Hormones and Homeostasis Flashcards
What do temperature and blood glucose concentration regulations systems have in common? What is different?
Similar (both have a…):
- negative feedback examples:
- regulated variable
- sensor (temp has >1: skin and __)
- double circuit (one circuit if too high; one if too low)
- effector (can have >1: glucose reg has insulin if too high and glucagon if too low)
- signal (message)
- set point and critical point
- controlled processes (adjust rates to achieve target point)
Temp only (not glucose):
- Multiple sensors in different places –> Integrative center (IC)
- Signals are neuronal in temp (hormonal in gluc)
Integrative center (IC)
(1) . Role of IC: Compares set-point to actual value, sends appropriate message to effectors.
(2) . Type of IC
- (a). Sensor/IC function may be combined, as in Glucose example.
- (b). Separate IC needed if there are multiple sensors, as in temp case. IC co-ordinates incoming information from multiple sensors
- (3). In this example, IC = hypothalamus (HT)
How are the following organs/body systems involved as effectors?
- Skeletal muscle
- Smooth muscle of peripheral blood vessels in skin
- Sweat glands
- Brain
Effectors can ↑ or ↓ heat LOSS. Can only ↑ heat generation.
[Therefore Humans have greater ability to cope with very cold than very hot.]
Skeletal muscle
- *Action to Raise Temp: *Contraction generates heat (shivering)
- Action to Lower Temp: None
Smooth muscle of peripheral blood vessels in skin
- Action to Raise Temp: Muscles contract; vessels constrict to reduce heat loss
- *Action to Lower Temp: *Muscles relax; vessels dialate to increase heat loss
Sweat glands
- *Action to Raise Temp: *None
- *Action to Lower Temp: *Produce sweat; evaporation increases heat loss
Brain
- Action to Raise Temp: Behavorial–put on coat, curl up
- *Action to Lower Temp: *Behavorial–take off coat
Afferent Signals
info goes away from sensors into IC
Efferent signals
info goes out of IC toward effectors
Regulation/regulated variable:
The variable (glucose level) you wish to keep at an approximately constant level is said to be “regulated.”
Control/controlled process:
The processes that alter levels of the regulated variable (glucose uptake, release or shivering, sweating, etc.) are said to be “controlled.”
IC Adjustments:
How does the IC adjust for body temp (ie: with fevers)?
- Fevers – Raise set point for body temperature and critical points for shivering/sweating
Shivering and sweating both kick in at higher temps. (You don’t have to cool off as much to start shivering and you need to heat up more to start sweating.)
- Raises set point (desired level) & actual level of internal body temperature.
Why fevers? High temperatures prevent bacteria from obtaining iron from host & improve immune function.
What are “Feedforward or anticipation” adjustments made by IC?
Planning ahead. Altering set points and/or critical points to adjust to anticipated factors. (Or you can think of it as just ignoring the usual critical points.)
- _ _Body temperature: Skin temperature affects critical temperature/set points for generating heat and/or shivering. If body is cold, but it’s warm outside, shivering can be postponed, saving energy, and you’ll still warm up. This is equivalent to lowering (or ignoring) set point/critical points for shivering, not changing set point of internal body temperature. Changes what effectors and what controlled processes you use to warm up, but not the end result.
- Secreting insulin when you start to digest food in the stomach, but before the digestion products (glucose, amino acids etc.) reach the blood. This way tissues will be ready to take up the glucose as soon as it enters the blood. (What allows uptake? What is triggered by insulin?)
What other components of internal milieu are regulated besides glucose, temperature?
Many nutrients like amino acids; concentrations of water, salts and ions (Na+, K+ etc.), gases (CO2, O2), waste products, volume & pressure of blood, and pH.
Which hormones are repsonsible for Maintenance of Homeostasis ?
insulin, glucagon, cortisol.
Regulate blood glucose/energy supplies and concentrations of substances in general. Maintain more or less constant conditions = homeostasis.
Which homones are responsible for Stress response?
cortisol, epinephrine.
Regulate heart rate, blood pressure, inflammation, etc.
Which hormones are repsonsible for Regulation of episodic or cyclic events ?
estrogen, insulin, oxytocin – regulate lactation, pregnancy, effects of eating, etc.
Which hormones are responsible for Growth/overall regulation ?
growth factors, tropic hormones
– regulate production of other hormones. (Note: not all GF’s are endocrines.)
How do effectors respond to insulin for glucose uptake?
a. Causes direct increase of glucose uptake by membrane transporters
b. Increases breakdown of glucose to provide energy
c. Increases conversion of glucose to ‘stores’
(1) . Glucose is converted to storage forms (fat, glycogen), AND
(2) . Breakdown of storage fuel molecules (stores) is inhibited.
d. Causes indirect increase of glucose uptake by increasing phosphorylation of glucose to G-P, trapping it inside cells
How does insulin work?
Insulin works through a special type of cell surface receptor, a tyrosine kinase linked receptor
(1). In resting skeletal muscle & adipose tissue –
- mobilizes GLUT 4 transporter (fac diff )
- -GLUT 4 protein – promotes fusion of vesicles containing the transporters with plasma membrane. No other hormone can cause this effect.
(2). In liver:
- Liver (& brain) can take up glucose without insulin –
- use different transporters (GLUT 1, 2 &/or 3–they do not use GLUT 4!) located permanently in the plasma membrane.
(a) . In liver: Insulin indirectly promotes glucose uptake in liver by increasing phosphorylation (trapping) and utilization of glucose.
(b) . Note: Insulin has no affect on glucose uptake in brain.
(3) . Working skeletal muscle: Insulin is not required for uptake of glucose in working skeletal muscle because exercise mobilizes GLUT4 in skeletal muscle. (Another good reason to exercise.)
insulin promotes utilization of glucose
(in many tissues)
- (1). Activates appropriate enzymes for synthesis of storage forms of metabolites – synthesis of glycogen, fat, and/or protein.
- (2). Inhibits enzymes for breakdown of stores.
- (3). Can promote utilization (breakdown) of glucose for energy.
d. Significance: Some effects of insulin are mimicked by other hormones, but mobilization of GLUT4 cannot be triggered by any other hormone. Therefore loss of insulin, or lack of response to insulin, is very serious, and causes diabetes type I or II, respectively.
What is the primary effector for release of glucose into blood?
liver
( Liver has phosphatase for G-6-P. Muscle and adipose tissue don’t.)
Role of Glucagon
_Receptor: _Glucagon works through a G protein linked receptor that triggers the cAMP pathway–> activates PKA.
Effects: Primary physiological effect is on liver; generally promotes production/release of glucose, not uptake or utilization.
Produced: both by breakdown of glycogen, and build up from lactate = gluconeogenesis.
Significance: can be mimicked by other hormones; no known medical condition caused by lack of glucagon.
Adrenal Gland
- Adrenal Medulla (nervous)
- Adrenal Cortex (epithelial)
Adrenal Medulla
- pathway stimulation?
- derived from what tissue?
- what does it secrete?
- What is the major hormone?
- What recepters does it have?
(1). Stimulated by nerves
(2). Derived from neural tissue; part of nervous system.
(3). Secretes compounds that can act as transmitters (when signal cell to cell) but
act as hormones (neuroendocrines) here – are released into the blood. Note same
compound can act as a transmitter or a neuroendocrine.
(4). Major hormone = epinephrine (adrenaline); also secretes some norepinephrine
(noradrenaline).
(5). Receptors. Receptors for epi and norepi on target cells are the same whether
the signal molecules are acting as hormones or as transmitters.
- All called adrenergic receptors
- Two major types – α & β.
Adrenal Cortex
- What stimulates it?
- What is it derived from?
- What does it produce?
- What axis is it part of?
(1) . Stimulated by a hormone (ACTH)ecture 17
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(2) . Derived from epithelial tissue
(3) . Produces steroids = corticosteroids. For structures see Sadava fig. 41.2 (b)
(41. 14).
(4) . Part of HT/AP axis
Pancreas
- How is it an endocrine gland?*
- How is it an exocrine gland?*
a. endocrine gland
(1). Secretes glucagon and insulin (& additional factors) into blood
(2). Insulin & glucagon control blood sugar balance
(3). Secretion of glucagon/insulin controlled by blood sugar levels and by input
from nervous system (in response to stress)
b. also exocrine gland – secretes digestive enzymes through duct to GI tract.
What’s the difference between endocrine & exocrine glands?
(1). Exocrine Gland
When gland forms, epithelial layer leaves duct to outside.
Secretion from gland flows into duct → outside or lumen.
- Examples:
- (i) sweat, mammary & tear glands → secretion → outside
- (ii) stomach glands & pancreas → secretion → lumen.
(2). Endocrine Gland
When gland forms, epithelial layer pinches off leaving no duct
Secretion (hormone) from gland enters blood.
- Example: gonads, pancreas, adrenal.
- (3) Both types get precursors for secretions from blood
catecholamines
(describe structure, receptors, and mechanisms of action)
- epinephrine (aka adrenaline), norepinephrine (aka noradrenaline), and dopamine.
- modified amino acids derived from tyrosine.
- All water soluble.
Receptors
- Multiple receptors, classified by ligands and responses to drugs
- (1). Dopamine has its own receptors, separate from the adrenergic receptors (for epi and
norepi). - (2). All adrenergic receptors bind to both epi and norepi. Some receptor types bind better to (have higher affinity for) one, some to the other, some equally well to both.
*Epinephrine acts mostly through beta adrenergic receptors.
*Norepinephrine mostly through alpha adrenergic receptors.
Mechanism of action:
- All receptors for all catecholamines are G protein linked; effects of hormones on any particular cell type depend on
(i) what receptors are present
(ii) what G protein each receptor activates. - Each G protein does one (or more) of the following:
- activate adenyl cyclase
- inhibit adenyl cyclase
- activate phospholipase C. (triggers the IP3 signaling pathway; details to be
- discussed later.)
- (iii) what target proteins are present in the cell that are ‘downsteam’ of (affectedby) the signaling pathway (cAMP or IP3 pathway).
goiter
(enlarged thyroid) -
2 types
- (a). When TH is low (hypothyroidism) – Lack of iodine or other factor → low level of TH
Low level of TH → lack of negative feedback to HT &/or AP → overproduction of TSH → goiter. - (b). When TH is high (hyperthroidism): Have high level of TH but still have too much stimulation of thyroid. Problem can be
i. Over production of TRH and/or TSH (due to tumors, failure of feedback, etc.), or
ii. Over stimulation of TSH receptors by other factors.
(4). What regulates or controls hormone levels? It’s different for TH & insulin.
(a). Levels of TH production (& levels of TSH & TRH) are
regulated by the hormone itself (TH). Same for cortisol, FSH, LH.
(b). Levels of insulin production are regulated by [Glucose] levels in
blood, not the hormone (insulin) itself. (Insulin secretion may also be
affected by signals from brain, anticipating a rise in blood [Glucose],
but is not regulated by hormone itself.)
Thyroglobulin synthesis and secretion
Q: (7-9)
Where in the cells of the anterior pituitary gland would you expect to find hormone receptors? Explain why.
- a) on the plasma membrane
- b) intracellular (in the nucleus)
- c) both
c. The cells of the anterior pituitary gland that secrete TSH are going to respond to stimulation from the hypothalamic TRH (which is a peptide hormone, and so stimulates membrane receptors) and are also sensitive to negative feedback from
TH Synthesis Diagram
<em>outside of class info</em>
- Thyroglobulin is synthesized in the rough endoplasmic reticulum and follows the secretory pathway to enter the colloid in the lumen of the thyroid follicle byexocytosis.
- Meanwhile, a sodium-iodide (Na/I) symporter pumps iodide (I-) actively into the cell, which previously has crossed the endothelium by largely unknown mechanisms.
- This iodide enters the follicular lumen from the cytoplasm by the transporter pendrin, in a purportedly passive manner.
- In the colloid, iodide (I-) is oxidized to iodine (I0) by an enzyme called thyroid peroxidase.
- Iodine (I0) is very reactive and iodinates the thyroglobulin at tyrosyl residues in its protein chain (in total containing approximately 120 tyrosyl residues).
- In conjugation, adjacent tyrosyl residues are paired together.
The entire complex re-enters the follicular cell by endocytosis.
* Proteolysis byvarious proteases liberates thyroxine and triiodothyronine molecules, which enter the blood by largely unknown mechanisms.
