1. The Endocrine System

2. Hypophyseal-Pituitary Axis
Site of Neural – Hormonal interaction
Sets temporal release of hormones
Responsible for stress reaction of hormones

3. The Hypothalamus & the Pituitary Gland-- Master Endocrine Glands!
Located in the brain, this region controls most endocrine secretions
Mainly regulatory hormones are released here. Most control the pituitary gland
The Pituitary Gland
Descending from the hypothalamus, this gland has two halves: anterior & posterior
The anterior half secretes mainly regulatory hormones
The posterior half secretes hormones, but manufactures none

4. Hormones secreted by the Hypothalamus & Anterior Pituitary Gland
GHRH (GH-releasing) GH (growth hormone)
SS (somatostatin, GH-inhib) “
CRH (corticotropin-rel) ACTH (adrenocorticotropic)
GnRH (gonadotropin-rel) LH (luteinizing hormone)
“ FSH (follicle-stimulating)
PRH (PRL-releasing) PRL (prolactin)
PIH (PRL rel-inhibiting) “
TRH (thyrotropin-rel) TSH (thyroid stimulating)        

5. What do these anterior pituitary hormones do?
Growth Hormone:
stimulates cells to grow and divide
increases amino acid transport rate and protein synthesis
increases fat metabolism
Typically, GH is secreted during sleep.
GH secretion increases when malnourished
GH influences bone growth via somatomedin:
GH in blood
GH arrives in liver
liver secretes somatomedin
cartilage divides
bones grow!

6. Problems with GH Too much GH in children leads to gigantism
Too much GH in adults leads to acromegaly
Too little GH in children leads to dwarfism

7. Other Anterior Pituitary Hormone Functions
ACTH:
works on the cortex of the adrenal gland, influencing the release of cortisol
stress can increase CRH secretion which will increase ACTH secretion
negative feedback when adrenal cortex hormones in blood decrease CRH secretion
LH & FSH:
LH in females and in males leads to sex hormone secretion
FSH in females causes growth and development of egg cell-containing follicles in the ovary, and causes estrogen secretion
FSH in males instigates sperm production
both hormones are regulated by GnRH, which is not significant in concentration until puberty

8. More Anterior Pituitary Hormone Functions
PRL:
In females, PRL promotes lactation
In males, PRL decreases LH secretion (note that too much PRL would then decrease androgen levels and cause sterility)
Controlled by both PRH and PIH
TSH:
works on thyroid gland to either cause or inhibit its secretion of hormones
works on thyroid gland to affect its growth (too much TSH leads to a goiter)
negative feedback via thyroid hormones in blood
stress or cold temperatures can change TSH secretion

9. The Posterior Pituitary Lobe
No hormones are made here. They are made in the hypothalamus and just released here.
Two peptide hormones are released from the posterior pituitary lobe (the neurohypophysis):
ADH (antidiuretic hormone or vasopressin)
OT (oxytocin)

10. Function of Posterior Pituitary Lobe Hormones
ADH:
as an “antidiuretic,” ADH decreases urine formation by having kidneys conserve water
also can contract smooth muscle cells, as found in blood vessels-- this causes an increase in blood pressure
ADH release triggered by osmoreceptors and inhibited by stretch receptors in blood vessels
OT:
In females, contracts the uterine wall smooth muscles
In females, helps to eject milk when lactating
No known function in males, although in both males and females, OT can have some antidiuretic effects

11. Hypothalamus & Anterior Pituitary
GHRH (GH-releasing) GH (growth hormone)
SS (somatostatin, GH-inhib) “
CRH (corticotropin-rel) ACTH (adrenocorticotropic)
GnRH (gonadotropin-rel) LH (luteinizing hormone)
“ FSH (follicle-stimulating)
PRH (PRL-releasing) PRL (prolactin)
PIH (PRL rel-inhibiting) “
TRH (thyrotropin-rel) TSH (thyroid stimulating)

12. Your book’s review diagram:

13. HPA Basics Hypophysis Neurohypophysis Adenohypophysis Third Ventricle
GRH, TRH, CRH, GnRH, Dopamine, Somatostatin
Neurohypophysis
Derived from Hypophysis
ADH, Oxytocin
Adenohypophysis
Derived from Rathke’s pouch
ACTH, LH, FSH, TSH, GH, PRL

16. Pituitary Diseases Primary Tumors Metastasis Empty Sella Hemorrhage
Adenomas
Craniopharyngioma
Metastasis
Empty Sella
Surgical, post-Sheehand’s
Hemorrhage
Sheehand’s syndrome
Hyperfunction
Prolactin
Insufficiency

17. The Endocrine Glands and Their Hormones
Pituitary Gland
A marble-sized gland at the base of the brain
Controlled by the hypothalamus or other neural mechanisms and therefore the middle man.
Posterior Lobe
Antidiuretic hormone: responsible for fluid retention
Oxytocin: contraction of the uterus

18. The Endocrine Glands and their Hormones
Pituitary Gland
Exercise appears to be a strong stimulant to the hypothalamus for the release of all anterior pituitary hormones
Anterior Lobe
Adrenocorticotropin
Growth hormone *
Thyropin
Follicle-stimulating hormone
Luteinizing hormone *
Prolactin

19. The Endocrine Glands and Their Hormones
Thyroid Gland
Located along the midline of the neck
Secretes two nonsteroid hormones
Triiodothyronine (T3)
Thyroxine (T4)
Regulates metabolism
increases protein synthesis
promotes glycolysis, gluconeogenesis, glucose uptake
Calcitonin: calcium metabolism

20. Thyroid

22. Thyroid Largest Endocrine organ in the body
Involved in production, storage, and release of thyroid hormone
Function influenced by
Central axis (TRH)
Pituitary function (TSH)
Comorbid diseases (Cirrhosis, Graves, etc.)
Environmental factors (iodine intake)

23. The Thyroid Gland
Structure: This bilobed gland contains many follicles. A follicle is a group of cells encircling a lumen. The lumen contains material called colloid (a glycoprotein) within it. As hormones are produced by the cells, the hormones are either released into the colloid or directly into the blood.
There are also extrafollicular hormone-secreting cells, called C cells. These are found between lumina.
Hormones Produced:
Thyroxine (T4) made in follicle
Triiodotyronine (T3) made in follicle
Calcitonin made by C cells

24. About the Thyroid Hormones...
T3 and T4:
Function: metabolism regulation (break down carbohydrates and fats, synthesize proteins)
Can only be made by follicular cells when iodides are available
Somewhat hydrophobic and get carried by proteins in the blood.
Controlled by anterior pituitary lobe TSH
T3 more effective, T4 more abundant
Calcitonin:
Function: decrease blood calcium levels and blood phosphate levels (by helping them get deposited in bone, and by stimulating excretion of them by kidneys)
Controlled by blood calcium levels and digestive chemicals
T4 and T3 are very similar molecules… T4 is also called thyroxine; it contains 4 iodine atoms in it. T3 (triiodothyronine)only has 3 iodine atoms in it. Iodine is not commonly found in our bodies within molecules. Iodine atoms tend to make ionic, not covalent, bonds in aqueous solutions. That’s why it may seem new to you to find this element in thyroxine and triiodothyronine.
Because we don’t need a lot of iodine in our bodies, when we do get it, we need to use it to make these hormones. If we don’t get iodine in our diets, we simply can’t make these hormones.
The salt we put on food has the chemical formula: NaCl. It used to be that this salt was sold in its pure form in stores. Also, some people were deficient in iodine in their diets, and health problems were discovered in those people. But now we can buy “iodized salt” in the supermarket. Iodized salt has some iodide ions in it (instead of some of the Cl ions). Ever since manufacturers started including iodide ions in our salt, people have been able to get their required levels of iodine in their diets.

25. Problems with the Thyroid Gland
Hyperthyroidism:
high metabolic rate, hyperactivity, sensitivity to heat, protruding eyes
Grave’s disease: when hyperthyroidism is due to an autoimmune problem (TSH is mimicked by autoantibodies)
Hypothyroidism:
in the adult: low metabolic rate, sensitivity to cold, sluggishness
in an infant: cretinism-- stunted growth, mental retardation, abnormal bone formation
Hashimoto’s disease: when hypothyroidism is due to an autoimmune problem (autoantibodies attack and destroy follicular cells)
goiter: no T3 and T4 can be made because not enough iodides were ingested.
On this slide, some serious thyroid gland problems are described. There are other problems that people have with their thyroid glands that are not as severe…
Some people have slight problems with their thyroid gland. If that problem causes too much thyroid hormone secretion, that person is said to have slight hyperthyroidism, and has increased metabolism. More often we hear of cases of slight hypothyroidism, where a person’s thyroid gland does not produce enough thyroid hormone… this causes a decreased metabolism, and often weight gain. People with slight hypothyroidism can usually take thyroid hormone as a medication to compensate for their naturally-occurring low levels.

26. Thyroid (cont) Regulates basal metabolic rate
Improves cardiac contractility
Increases the gain of catecholamines
Increases bowel motility
Increases speed of muscle contraction
Decreases cholesterol (LDL)
Required for proper fetal neural growth

27. Thyroid Physiology Uptake of Iodine by thyroid
Coupling of Iodine to Thyroglobulin
Storage of MIT / DIT in follicular space
Re-absorption of MIT / DIT
Formation of T3, T4 from MIT / DIT
Release of T3, T4 into serum
Breakdown of T3, T4 with release of Iodine

28. Iodine uptake Na+/I- symport protein controls serum I- uptake
Based on Na+/K+ antiport potential
Stimulated by TSH
Inhibited by Perchlorate

29. Secretion of Thyroid Hormone
Stimulated by TSH
Endocytosis of colloid on apical membrane
Coupling of MIT & DIT residues
Catalyzed by TPO
MIT + DIT = T3
DIT + DIT = T4
Hydrolysis of Thyroglobulin
Release of T3, T4
Release inhibited by Lithium

30. Thyroid Hormones

31. Thyroid Hormone Majority of circulating hormone is T4
Total Hormone load is influenced by serum binding proteins (TBP, Albumin, ??)
Thyroid Binding Globulin 70%
Albumin 15%
Transthyretin 10%
Regulation is based on the free component of thyroid hormone

32. Hormone Binding Factors
Increased TBG
High estrogen states (pregnancy, OCP, HRT, Tamoxifen)
Liver disease (early)
Decreased TBG
Androgens or anabolic steroids
Liver disease (late)
Binding Site Competition
NSAID’s
Furosemide IV
Anticonvulsants (Phenytoin, Carbamazepine)

33. Hormone Degredation T4 is converted to T3 (active) by 5’ deiodinase
T4 can be converted to rT3 (inactive) by 5 deiodinase
T3 is converted to rT2 (inactive)by 5 deiodinase
rT3 is inactive but measured by serum tests

34. Thyroid Hormone Control

35. TRH Produced by Hypothalamus Release is pulsatile, circadian
Downregulated by T4, T3
Travels through portal venous system to adenohypophysis
Stimulates TSH formation

36. TSH Produced by Adenohypophysis Thyrotrophs Upregulated by TRH
Downregulated by T4, T3
Travels through portal venous system to cavernous sinus, body.
Stimulates several processes
Iodine uptake
Colloid endocytosis
Growth of thyroid gland

37. TSH Response

38. Iodine states
Normal Thyroid
Inactive Thyroid
Hyperactive Thyroid

39. Hypothyroid
Symptoms – fatigability, coldness, weight gain, constipation, low voice
Signs – Cool skin, dry skin, swelling of face/hands/legs, slow reflexes, myxedema
Newborn – Retardation, short stature, swelling of face/hands, possible deafness
Types of Hypothyroidism
Primary – Thyroid gland failure
Secondary – Pituitary failure
Tertiary – Hypothalamic failure
Peripheral resistance

40. Hypothyroid Cause is determined by geography Diagnosis Treatment
Low FT4, High TSH (Primary, check for antibodies)
Low FT4, Low TSH (Secondary or Tertiary, TRH stimulation test, MRI)
Treatment
Levothyroxine (T4) due to longer half life
Treatment prevents bone loss, cardiomyopathy, myxedema

41. Goiter Endemic goiter Goiter in developed countries Other causes
Caused by dietary deficiency of Iodide
Increased TSH stimulates gland growth
Also results in cretinism
Goiter in developed countries
Hashimoto’s thryoiditis
Subacute thyroiditis
Other causes
Excess Iodide (Amiodarone, Kelp, Lithium)
Adenoma, Malignancy
Genetic / Familial hormone synthesis defects

42. Hyperthyroid
Symptoms – Palpitations, nervousness, fatigue, diarrhea, sweating, heat intolerance
Signs – Thyroid enlargement (?), tremor
Lab workup
TSH
FT4
RAIU
Other Labs
Anti-TSH-R Ab, Anti-TPO Ab, Anti-TBG Ab
FT3
FNA
MRI, US

43. Hyperthyroid Common Causes Rare Causes *Graves Adenoma
Multinodular Goiter
*Subacute Thyroiditis
*Hashimoto’s Thyroiditis
Rare Causes
Thyrotoxicosis factitia, struma ovarii, thyroid metastasis, TSH-secreting tumor, hamburger

46. The Endocrine Glands Parathyroid Glands Secretes parathyroid hormone
regulates plasma calcium (osteoclast activity)
regulates phosphate levels

47. Calcium Regulation
Parathyroid

48. Calcium
Required for muscle contraction, intracellular messenger systems, cardiac repolarization.
Exists in free and bound states
Albumin (40% total calcium)
Phosphate and Citrate (10% total calcium)
Concentration of iCa++ mediated by
Parathyroid gland
Parafollicular C cells
Kidney
Bone

49. Parathyroid Gland
This gland only secretes one hormone: Parathyroid Hormone (or PTH)
PTH function (we began learning this when we studied bone):
increases blood calcium (Ca2+) levels and decreases blood phosphate (PO42-) levels

50. PTH function (continued)
How does PTH work?
PTH causes Ca2+ & PO42- to be released from bone into blood (by increasing osteoclast activity)
PTH causes the kidneys to remove PO42- ions from the urine
PTH increases vitamin D production, so that you absorb more Ca2+ during digestion
PTH is regulated by blood calcium levels-- not by other glands!

51. Parathyroid Hormone Produced by Parathyroid Chief cells
Secreted in response to low iCa++
Stimulates renal conversion of 25-(OH)D3 to 1,25-(OH)2D which increases intestinal Ca++ absorption
Directly stimulates renal Ca++ absorption and PO43- excretion
Stimulates osteoclastic resorption of bone

52. Calcitonin
Produced by Parafollicular C cells of Thyroid in response to increased iCa++
Actions
Inhibit osteoclastic resorption of bone
Increase renal Ca++ and PO43- excretion
Non-essential hormone. Patients with total thyroidectomy maintain normal Ca++ concentrations
Useful in monitoring treatment of Medullary Thyroid cancer
Used in treatment of Pagets’, Osteoporosis

53. Vitamin D Sources Metabolism Function Food – Vitamin D2
UV light mediated cholesterol metabolism – D3
Metabolism
D2 and D3 are converted to 25(OH)-D by the liver
25(OH)-D is converted to 1,25(OH)2-D by the Kidney
Function
Stimulation of Osteoblasts
Increases GI absorption of dietary Ca++

54. Hypocalcemia Decreased PTH Resistance to PTH Vitamin D abnormalities
Surgery
Hypomagnesemia
Idiopathic
Resistance to PTH
Genetic disorders
Bisphosphonates
Vitamin D abnormalities
Vitamin D deficiency
Rickets (VDR or Renal hyroxylase abnormalities)
Binding of Calcium
Hyperphosphate states (Crush injury, Tumor lysis, etc.)
Blood Transfusion (Citrate)

55. Hypercalcemia Hyperparathyroidism Malignancy Granulomatous Diseases
Primary, Secondary, Tertiary
MEN Syndromes
Malignancy
Humoral Hypercalcemia
PTHrP (Lung Cancer)
Osteoclastic activity (Myeloma, Lymphoma)
Granulomatous Diseases
Overproduction of 1,25 (OH)2D
Drug-Induced
Thiazides
Lithium
Milk-Alkali
Vitamin A, D
Renal failure

56. Hypercalcemia Signs & Symptoms Medical Treatment Surgical Treatment
Bones (Osteitis fibrosa cystica, osteoporosis, rickets)
Stones (Renal stones)
Groans (Constipation, peptic ulcer)
Moans (Lethargy, depression, confusion)
Medical Treatment
SERM’s (Evista)
Bisphosphonates (Pamidronate)
Calcitonin (for severe cases)
Saline diuresis
Glucocorticoids (for malignant/granulomatous diseases)
Avoid thiazide diuretics
Surgical Treatment
Single vs. Double adenoma – simple excision
Multiple Gland hyperplasia – total parathyroid with autotransplant vs ½ gland excision

57. Primary Hyperparathyroidism
Diagnosis
Signs & Symptoms
Elevated serum calcium
Elevated PTH
Etiology
Solitary Adenoma (80-85%)
Double Adenomas (2-4%)
Muliple Gland Hyperplasia (10-30%)
Parathyroid Carcinoma (0.5%)
MEN syndromes (10% of MGH have MEN 1)

58. Parathyroidectomy 1990 NIH Guidelines Other considerations
Serum Ca++ > 12 mg/dl
Hypercalciuria > 400 mg/day
Classic symptoms
Nephrolithiasis
Osteitis fibrosa cystica
Neuromuscular disease
Cortical bone loss with DEXA Z score < -2
Reduced creatinine clearance
Age < 50
Other considerations
Vertebral osteopenia
Vitamin D deficency
Perimenopause

59. The Endocrine Glands Adrenal Medulla
Situated directly atop each kidney and stimulated by the sympathetic nervous system
Secretes the catecholamines
Epinephrine: elicits a fight or flight response
Increase H.R. and B.P.
Increase respiration
Increase metabolic rate
Increase glycogenolysis
Vasodilation
Norepinephrine
House keeping system

60. The Endocrine Glands Adrenal Cortex
Secretes over 30 different steroid hormones (corticosteroids)
Mineralocorticoids
Aldosterone: maintains electrolyte balance
Glucocorticoids
Cortisol:
Stimulates gluconeogenisis
Mobilization of free fatty acids
Glucose sparing
Anti-inflammatory agent
Gonadocorticoids
testosterone, estrogen, progesterone

61. The Endocrine Glands Pancrease: Located slightly behind the stomach
Insulin: reduces blood glucose
Facilitates glucose transport into the cells
Promotes glycogenesis
Inhibits gluconeogensis
Glucagon: increases blood glucose

62. The Endocrine Glands Gonads Kidneys (erythropoietin)
testes (testosterone) = sex characteristics
muscle development and maturity
ovaries (estrogen) = sex characteristics
maturity and coordination
Kidneys (erythropoietin)
regulates red blood cell production

63. The Endocrine Response to Exercise
Table 5.3 Page 172

64. Regulation of Glucose Metabolism During Exercise
Glucagon secretion increases during exercise to promote liver glycogen breakdown (glycogenolysis)
Epinephrine and Norepinephrine further increase glycogenolysis
Cortisol levels also increase during exercise for protein catabolism for later gluconeogenesis.
Growth Hormone mobilizes free fatty acids
Thyroxine promotes glucose catabolism

65. Regulation of Glucose Metabolism During Exercise
As intensity of exercise increases, so does the rate of catecholamine release for glycogenolysis
During endurance events the rate of glucose release very closely matches the muscles need (fig 5.9, pg. 174)
When glucose levels become depleted, glucagon and cortisol levels rise significantly to enhance gluconeogenesis.

66. Regulation of Glucose Metabolism During Exercise
Glucose must not only be delivered to the cells, it must also be taken up by them. That job relies on insulin.
Exercise may enhance insulin’s binding to receptors on the muscle fiber.
Up-regulation (receptors) occurs with insulin after 4 weeks of exercise to increase its sensitivity (diabetic importance).

67. Regulation of Fat Metabolism During Exercise
When low plasma glucose levels occur, the catecholamines are released to accelerate lypolysis.
Triglycerides are reduced to free fatty acids by lipase which is activated by: (fig. 5.11, pg. 176)
Cortisol
Epinephrine
Norepinephrine
Growth Hormone

68. Hormonal Effects on Fluid and Electrolyte Balance
Reduced plasma volume leads to release of aldosterone which increases Na+ and H2O reabsorption by the kidneys and renal tubes.
Antidiuretic Hormone (ADH) is released from the posterior pituitary when dehydration is sensed by osmoreceptors, and water is then reabsorbed by the kidneys.

69. Adrenal Glands
An adrenal gland is found on top of each kidney. Each adrenal gland has two regions that carry out separate functions!
The adrenal medulla
The adrenal cortex
We will cover each of these two regions separately in the next few slides.

70. The Adrenal Medulla
Acts very much like a part of the sympathetic nervous system (fight or flight)
Secretes two amines:
norepinephrine (20%)
epinephrine (80%)
Stimulated by preganglionic neurons directly, so controlled by the hypothalamus as if part of the autonomic nervous system, NOT by tropic hormones

71. The Adrenal Cortex Acts like a regular endocrine organ
Secretes many hormones, but most importantly secretes the following steroids:
aldosterone
cortisol
sex hormones
Aldosterone and cortisol require further explanation (while sex hormone production will be covered later this semester)

72. More about Adrenal Cortex Hormones
Aldosterone:
Considered a mineralocorticoid
Regulates “mineral electrolyte” levels in the blood (for example: Na+ and K+ ions)
How is aldosterone controlled?
blood plasma ion concentrations affect its secretion directly (but not always strongly)
kidney secretes renin in response to altered electrolyte levels, which triggers angiotensin activation in the blood, which leads to aldosterone secretion
ACTH from the anterior pituitary can cause aldosterone secretion
Cortisol:
Considered a glucocorticoid
Overall effect of cortisol:
Helps to keep blood glucose concentration within a normal range between meals
Specific actions of cortisol:
increases amino acid concentration in the blood (by inhibiting protein synthesis in select tissues)
promotes use of fat for energy production in our bodies (rather than glucose)
stimulates the liver to synthesize glucose (not from carbohydrates, but from amino acids and glycerol), called gluconeogenesis
This slide mentions the terms “mineralocorticoid” and “glucocorticoid.” What do these terms mean? Well,they sound and look long and complicated, but they really are not.
A “corticoid” is any hormone made in the CORTEX of the adrenal gland. That should seem straightforward.
The mineralo- and gluco- parts simply reflect what they do. A mineralocorticoid is a hormone that is made in the adrenal cortex that regulates the levels of specific minerals in the blood. A glucocorticoid is a hormone that is made in the adrenal cortex that regulates glucose levels in the blood.
It’s that simple.

73. The Pancreas
This gland has both endocrine and exocrine functions… we’ll only cover the endocrine portion now (exocrine is for digestion)
The endocrine portion of the gland contains three types of cells, each making a different hormone, arranged into groups called Islets of Langerhans
alpha cells: secrete glucagon
beta cells: secrete insulin
delta cells: secrete SS (somatostatin)
Note that these pancreatic hormones are involved in blood glucose regulation, and problems with them can lead to diabetes.
In this slide, the term “endocrine” is compared with “exocrine.” You learned these terms way back in A&P1, when we studied tissues. Back then, you learned these terms in reference to glands in epithelial tissues.
Endocrine glands secrete their hormones into the blood. Exocrine glands secrete their substances into ducts.
We learned about some exocrine glands when we learned about sweat and sebaceous glands in the skin. Now, in this chapter, we are learning about endocrine glands. Endocrine glands affect the tissues in a body by travelling throughout the body in blood.
The pancreas secretes some hormones into the blood. These are hormones that are very important in regulating our blood glucose levels. The pancreas also secretes chemicals into a duct that feeds into our digestive tract to assist in digestive functions. This exocrine function has its effect in a much more regionally-restricted manner.

74. Blood Glucose Regulation by the Pancreas
Glucagon:
It works on the liver to cause the production of glucose via:
glycogenolysis
gluconeogenesis
It is regulated by blood glucose levels directly:
secreted when blood glucose drops (before next meal)
Prevents hypoglycemia
Insulin:
It works on the liver to remove glucose from the blood via:
making glycogen
preventing gluconeogenesis
increasing glucose transport into cells
It is also regulated by blood glucose levels directly
Prevents hyperglycemia
Note: glucagon and insulin work in opposition, and their combined effects control blood glucose

75. Pineal Gland Secretes only one hormone: melatonin
Involved in your circadian rhythm (your recognition of day and night times):
melatonin secretion decreases in the day
melatonin secretion increases at night
Melatonin is also involved in longer rhythms, like monthly and seasonal… and is thought to be involved in the female menstrual cycle and maybe in the onset of puberty

76. Other Endocrine Glands
Thymus Gland: secretes thymosins which are involved in white blood cell production
Reproductive glands (the gonads): the ovaries and the testes produce sex hormones
Others: too specific for now, we’ll get to them as we continue this semester.
The gonads (reproductive glands) are quite complicated. They do have an important endocrine role, but we cannot delve into that in this unit. You will learn all about their role when we do the reproductive system!