroyed by autoimmune attack Glucose is unable to enter resting muscle or adipose

cells

Rate of fat synthesis lags behind rate of lipolysis

Fatty acids are converted to ketone bodies, producingketoacidosis

Increased glucagon levels stimulate glycogenolysis

in liver

19-51

Effects of Uncontrolled Type I Diabetes

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y

Fig 19.12

19-52

Hypoglycemia

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yp g y

Reactive hypoglycemia is oversecretion of insulin due to anexaggerated response ofb cells to a rise in glucose

Occurs in people who are genetically predisposed to type II diabetes

Symptoms include tremors, hunger, weakness, blurred vision, & confusion

Fig 19.14

19-54

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Miscellaneous Glands &

Hormones

11-65

Pineal Gland

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Is located in basal

forebrain near

thalamus

Secretes melatonin

in response to

activity of

suprachiasmaticnucleus (SCN) of

hypothalamus

Fig 11.32

11-66

Pineal Gland continued

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SCN is primary timing center for circadian rhythms

Reset by daily light/dark changes

Melatonin is involved in aligning physiology withsleep/wake cycle & seasons

Secreted at night & is inhibited by light

Inhibits GnRH (antigonadotropic) in many animals

11-67

Thymus

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Is located aroundtrachea belowthyroid

Produces T cellsof immunesystem &hormones that

stimulate them

Fig 11.3311-68

Sex & Reproductive Hormones

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Gonads (testes & ovaries) secrete steroid hormonestestosterone, estrogen, & progesterone

Placenta secretes estrogen, progesterone, hCG, and

somatomammotropin

11-69

Estrogen

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Causes epiphyseal discs (cartilaginous growthplates) to seal (ossify) which stops growth

Is necessary for proper bone mineralization &

prevention of osteoporosis Stimulates osteoblast activity & suppresses

formation of osteoclasts

19-73

Autocrine & Paracrine Regulation

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Autocrine regulators are produced & act within

same tissue of an organAll autocrines control gene expression in target cells

Paracrine regulators are autocrines that are produced

within one tissue & act on different tissue in same organ.Autocrines & paracrines include:

Cytokines (lymphokines, interleukins)

Growth factors (promote growth & cell division)

Neutrophins (provides trophic support for normal &regenerating neurons)

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Table 11.2

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Table 11.7

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Table 11.8