BSCI 1511 Study Guide - Midterm Guide: Adenylyl Cyclase, Guanylyl Cyclase, Anterior Pituitary

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Bio Exam 1 Review
I. Hormones
a. Growth Hormone
i. Produced & released in anterior pituitary
b. Thyroid stimulating hormone (TSH)
i. Produced by anterior pituitary
ii. Ultimately leads to thyroxine production
c. Thyroxine
i. Increases metabolic rate
ii. End results of TSH
d. Insulin
i. Binds to RTK receptor
ii. Decreases blood glucose
iii. Initiates glycolysis
iv. Inhibits glycogen breakdown
v. Promotes glycogen synthesis
vi. Alters gene transcription
vii. Released into blood by beta cells of pancreas
1. When this happens, body cells take up more glucose from blood
cells
viii. Type 1 Diabetes is caused by a deficiency of insulin
e. Parathyroid hormone (= Ca2+ IN)
i. Increases blood calcium levels
f. Calcitonin (= Ca2+ OUT)
i. Promotes calcium deposit in bone (out of blood)
ii. Secreted by thyroid
iii. Opposes parathyroid hormone
g. GnRH
i. Induces release of gonadotrophins (FSH and LH) from anterior pituitary
1. Called gonadotrophins b/c act on gonads & support
gametogenesis
ii. More GnRH = more LH
h. Inhibin
i. Released by Sertoli cells
ii. Causes decrease in FSH release from pituitary (negative feedback)
i. Steroid hormones
i. Act on cells by binding to soluble, intracellular receptors
1. Only certain cells have these receptors
ii. Generally exert effects by causing changes in gene transcription
1. AKA initiate gene transcription
iii. Act slowly b/c they turn genes on or off and it takes time for gene
products to build up or be depleted
iv. Anabolic steroids interfere w/ negative feedback loops necessary for
control of gonadotropin release
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1. Can inhibit GnRH, LH, and FSH release
v. Examples:
1. Testosterone
2. JH in insects
j. Adrenal hormones
i. Adrenal gland is stimulated by secretion of ACTH by anterior pituitary
ii. 2 parts:
1. Adrenal cortex = mineralocorticoid hormones & glucocorticoid
hormones
a. Long-term stress
2. Adrenal medulla = epinephrine & norepinephrine
a. Short-term stress
k. Human chorionic gonadotrophin (HCG) = secreted by blastocyst, maintains the
corpus luteum
i. Basis for pregnancy tests (secreted in urine)
l. Melatonin
i. Produced in pineal gland
ii. Represses the growth and spermatogenesis w/in the testes
1. AKA less sperm growth at night
m. Oxytocin
i. Produced in posterior pituitary (RARE!)
ii. Stimulates uterine contractions during labor
n. FSH
i. Stimulates Sertoli Cells in seminiferous tubules
1. Provide nutrients & support to developing sperm
ii. Peaks at ovulation in ovarian cycle
o. Prolactin
i. Hormone that makes you produce milk
ii. Secreted by anterior pituitary
iii. Hypothalamic prolactin releasing hormone starts cascade
iv. Positive feedback loop
p. Glucagon
i. Pancreatic hormone
ii. Triggers breakdown of glycogen to glucose in liver cells
iii. GPCR pathway
q. LH
i. Surge in this hormone at end of follicular development= signal for
ovulation
1. Thus, rise of LH = predictor for ovulation
ii. Stimulates growth & development follicle, which then starts producing
estrogen
iii. As estrogen is secreted, LH levels rise, follicle ruptures, & egg is released
1. Estradiol peak causes LH peak
a. Estradiol peaks occurs a few days before ovulation
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iv. Produced in anterior pituitary, which is stimulated by GnRH
v. Acts on gonads: ovaries in women & Leydig cells in testes of males
1. Activates Leydig Cells, which increase output of testosterone
r. Progesterone
i. Secreted by corpus luteum
ii. Peaks several days after ovulation has occurred
1. BAD measure for predicting ovulation
iii. Thickens endometrium to prepare for implantation
iv. Concentration increases after fertilization
v. Abortion pill = blocks progesterone receptors in uterus
1. No progesterone = no pregnancy
a. Induces menstruation
s. Epinephrine
i. Neuro-hormone
ii. In liver, causing glycogen breakdown and thus release of glucose
1. Causes blood glucose levels to rise
iii. Works same as glucagon basically
II. Signal Transduction Pathways (Reception Transduction Response)
a. Signal transduction pathways allow for amplification and tight regulation
b. cAMP
i. cAMP-phosphodiesterase inhibits cAMP production
1. If remove this, have prolonged effects of epinephrine
ii. cAMP activates PKA
c. GPCRs
i. 7 transmembrane domains
ii. Work with G proteins
1. Bind GDP & GTP
a. GDP replaced by GTP when ligand binds GPCR
b. Hydrolyzes GTP to GDP to inactivate itself
2. Alpha, beta, gamma subunits
d. GPCR -Epinephrine
i. Binds to GPCR, activating it
1. G protein binds, alpha subunit changes GDP GTP , activating it
ii. G protein activates adenyl cyclase, which converts ATP to cAMP
1. cAMP (2nd messenger) PKA (binds regulatory subunits,
releases catalytic subunits, leading to end results) ____
a. In Liver = glucose!
i. Inhibition of glycogen synthesis, promotion of
glycogen breakdown
b. In skeletal muscle = vasodilation
c. In intestines = vasoconstriction
iii. *Cholera toxin modifies a G-protein so that it cannot hydrolyze GTP
1. makes it so adenylyl cyclase is irreversibly activation
constantly high levels of cAMP
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