Growth Hormone, Growth Factor, and Growth Diseases

Question 1

How many cells in the adult human body? How many cell types?

Answer 1

Around 37 million cells of over 200 different types.

Question 2

What is the placenta? Why is it necessary for growth?

Answer 2

An endocrine organ produced during pregnancy which supplies the developing fetus with nutrients as well as endocrine molecules.

Question 3

What is the leading cause of low birth-weight infants? What else can affect fetal development?

Answer 3

Poor maternal nutrition. Drugs, illness, smoking, and fitness can also affect growth and mental development.

Question 4

What long-term repercussions result from an infant having low birth-weight?

Answer 4

Greater odds for that child (if female) to give birth to another low birth-weight child. Low birth-weight is also associated with chronic diseases like obesity.

Question 5

At what 5 stages of development do humans experience accelerated growth?

Answer 5

1. Fetus
2. Immediately after birth
3. Two years olf
4. Seven years old
5. Puberty

Question 6

What nutrient during childhood has the most impact on final adult height? What other nutrients can affect height?

Answer 6

Protein is the greatest determiner, but minerals (ex: calcium) and vitamins A and D also play a role.

Question 7

Is vitamin D a true vitamin? Why? Why not?

Answer 7

No, it’s actually a hormone which binds to nuclear receptors and alters transcription of many cellular processes.

Question 8

Why is breast milk considered the best source of nutrition for infants?

Answer 8

Any amount of breast milk can induce changes in DNA methylation which is thought to improve development.

Question 9

What condition results from having too much growth hormone (AFTER PUBERTY)? Describe.

Answer 9

Acromegaly. High growth hormone causes high insulin-like growth factor 1 which stimulates the proliferation of bone, cartilage, and soft tissue.

Question 10

How can acromegaly be treated?

Answer 10

Using growth hormone receptor antagonists can block its growth stimulating effects.

Question 11

What characteristics develop as someone with acromegaly ages?

Answer 11

Size of nose, lips, and skin folds keep increasing throughout their life because of excess growth hormone production.

Question 12

What is gigantism? At what stage of human development does it occur? How can this be caused?

Answer 12

A condition which occurs before puberty involving excessive growth due to high levels of growth hormone. Possibly due to somatotroph-releasing tumours.

Question 13

What causes Laron’s dwarfism?

Answer 13

Caused by growth hormone receptor defect or insulin-like growth factor 1 defect.

Question 14

How come some kids are just shorter than normal?

Answer 14

“Normal short kids” may just have low growth hormone binding protein.

Question 15

How can ectopic tissue cause acromegaly or gigantism?

Answer 15

Tumour in a tissue (with GH receptors) other than the anterior pituitary causing upregulation of growth hormone.

Question 16

What factors contribute to psychosocial dwarfism?

Answer 16

Environmental factors during development can cause reduced growth (can be social, nutritional, or even altitude).

Question 17

How was growth hormone replacement therapy used to treat undersized children and aids? What issue arose? How was this problem solved?

Answer 17

Took GH from cadavers, but led to Creutzfeld-Jakob disease (prions in the brain, cause brain holes). Solved by creating human GH in mice and taking that instead.

Question 18

How do growth factors stimulate growth?

Answer 18

Have mitogenic properties and stimulate growth via proliferation and/or differentiation.

Question 19

What are proto-oncogenes? What can they become?

Answer 19

A category of genes with either replicative or apoptotic function that when mutated become cancer-causing oncogenes.

Question 20

What occurs in nerve cells which stop being stimulated?

Answer 20

The cells die.

Question 21

What 5 important growth factors make use of cytokine receptors?

Answer 21

1. Growth hormone
2. Erythropoietin (RBCs)
3. Cytokines (immune fxn.)
4. Colony stimulating factors (WBCs)
5. Transforming growth factor beta

Question 22

How is tyrosine kinase associated with growth HORMONE cytokine receptors?

Answer 22

Cytokine receptors recruit accessory proteins which have tyrosine kinase domains.

Question 23

How is tyrosine kinase associated with growth FACTOR receptors?

Answer 23

The receptor has its own associated tyrosine kinase domain which phosphorylates other proteins.

Question 24

What 6 main growth factors which use growth factor receptors were discussed in class?

Answer 24

1. Insulin-like growth factor 1
2. Insulin-like growth factor 2
3. Insulin
4. Epidermal growth factor
5. Nerve growth factor
6. Platelet derived growth factor

Question 25

How does insulin-like growth factor 1 affect child development?

Answer 25

Responsible for protein synthesis a well as cell proliferation. Acts on growth hormone by negative feedback.

Question 26

How does insulin-like growth factor 2 affect the developing fetus?

Answer 26

Fetal growth hormone (esp. liver), mediates growth hormone effects.

Question 27

How does insulin act as a growth factor for a developing fetus?

Answer 27

Important for carbohydrate metabolism but also fetal growth.

Question 28

What effect does epidermal growth factor have on the developing fetus? How can it be affected by a mother who smokes during pregnancy?

Answer 28

Primes the fetal gut to absorb nutrients, also plays a role in fetal growth. Cause of low birth-weight and delayed growth for children of smoking mothers.

Question 29

What function does nerve growth factor serve in the body?

Answer 29

Promotes growth and maintenance of sympathetic NS and some sensory neurons.

Question 30

What is the biological purpose of platelet derived growth factor?

Answer 30

Stimulates wound healing. Allows damaged cells to respond to insulin-like growth factor 1.

Question 31

What 6 main steps outline the function of growth factor receptors?

Answer 31

1. Dimerization upon ligand binding 2. Autophosphorylation 3. Recruit accessory proteins 4. Recruited proteins phosphorylate 5. Signalling complex forms 6. Intended effect (cell division, etc.)

Question 32

When growth factor receptors autophosphorylate, what residues are recognized by SH2 domains on accessory proteins?

Answer 32

Phosphorylated tyrosine residues (in certain contexts).

Question 33

After growth factor receptors autophosphorylate, what is recognized by SH3 domains on accessory proteins?

Answer 33

Proline-rich areas, usually on other accessory proteins which have already been recruited.

Question 34

What is an Src?

Answer 34

A proto-oncogenic tyrosine kinase.

Question 35

What are 4 examples of phosphorylation cascades?

Answer 35

1. MAPK 2. PI3K 3. PKB 4. Ras/ERK

Question 36

What is RAS?

Answer 36

Rat sarcoma, a small G protein. Also a common oncogene.

Question 37

What is growth factor receptor bound protein 2 (GRB2)? What is it's function?

Answer 37

It is a protein which contains both SH2 and SH3 domains (like growth factor receptor accessory proteins).

Question 38

What disease is associated with an excess of growth factor? How can this disease promote itself (positive feedback regulation)?

Answer 38

Cancer. Tumours can cause increased growth factor secretion.

Question 39

What disease is associated with a lack of growth factor?

Answer 39

Failure to grow/thrive. Apoptosis.

Question 40

What condition is caused by an overabundance of insulin-like growth factor 1? How does it relate to growth hormone?

Answer 40

Acromegaly. IGF-1 levels directly reflect GH levels. High growth hormone levels increase the levels of insulin-like growth factor 1.

Question 41

How does Rous sarcoma virus affect cell growth? What is it?

Answer 41

A retrovirus (acts as a viral mimic) which can cause cancer (an oncovirus). Reverse transcribes its RNA into cDNA then integrates into the host DNA.

Question 42

What is v-src? How does it affect the cell?

Answer 42

An active kinase inserted into a cell by a virus that mimics regular src (c-src, proto-oncogene) tyrosine kinase but can't be regulated (oncogene).