HUMAN ANATOMY

ENDOCRINE SYSTEM II

I. INTRODUCTION
II. THE PANCREAS
III. THE GONADS
IV. THE PINEAL GLAND
V. THE THYMUS

I. INTRODUCTION

II. THE PANCREAS

* Gross anatomy
Large, soft, gray-pink colored gland with many lobules
Each lobule defined by connective tissue septa
Considered a tubuloacinar gland
Acini = grape-like cluster of cells
Therefore- the pancreas has many grape-like clusters of secretory
cells connected by numerous passageways (tubules or
ducts)
Shaped like a tadpole
Location = upper abdominal cavity behind stomach
Head = in R abdomen within the “C” of duodenum
Body = extends to L
Tail = in mesentery near hilum of spleen

* Function of the pancreas

Exocrine portion
Makes up most of gland - composed of pear shaped serous acini
Secretes aqueous product (water & enzymes) into ducts
Endocrine portion
Scattered small clusters of cells- called the islets of Langerhans
Secretes hormones into blood

* Endocrine portion of the pancreas

Islets of Langerhans = scattered islands of secretory cells that release hormones
Secretes [2] antagonistic polypeptide hormones - that influence carbohydrate
metabolism
1. Insulin
Function = LOWERS blood glucose
Moves glucose out of blood & into cells (especially liver, muscle
& adipose)
2. Glucagon
Function = INCREASES blood glucose
Mechanisms
 Glycogenolysis = breaks down liver glycogen into glucose
Glyconeogenesis = new glycogen synthesized by liver
Islet cell types
Alpha cells
Large cells - mostly in periphery of Islet
Manufactures & releases glucagon
Beta cells
Small cells - most in central area
Manufactures & releases insulin

Both cells types have features of protein producing cells

Moderate amounts of rER
Active Golgi
MANY secretory granules

Delta cells
LARGEST cell type
Manufactures & releases somatostatin – hormone that INHIBITS
growth hormone

* Blood Sugar Metabolism

Role of Insulin in glucose uptake
Unrefined carbohydrates are eaten  broken down into smaller sugars by
enzymes in mouth & intestines  absorbed (via intestines) into
blood
Acid from stomach entering small intestine stimulates pancreas to release
insulin into the blood
Insulin binds to special receptor on cell surface (mostly on liver, muscle,
adipose cells)

Inside cell- the receptor changes shape and sends a molecular signal that
activates sugar transport channel vesicles
Vesicles respond - and carry sugar transport channels (protein
entryways) to the cell membrane
Once inserted in membrane - the transport channels allow sugar to cross
membrane and enter cell from blood

Sugar is used by cell – to generate energy (ATP) within the mitochondria

If excess sugar present – it is stored as glycogen – or fat

Nutrients needed for process to run effectively

Minerals = vanadium, chromium, magnesium
Fatty acids = CLA (conjugated linoleic acid), lipoic acid
Vitamins = inositol,, vit-E

Problems with blood sugar regulation

 Inactivity, excess sweets, high quantities of refined/processed foods
consumed… result in rapid increase in blood sugar levels
Pancreas responds – releasing a proportionally HIGH amount of insulin
If this pattern continues – 3x/day, week after week, month after month,
year after year….
Cell receptors may become un-responsive to insulin

Eventually… individual may suffer Sydrome X (Metabolic Syndrome)

Cluster of symptoms - including varying degrees of glucose
intolerance, high HDL and/or triglicerides, high blood
pressure, upper body obesity, coronary heart disease,
stroke, polycystic ovary syndrome (increases androgen
levels), colorectal cancer, breast cancer

Contributing factor = diet deficient in nutrients

System components (membranes, insulin receptors) cannot
be maintained or properly constructed
Result - sugar remains in blood
Transport channel vesicles may have difficulty in fusing
with cell membrane
Result - sugar remains in blood
Increased activity of other factors that are normally
suppressed in a healthy cell
Phosphotyrosine phosphatases
Tumor Necrosis Factor alpha (TNF)
Nuclear factor-kappaB
Result – cell and/or tissue damage

Ultimately- a poor diet may alter gene expression… which

controls blood sugar metabolism
Result = reduction in fat, sugar utilization by mitochondria
Result = altered fat metabolism

Diabetes Mellitus
Mellitus (sweet urine)
A group of diseases
High glucose in urine results in HYPERglycemia  which in turn
causes polyuria (high urine output), polydispsia (great
thirst), and polyphagia (great hunger- thus eating)
Type I Diabetes
Called ‘insulin dependent’ diabetes
Cause = LOW insulin production by Islet cells
Result = glucose cannot enter cells – thus they starve
Because glucose cannot be used- the body uses fatty acids
to make ATP (energy)
Keytones – are breakdown products of fatty acids
 These molecules cause the local tissue pH to
fall  which may produce cell death
Type II Diabetes
Called ‘maturity onset’ diabetes
MOST diabetes cases in US
General cause = receptors on the surface of target cells
become LESS senstive to insulin
Treatment = facilitate receptor repair by altering food type
intake, number of meals (from 3 to 6), exercise
Gestational Diabetes
Occurs during pregnancy
Possible damage to fetus

Diabetes Insipidus
Cause = tumor or brain trauma to neurohypophysis (posterior part of
pituitary) causes HYPOsecretion of ADH (anti-diuretic hormone)
Result = large volumes of urine produced  which in turn causes
dehydration/thirst, often bedwetting in children

II. GONADS - TESTES (MALE)

* Anatomy of the seminiferous tubules
Major structural component – fills each teste
Massively coiled tube
Function = produce sperm
Layers
Tunica propria = OUTER capsule of fibroelastic tissue
[4] Inner layers of epithelial cells = primary & secondary
spermatocytes, spermatids, spermatozoa
Surround lumen
Called “germinal epithelium”
Function = to produce gametes – reproductive cells called
spermatozoa
Spermatogonia
Large cells lying against wall of seminiferous
tubule
Function = divide by meiosis to produce
spermatocytes  develop into spermatozoa
Sertoli cells
HUGE cells lying against wall of seminiferous tubule

* Sertoli cells
Histology
Many cytoplasmic extensions that form a meshwork
! Developing spermatocytes nestle within meshwork
Functions
 Supportive
Mechanically hold developing sperm on luminal & lateral surfaces
Provide nutrients to developing spermatocytes
Phagocytosis
Remove waste produced by developing spermatocytes
Consume degenerating spermatocytes
Secretion
In the Embryo
MIS (Mullerian inhibitory hormone)
Suppress formation of mullerian ducts – which in
females will later develop into the uterus &
vagina
In the Adult
ABP (Androgen binding protein)
Binds testosterone to Sertoli cell membrane
Testosterone required for sperm
development
FSH promotes ABP secretion
Inhibin
Inhibits FSH (pituitary) = feedback control for
spermatogenesis

* Interstitial (Leydig) cells

Located BETWEEN the seminiferous tubules
Often close to nerves
Function
Produces the hormone testosterone
Controls development & maintenance of male secondary sex
characteristics
Maintains structures of the entire male reproductive tract
Controls spermatogenesis
Controls sex drive
Increases cellular metabolism

III. GONADS - OVARIES (FEMALE)

* Gross anatomy of ovaries
Small, PAIRED organs located in the upper pelvic cavity – on lateral sides of
uterus
The size & shape of almonds
Suspended from body wall by several ligaments

* Functions
Produces gametes – reproductive cells called eggs or ova (singular = ovum)
Produces hormones
 Estrogen
Progesterone

* Ovarian cycle
Ova are held within follicles
Follicle = a group of cells surrounding each ovum
During each menstrual cycle- the layers of follicular cells around the
ovum proliferate
Follicle life cyle
Primordial follicle stage
Formed during fetal life
1 Layer of sqamous -or- cuboidal cells surrounding ova
Primary follicle stage
At puberty- the menstrual cycle begins
During each menstrual cycle- FSH from the adenohypophysis
stimulates follicle cells (in ovary) to proliferate
Primary follicle = when several layers of cuboidal cells surround
an ova
Theca interna
Inner layer of cells
Function = to secrete the hormone estrogen
Estrogen acts to support growth of follicles,
maintain uterine lining, support
female secondary sex
characteristics…
Secondary follicle stage
As the menstrual cycle continues- FSH continues to act – and the
primary follicle gains additional cell layers
Secondary follicle = [2] major layers now present
Theca interna
Inner layer of cells secreting estrogen
Theca externa
Ring of small compact cells around interna
Tertiary (Mature or Graffian) follicle stage
Fluid accumulates within area in follicle
Tertiary follicle = is the stage that is ready for ovulation

* Ovulation
At mid-point of monthly cycle- 1 follicle is more developed than others
The triggers…
Surge of LH - from adenohypophysis
Surge of estrogen - from theca interna cells of ovary
MAX output of estrogen - during day 14 of cycle
Ovulation takes place on day 14

Estrogen peak flow acts upon hypothalamus

 The hypothalamus SHUTS DOWN FSH (from pituitary)  which
effectively stops follicle growth
The hypothalamus INCREASES LH (from pituitary)  which
triggers ovulation & corpus luteum formation

After ovulation - the follicle undergoes series of structural changes

Corpus hemorrhagicum
Recently ovulated follicle filled with blood clot
Corpus luteum
(L. corpus =body , luteum = yellow)
A revived corpus hemorrhagicum
Certain cells are transformed and begin secreting progesterone
Main function of progesterone - act on uterine lining to
maintain it, and keep it from coming off (menses) if
pregnancy occurs
LH maintains cells within the corpus luteum

NO fertilization after ovulation

Corpus luteum of menstruation develops
Functions
Progesterone secretion
Provides negative feedback to hypothalamus
Result = LH SHUTS OFF
When LH shuts off- the corpus luteum cells die
Result = Progesterone cannot be produced-
and blood levels decline
! In effect… progesterone shuts
itself off
When progesterone levels fall- the uterine lining
comes off (menes)
Estrogen secretion
Since the corpus luteum degenerates- estrogen
production stops- thus it’s inhibition on FSH
(via the hypothalamus) is stopped- and FSH
starts flowing – which causes a new group
of follicles to begin to develop within the
ovary
Lifetime =10-14 days
! Cycle begins again

Fertilization & implantation (pregnancy) after ovulation

Corpus luteum of pregnancy
Cell layers enlarge
Secretes progesterone – until the placenta can take over
Placental hormones
Estrogen
 Progesterone
Human chorionic gonadotropin (HCG)
Human chorionic somatomammotropin (HCS)
Function = maintain uterine lining- and nourish & protect
developing fetus
At partuition
Follicle cells undergo rapid degeneration
Replaced by corpus albicans -a fibrous scar lasting months to
years

IV. PINEAL GLAND

* Gross anatomy
Flat, small gland located below posterior end of corpus callosum
Lobules of cells separated by septa
Comprised of un-myelinated nerves & blood vessels

* [2] cell types

1. Pinealocytes
MOST of the gland
Resemble neurons
Processes often extend & terminate on capillaries
Function - to produce the hormone melatonin
May aid regulation of sleep-wake patterns

2. Interstitial cells
Dispersed among clumps of pinealocytes
Forms thin capsule - sends septa into gland to form incomplete
lobules
Structural studies suggest they are a type of astrocyte

V. THYMUS
* Gross anatomy
First lymphoid organ to develop
At birth – a large (12-15g) bilobed body in superior part of chest
Lipid infiltration begins at birth
Year 2 – gland has doubled in size
Later in life – it regresses until nearly wholly replaced by adipose tissue
Lymphocytes continue to proliferate thru life - to maintain T cell supply

Capsule
Made from thin connective tissue
Septa = from capsule penetrate gland & divide it into IN-complete lobules
 Parenchyma (functional tissue)
1. Cortex = outer dark staining zone
Closely packed lymphocytes
2. Medulla = inner lighter staining zone
Fewer lymphocytes here

* Cell types
1. Epitheliocytes (epithelial-reticular cells)
!!! “Reticulum” (meshwork) of thymus gland is made up of long slender
cell processes of E-R cells
Produces the hormone thymosin
Regulates T-cell maturation and proliferation in thymus &
periphery
2. Lymphoctyes
Maturing T-cells – sometimes called thymocytes
! Few reach maturity (those that recognize foreign Ag)
Most T-cells that are anti-self - are destroyed
3. Macrophages

* Essential for life?

Thymctomized adults  little / no effect
Thymctomized newborn mice = fail to develop immunological competance  die
early from infections
Lymph nodes fail to develop  no T cell populations

* Primary site for T-lymphocyte (T-cell) production

T cells migrate from bone marrow to thymus – where they mature and proliferate
Become immuno-competent ONLY after leaving
Types
Cytotoxic (killer) T cells
Recognize antigens (virus , tumor , transplant)
Need aid from Helper-T cells to kill invader
Helper T cells
Activated by macrophages - who present them with specific
antigens they have consumed
Secrete cytokines = chemicals that stimulate T-cell proliferation &
activation
Suppressor T cells
Dampen the bodies immune response – to keep it from getting out
of control
Memory T cells
Recognize antigen it has experienced before - then quickly
produces a clone of cells in response