Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
68 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Where are somatotropes located?
|
Anterior pituitary
|
|
|
|
What produces growth hormone?
|
Somatotropes
|
|
|
|
Growth hormone stimulates the production of what in the liver?
|
Insulin-like Growth Factor (IGF-1)
|
|
|
|
T/F
GH has direct physiological actions on non-endocrine organs. |
True!
|
|
|
|
Growth hormone causes growth of almost all tissues of the body that are capable of growing via what 4 general processes?
|
Increased size of cells
Increased mitosis Increased number of cells Specific differentiation |
|
|
|
Growth hormone is a 191 amino acid protein similar to what 2 hormones, with some overlap in activity?
|
prolactin and human placental lactogen
|
|
|
|
What signaling pathway is GH linked to?
|
JAK/STAT
|
|
|
|
a) GH binds to what to increase its biological half life?
b) What percentage of GH is bound to the extracellular domain of this GH receptor? c) How does this increase its half-life? d) What is the half life of circulating GH? |
a) GH-binding protein (GHBP)
b) 50% c) By making it less available for degradation by liver and kidney d) about 20 minutes |
|
|
|
What individuals lack normal GH receptors but have normal GH secretion?
|
Laron Dwarfs
|
|
|
|
T/F
Laron dwarfs have detectable levels of binding protein in their serum. |
False!
They do NOT have detectable levels of binding protein in their serum. |
|
|
|
Release of GH from somatotropes is predominately stimulated by what?
|
GHRH from the Hypothalamus
|
|
|
|
Synthesis and release of GH from somatotropes is inhibited by what?
|
Hypothalamus via somatostatin.
Somatostatin is also found in other areas of the body. |
|
|
|
What is the primary negative feedback of GH?
|
IGF-1 (long feedback loop)
|
|
|
|
What is the short negative feedback loop on GH?
|
GH itself exerts negative feedback
|
|
|
|
How does IGF-1 indirectly inhibit GH release? (2 ways)
|
1. By increasing secretion of somatostatin from nuclei in the periventricular region of the hypothalamus.
2. By suppressing GHRH release from the arcuate nucleus in the hypothalamus. |
|
|
|
When is GH primarily released?
|
During slow wave sleep
|
|
|
|
T/F
Serum GH levels are useful even if the exact sampling time is unknown. |
False!
Serum GH values NOT useful unless exact sampling time is know. |
|
|
|
What is a better indicator than GH levels?
Why? |
IGF-1 levels
Because its secretion is regulated by GH, and it has a longer circulating half-life than buffers pulsatile and diurnal changes in secretion. |
|
|
|
GH acts directly on which types of tissue to regulate metabolism?
|
Liver, muscle and adipose
|
|
|
|
T/F
The overall goal of GH is to shift metabolism to carbohydrate use to conserve lipid and protein use. |
False!
Overall goal to shift metabolism to lipid use to conserve carbohydrate and protein. |
|
|
|
What are the 3 general metabolic effects of GH?
|
1. GH is a protein anabolic hormone
GH is a lipolytic hormone: Activates hormone sensitive lipase and mobilizes neutral frats from adipose results 3. GH alters carbohydrate metabolism. Bottom line: GH enhances body protein, reduces fat stores and conserves carbohydrate. |
|
|
|
Which of the following is NOT a protein anabolic property of GH?
a) Enhanced amino acid transport through the cell membrane b) Enhanced RNA translation to cause protein synthesis by ribosomes c) Increased nuclear transcription of DNA to from RNA d) Increased proteolysis |
d - GH actually decreases proteolysis
|
|
|
|
Lipolysis caused by GH activates hormone sensitive lipase and mobilizes neutral fats. What is the effect in adipose tissue, blood, liver and skeletal muscle?
|
Increased mobilization of FAs from adipose tissue
Increased FFAs in blood Increased uptake and use of FAs in skeletal muscle and liver |
|
|
|
Decreased glucose uptake in tissues (which is secondary to the increases in serum FFA) coupled with increased glucose production by the liver can lead to what state in the blood?
|
Hyperglycemic effects
Increased insulin secretion |
|
|
|
The increase in FFA oxidation in liver increases liver a)_________ and stimulates b)____________ and glucose production from c)________ and d)__________.
|
a) Acetyl-CoA
b) gluconeogenesis c) lactate d) glycerol |
|
|
|
What hormone in skeletal muscle and adipose is anatagonized by GH?
|
Insulin
|
|
|
|
a) Excess GH secretion can lead to what condition?
b) What cells become damaged? |
a) Diabetes Mellitus
Insulin levels necessary to maintain normal glucose levels increases b) This damages pancreatic b cells. |
|
|
|
The following indirect actions of GH lead to what overall effect?
Increases deposition of protein by chondrocytic and osteogenic cells Increases rate of reproduction of these cells Increases rate of conversion of chondrocytes into osteogenic cells |
Increases growth of skeletal frame
|
|
|
|
Where do long bones grow in length?
|
At the epiphyseal cartilage
|
|
|
|
T/F
Osteoclasts remove old bone. |
True!
OsteoBlasts - Build bone! OsteoClasts - Crush bone! |
|
|
|
Which is strongly stimulated by GH, osteoclasts or osteoblasts?
|
Osteoblasts
|
|
|
|
GH fails to cause growth of the skeletal frame without what 2 things?
|
Insulin and carbohydrates that are needed for energy and enhanced AA and glucose transport
|
|
|
|
Many GH actions are mediated by a group of proteins called:
|
Somatomedins
|
|
|
|
Name the principle somatomedin.
|
The principle somatomedin is Insulin-Like Growth Factor I (IGF-1) or Somatomedin C
|
|
|
|
How does IGF-1 act on target cells? (ex: chondrocytes and osteocytes)
|
Like GH, IGF-1 acts on target cells (e.g. chondrocytes and osteocytes) via membrane tyrosine kinase receptors.
|
|
|
|
T/F
Somatomedins are structurally similar to insulin and posses strong insulin-like functional activities |
False!
Somatomedins are structurally similar to insulin, but possess only weak insulin-like functional activities |
|
|
|
Besides the liver, where else is circulating IGF-1 secreted when stimulated by GH?
|
It is also secreted in cartilage, bone, & muscle
|
|
|
|
When does IGF-1 act as an autocrine or paracrine agent?
|
When it is secreted in cartilage, bone and muscle (not liver)
|
|
|
|
What is IGF bound to when being transported in serum?
What does IGF associate with after this? |
IGF binding protein (IGFBP)
Acid labile subunit (ALS) |
|
|
|
Production of IGF, IGFBP and ALS are all stimulated by what hormone?
|
GH
|
|
|
|
IGFBP/ALS/IGF-1 complex mediates ___________ and _____________ of IGF-1.
|
transport and bioavailability
|
|
|
|
What is the effect of IGFBP on IGF action and half-life?
|
IGFBP usually inhibits IGF action but they also serve to increase circulating half-life of IGF (~10-12hr)
|
|
|
|
How are locally activated IGF's generated?
|
IGFBP proteases degrade IGFBP and generate locally active IGF’s
|
|
|
|
What does the pubertal peak rate in height increase correspond to at around age 12?
|
serum IGF-1 levels
|
|
|
|
What does GH cause in adipose tissue?
|
Decreased glucose uptake
Increased lipolysis Overall -> Decreased Adiposity |
|
|
|
What does GH cause in the liver?
|
Increased RNA synthesis
Increased protein synthesis Increased gluconeogenesis Increased IGFBPs Increased IGFs |
|
|
|
What do GH and IGF cause in the muscle?
|
Decreased glucose uptake
Increased amino acid uptake Increased protein synthesis Overall -> Increased lean body mass |
|
|
|
What do GH and IGF cause in the kidney, pancreas, intestine, islets, parathyroids, skin, connective tissue, bone, heart and lung?
|
Increased protein synthesis
Increased RNA synthesis Increased DNA synthesis Increased cell size and number Overall -> Increase in organ size and organ function |
|
|
|
What do GH and IGF cause in chondrocytes?
|
Increased amino acid synthesis
Increased protein synthesis Increased DNA synthesis Increased RNA synthesis Increased collagen Increased chondroitin sulfate Increased cell size and number Overall -> Increase in linear growth |
|
|
|
Do the following inhibit or stimulate GH secretion?
Decreased blood glucose Decreased blood free fatty acids Starvation or fasting, protein deficiency Trauma, stress, excitement Exercise Testosterone , estrogen Deep sleep (stages II and IV) Growth hormone-releasing hormone |
Stimulate
|
|
|
|
Do the following stimulate or inhibit GH secretion?
Increased blood glucose Increased blood free fatty acids protein deficiency Aging Obesity Growth hormone inhibitory hormone (somatostatin) Growth hormone (exogenous) Somatomedins (insulin-like growth factors) |
Inhibit
|
|
|
|
T/F
Strenuous exercise causes a burst in GH. |
True!
|
|
|
|
When there are ample nutrients...
a) Amino acids ________ GH and insulin b) High serum glucose increases ________ secretion c) High GH, insulin and nutrient promote _______ |
a) increase
b) insulin c) growth |
|
|
|
When there are high calories, low amino acids...
a) High carbs _______ insulin secretion b) But low amino acid inhibits ________ and ________ production c) Dietary _____ and ______ used for energy but not good conditions for growth |
a) increases
b) GH and IGF c) carbs and fats |
|
|
|
When fasting, overall low nutrient availability...
a) Low carbs and fats increase _____ levels and lower _______ levels b) however _____ levels are low, conditions do not favor growth. c) GH is beneficial because it promotes __________ while attempting to minimize tissue _______ loss. d) With less insulin, peripheral tissue glucose use is ________, sparring glucose for essential tissues such as ________ |
a) GH, insulin
b) IGF c) fat mobilization, protein d) decreased, brain |
|
|
|
When there is protein deficiency, does carbohydrate treatment decrease GH levels?
What about protein treatment? |
Carb - not really
Protein - yes! |
|
|
|
What does GH deficiency leads to if developed before puberty?
|
Short stature (dwarfism)
|
|
|
|
What do many cases of GH deficiency result from?
In this case, what will happen to sexual development? |
Panhypopituitarism (all anterior pituitary hormones are deficient)
They will not be sexually mature and remain infertile. |
|
|
|
T/F
In GH deficiency, parts of the body develop in inappropriate proportion. |
False!
Parts grow in appropriate proportion, but the rate of development is greatly decreased and there is a decreased capacity to promote cartilage and long bone growth. |
|
|
|
With GH deficiency, only GH is deficient in how many of cases?
|
In 1/3rd
|
|
|
|
In Laron Dwarfism, what hormone is low?
Why? |
Low somatomedin C (IGF-1)
Receptor insensitivity to GH so liver does not produce IGF-1 |
|
|
|
How is GH deficiency treated?
|
Treatment with Human Growth Hormone
|
|
|
|
What is GH excess usually caused from?
|
Pituitary adenomas
|
|
|
|
What does adolescent onset of GH excess cause?
|
Gigantism: increased bone length and bone thickness
|
|
|
|
dolor
|
pain, grief, sorrow
|
dolōris
|
|
|
Chronic elevation of GH leads to metabolic effects on lipolysis and glucose uptake result in what?
|
Abnormally high levels of blood glucose - Pituitary Diabetes
|
|
|
|
a) The excessive stimulation of insulin in pituitary diabetes results in ______________ tissues, which further impairs plasma glucose uptake
b) What type is this? |
a) “insulin insensitive”
b) Type II |
|
|
|
a) "Insulin insensitive" tissues in pituitary diabetes eventually lead to “burn-out” of ____________ cells.
b) What type of pituitary diabetes is this? |
a) pancreatic β-islet
b) Type I |
|
