Download 8-9 (Cotlin)

Endocrinology: 8:00-9:00 am
Scribe: Maggie Law
Friday, November 6, 200
Proof: Ashley Hollady
Dr. Cotlin
Thyroid, Parathyroid, and Adrenal Glands
Page 1 of 7
BL=basolateral; ZG= zona glomerulosa; ZF=zona fasciculata; ZR=zona reticularis
I. The Endocrine Systems; Thyroid, Parathyroid and Adrenal Glands [S1]: skipped
II. Thyroid and Parathyroid Glands [S2]
a. Skipped, already covered
III. Blood supply to the thyroid [S3]
a. skipped
IV. The Thyroid Gland [S4]
a. skipped
V. Functional and Structural Unit [S5]
a. Concept of a thyroid follicle—all of them are highly polarized structures so that their apical surface.
b. Pars intermedia is not polarized.
c. The following cells will secrete T3 and T4- colloid; parafollicular will secrete calcitonin.
VI. Follicular Cells [S6]
a. skipped
VII. EM of Thyroid Follicular cell [S7]
a. Basolateral region; lots of active processes going on with mitochondria and rough ER. T3 and t4 made on a
scaffold of thyroglobulin.
b. Producing thyroglobulin—specific protein to the thyroid, the follicular cells, they are producing this, up-taking
iodine always at the basolateral side of the cell.
c. See iodine receptors as well as receptors for TSH.
d. In the apical region this is essentially colloid—you will see microvilli, little surfaces processes and once they are
activated to secrete hormone, these will put out large fillapodia and kind of re-ingest the colloid =Remember this
association.
e. The colloid is totally separate from all the tissue around it--surrounded by follicular cells.
f. THIS IS WHERE THE AUDIO PICKED UP AT—ABOVE IT JUST WHAT I HAD TYPED IN CLASS.
VIII. Parafollicular Cells [S8]
a. Parafollicular cells secrete calcitonin in the blood and have the effect of lowering the calcium concentration in
the blood.
IX. Thyroid Gland [S9]
a. skipped
X. Synthesis of Thyroid Hormone [S10]
a. 2 things dependent on producing T3 and T4---collectively thyroid hormone.
i. 1. Stimulation by the TSH, which is released from anterior pituitary into circulation; these cells have
receptors for TSH at the basolateral and also have iodine transporters. Both things are necessary.
1. First you have stimulation of the cells and then you have to have adequate supply of iodine; this is
the primary place in body where you use iodine.
ii. Transport iodine at basolateral surface; it’s actively taken up, transported across the cell in a transcellular
process and released at apical surface; on the extracellular side of the apical surface there is thyroid
peroxidases that oxidizes iodine and it’s going to be incorporated into thyroglobulin.
iii. Iodine is being taken up, transported, and oxidized at the apical surface; thyroglobulin is being made and
secreted at the apical surface as well.
iv. Iodine, colloid, thyroglobulin are in the colloid, thyroglobulin becomes iodinated at the apical membrane on
the extracellular side— the thyroglobulin is like a scaffold for making T3 and T4.
1. This results in mono and di-iodo-tyrosine molecules; tyrosine is where the iodine is attached; those
are the amino acids that are modified.
v. The colloid is a storage spot for T3 and T4, or in this case, iodinated thyroglobulin—do not actually
generate T3 and T4 until it is taken back up into the cell and processed.
vi. In colloid is iodinated thyroglobulin—is just a storage reservoir, have several months supply if you need it—
it will just sit there and it’s kind of a resting situation.
vii. These cells are cuboidal in a resting situation, but once they are stimulated they become much more
polarized and columnar .
viii. Now you have sufficient iodine and iodinated thyroglobulin.
1. Once you get the signal, the TSH, that binds to the receptors and activates a signaling process—first
thing that happens is the cell is activated to take up the colloid; the fillipodia that will engulf these
and are capable of taking in large amounts in a pinocytosis-like way.
2. The vesicles fuse with lysosome or late endosome, something with a lower pH—the more acidic
vesicles—and that’s where we see digestion of the thyroglobulin molecules.
3. Digestion and cleaving of the mono and di-iodo-tyrosin, you get releasing of the T3 and T4.
Endocrinology: 8:00-9:00 am
Scribe: Maggie Law
Friday, November 6, 200
Proof: Ashley Hollady
Dr. Cotlin
Thyroid, Parathyroid, and Adrenal Glands
Page 2 of 7
ix. T3 and T4 are generated and secreted at the BL surfaces; the cell tries to recycle it’s iodine and
thyroglobulin; the iodine is cleaved from the MIT (mono-iodo-tyrosine) and DIT (di-iodo-tyrosine) and can
be reused.
x. T3 and T4 are distributed—there is lots of vasculature in this, so they will secreted on the BL side and
directly enter the connective tissue of the vasculature into the blood stream.
XI. Release of Thyroid Hormones [S11]
a. skipped
XII. Images [S12]
a. Here a tyrosine molecule with a hydroxyl group.
b. There are certain positions on the benzene ring that are going to iodinated.
c. Mono would have one iodine molecule attached. Di-iodo-tyrosine has 2.
d. If you put the mono and the di-iodo together, you will get a molecule of T3.
e. If you put 2 di-iodo’s together , you can get T4 molecules.
f. Have the thyroglobulin with all the tyrosines, that are scaffolded and iodinated are all over the place, it can be
taken up and processed and the result is these two molecules.
g. Active molecules-The T3 is a molecule with 3 iodine’s; T4 has 4 iodine’s; any extra iodine molecules are just
recycled.
h. These are bulky and hydrophobic but that have reactive groups on end; in circulation they are bound to thyroid
hormone binding protein.
i. That’s true for most hormones; they are not circulating freely but are usually bound to some accessory
molecules.
XIII. Physiological Effects of T3 and T4 [S13]
a. Bind to proteins in the plasma and slowly be released; they are bound to intracellular proteins and slowly diffuse
over days.
b. Both of them have nuclear hormones—they can get through plasma membrane, get to nucleus and stimulate
many genes involved in metabolism.
c. These are slow acting and don’t cause an immediate reaction in the cell; you do something by turning on gene
expression—a slower effect, but a more long lasting effect.
d. Circulating in blood stream is mostly T4; T3 has a much shorter half life (less than a day) whereas T4 has a
longer half life of almost a week.
e. Cell can take T4 and cells can convert it to T3; T4 is more stable and it can be used to generate T3.
f. T3 has a much more potent activity and can bind with higher affinity to most cells. Cells will preferentially use
T3.
XIV.
T3 and T4 Functions [S14]
a. Overview—T3 and T4 functions—these control most of your resting metabolic activities—increase metabolic
rate, promote the use of energies and protein synthesis, normal cardiac function, normal neuronal development,
promotes body growth. If you don’t have normal levels, you will decrease all of these things.
i. T3 and T4 are used all over your body for resting and normal metabolic functions.
XV. Clinical Correlations [S15]
a. Graves’ Disease
i. Autoimmune disease in which the thyroid is constantly stimulated
1. Person affected would have hyperplasia and hyper stimulation all the time.
2. These patients have heart arrhythmias, muscle fatigue because they are always activating things
when they are not supposed to.
b. Hypothyroidism—not producing enough T3 and T4.
i. More prone to infection, metabolic functions slow, lethargy, etc.
ii. Goiter-when you have insufficient dietary iodine—you need it to build all the stuff but can’t make the
hormone because you don’t have iodine.
XVI.
The Parathyroid Glands [S16]
a. Very small glands imbedded and encapsulated in the thyroid tissue—have a thin connective tissue coating
b. They produce PTH, which acts to increase calcium levels in blood.
XVII. Histology of Parathyroid Glands [S17]
XVIII. Histology [18]
a. Two types of cells
i. Oxyphil—not sure what they produce on a functional level as far as their secretions
ii. Chief cells—primary secretory cell of the parathyroid gland and these release parathyroid hormone
XIX.
Thyroid and Parathyroid Glands [S18]
a. You can see the non-uniformity of all the follicles—not all the same size and shape.
XX. Parathyroid glands of an adult [S19]
Endocrinology: 8:00-9:00 am
Scribe: Maggie Law
Friday, November 6, 200
Proof: Ashley Hollady
Dr. Cotlin
Thyroid, Parathyroid, and Adrenal Glands
Page 3 of 7
a. Tends to accumulate fat as adult gets older—see the dark cells vs. the light cells.
i. The dark and grainy cells are the chief cells producing the PTH.
ii. The lighter ones are oxyphils.
XXI.
Histology Slide [S20]
a. Small, encapsulated with lots of blood vessel around them; embedded right in the thyroid tissue itself.
XXII. Effects of Parathyroid Hormone [S21]
a. Calcitonin—toning something down, so you are lowering calcium.
b. PTH is the reverse--increases calcium.
i. Need calcium stores for a lot of things—action potentials, at the nerve terminals.
ii. Many of the secretory, regulatory secretions require an influx of Calcium.
iii. Always need Ca high outside the cell, low inside the cell, and high in the ER because Ca is used for muscle
contraction and basic signal transduction pathways all over the body.
c. Want to increase Ca and release stores of it in our body there are a few places to go.
i. PTH’s most active sites are osteoclasts. These are macrophage cells in the bone that digest bone; acts on
the osteoclasts to active them and acts on this lineage to produce more osteoclasts by stimulating the
progenitors.
ii. Absorption of Ca in the intestine—take up more from food sources
iii. Conservation of Ca by the kidney--acts on the tubules and the collecting ducts to retain Ca so you don’t
loss it in the urine.
iv. Also stimulates the conversion of active vitamin D; active vitamin D can be a cofactor for increased Ca
uptake .
v. All these things together have one goal—to increase Ca in the blood stream!
vi. Lose the high extracellular Ca; blood is just the extracellular media, lots of bad things can happen.
vii. Muscles and nerves require Ca.
XXIII. PTH Synthesis and Action [S22]
a. PTH is secreted as prohormone;
b. Traffics through the ER and the Golgi like any other secreted protein; pro-sequence is removed in the Golgi and
the mature hormone is secreted, so there are a couple of different processing steps to go through.
c. What stimulates its release? Unlike the a lot of the other things that have a hormone from the anterior pituitary
that binds and actives, this is NOT under the control of TSH.
d. It simply responds to Ca levels; there are Calcium sensors in the chief cells with receptors on the surface; when
these things are triggered by low Ca concentrations, that stimulates the cell directly to release PTH.
e. Not under any kind of pituitary control—simply responds to Ca levels; when Ca levels are sufficiently high, this
process of synthesis and secretion is down regulated.
f. The receptor signals through a G-protein receptor, adenylate cyclase, to produce cAMP—as you except the
receptors are on osteoclasts primarily and also tubular epithelial cells in the kidneys.
g. Release calcium through bone digestion and conserve Ca through the urine production process.
XXIV. PTH and Calcitonin [S23]
a. Both are controlled by circulating Ca; They work in opposing fashions
XXV. Clinical Correlations [S24]
a. Can have hypo or hyper parathyroid.
XXVI. The Suprarenal Glands [S25]
a. Suprarenal Glands and Adrenal Glands are the same thing; suprarenal because of where they sit on top of the
kidneys.
b. Small little glands (3 to 5 cm by 1 cm) sitting on top of the kidney; totally encapsulated with its own little
connective tissue surrounding it; usually has some adipose tissue sitting around it.
c. 2 basic classes of molecules made here—lots of our steroids are manufactured and secreted in the adrenal
glands as well as catchacholamines (epi and NE).
d. 2 different regions
i. Cortex—responsible for steroid synthesis
ii. Medulla-catchacholamines
e. Both are from very different embryonic origins similar to what we saw with the pituitary (part from ectoderm and
part was nerve tissue).
XXVII. Blood Supply [S26]
a. Very vascular tissue—has superior, medial and inferior suprarenal arteries; set so the blood will enter all over
like little cones; the arterial supply is around the periphery and will all leave by a central vein.
b. There are lots of arterial branches that supply the adrenal gland, but one adrenal vein drains the entire contents
of the gland.
XXVIII. Development [S27]
Endocrinology: 8:00-9:00 am
Scribe: Maggie Law
Friday, November 6, 200
Proof: Ashley Hollady
Dr. Cotlin
Thyroid, Parathyroid, and Adrenal Glands
Page 4 of 7
a. Cortex, all three layers, derived from from mesoderm.
b. Medulla derives from neural crest cells.
c. As the medulla is developing, the fetal cortex only has two layers; the third layer won’t develop until after birth.
XXIX. Structure of the Adrenal Gland [S28]
a. Surrounded by a capsule w/ 3 layers
b. Three layers of the cortex
i. Glomerulosa
ii. Fasciculata
iii. Reticularis
c. In a circular pattern—underneath the cortex, the immediate layer surrounding the entire gland is the ZG which is
very thin.
d. The ZF is shown in light purple. The ZR is the light green.
e. These three layers make of the cortex from mesodermal origin.
f. Medulla is in the central region and derives from neural crest cells.
g. See a situation where you have direct and physical contract of the nerve system in endocrine tissue, similar to
the pituitary gland.
XXX. Organization of cells in the Adrenal glands [S29-30]
a. Have capsular arteries; all the branches--superior, medial, inferior will insert into the capsule and then we will
see a plexus and branching throughout.
i. Glomerulosa cells— primarily secrete mineralcorticoids.
ii. Fasciculata, the largest, will produce glucocorticoids.
iii. Reticularis—produces androgens—sex hormones.
iv. Medulla—two types of cells secreting epi and NE.
XXXI. Blood Supply to adrenal Glands [S31]
a. See branches that will penetrate the cortex and from sinusoids around all of the cells and have some arteries
that will go directly through the cortex to the medulla.
b. Plexus with capillaries—secrete contents directly into the vasculature.
c. Along the fasciculata, see these longitudinal sinusoids with a fenestrated epithelium; see these cells with spaces
inside of them that are sinusoid cavities; they capillarize again in the reticularis and then in the medulla.
d. Medulla has its own fresh arterial blood supply—does receive venous blood from the cortex; all of the blood will
drain into the medulla, whether it’s the venous blood from the cortex or the fresh blood feeding the medulla—all
will drain into a central medullary vein—each adrenal gland has multiple arterial inputs but a single venous
output.
XXXII. Blood supply to the adrenal Gland [S32]
a. The whole thing is surrounded by capsule, cortex, and medulla.
b. Here are the capillary beds, all of the sinusoids, more capillary beds, and then these kind of larger, dense ones
are the ones feeding the medulla.
XXXIII. Blood Supply to Suprarenal glands [S33]
a. This is a cast of the vasculature
b. All of the smaller longitudinal vessels are the sinusoids draining the cortex and the thick, puffier ones are the
long, cortical arteries that will go straight to the medulla.
c. Shows the central medullary vein.
XXXIV. The Adrenal Cortex [S34]
a. Three concentric zones and three classes of steroid hormones.
b. The steroid hormones, regardless of what they are (mineralcorticoid, glucocorticoid, etc.), are NOT stored; they
are made on demand!
c. However, cholesterol is stored; the main source is LDL; all of these cell types take up LDL and store high
concentrations of cholesterol only on demand!
d. Upon stimulation, you will see LDL is freed and used for synthesis of whatever the hormone is.
e. These are slow acting kind acting process because they have to get the signal, make it, and release it—not an
immediate result.
f. Like the thyroglobulin stored (T3 and T4) that was only released and processed upon stimulation.
g. Not storing the hormone, they are storing the LIPID to make the hormone.
XXXV. Layers of the Adrenal Cortex [S35]
a. Glomerulosa—smaller layer; named b/c it look like the glomeruli of the kidney.
b. Fasciculata—tend to be in parallel arrays with doublets of cells are each side; each is surrounded by sinusoids
c. This shows a diagram of the reticularis.
XXXVI. Zone Glomerulosa [S36]
a. All stimulated at some level by the adrenocorticotropic hormones that come from the pituitary gland.
Endocrinology: 8:00-9:00 am
Scribe: Maggie Law
Friday, November 6, 200
Proof: Ashley Hollady
Dr. Cotlin
Thyroid, Parathyroid, and Adrenal Glands
Page 5 of 7
b. Receptors on these cells will have receptors for ACTH; the cells here also respond to angiotensin II to produce
aldosterone and deoxycorticosteriod.
c. These are the 2 primary mineralcorticoids that are secreted by glomerulosa.
d. Function is controlling fluid and electrolyte balance.
e. Think of things with RER producing lots of things with proteins; SER is involved in production of lipids and all
these cells will have high concentrations of SER relative to what we would see in other cells that are not dealing
with hormones.
f. These cells make little glomeruli-like structures---like any other epithelial cells, they will be connected by gap
junctions and desmosomes to keep the integrity of the cells.
g. Cells will secrete on the BL side because the BL side is what connects to the vasculture.
XXXVII. Hormones of the ZG [S37]
a. Primary target is the distal convoluted tubule in the kidney to help regulate water balance and homeostasis-Water conservation.
b. Also targets the gastric mucosa, sweat glands, and salivary glands—stimulating the uptake of sodium, the
salvaging of the sodium.
c. Take up salts and water comes back in as well; primary goal here is regulating water.
XXXVIII.
Renin Angiotensin-aldosterone System [S38]
a. Renin triggers the angiotensinogen to become angiotensin I.
b. Conversion of angiotensin I to angiotensin II.
c. Angiotensin II, in addition to ACTH will stimulate the cells of the glomerulosa; when you here angiotensin acts
on the adrenal gland to produce aldosterone, it’s acting on the cells of the ZG.
d. Aldosterone will feedback and act on the kidney to help conserve the water.
e. This process will turn down the cycle.
f. In addition to the ACTH, these cells are under the control of the rennin-angiotensin system as well.
XXXIX. Zone Fasciculata [S39]
a. The fasciculat is the largest region of the cortex.
b. Produces lots of cortisol and corticosteroids which will be involved in fat and protein metabolism.
c. Cells are much larger and puffier; the cells are called spongocytes b/c they look like sponges.
d. Accumulate the largest concentration of lipid droplets relative to the other sites in the cortex; lots and lots of
SER and lots and lots of lipid droplets. It produces a lot of cortisol.
XL. Hormones of ZF [S40]
a. Wide range of functions
i. Liver—anabolic effect—promote fatty acid synthesis, amino acid synthesis, utilization of glucose.
ii. Can have a catabolic effect in some tissue and stimulate lipid breakdown—these can do lots of different
things and are going to be tissue and cell specific.
iii. Very high concentrations have exhibit an anti-inflammatory effect.
iv. Lots of people take steroid for illness to reduce inflammation and inhibit the ongoing inflammatory
responses like the recruitment of macrophages—know when you are getting the recruitment of all the white
blood cells, you get inflammation.
v. Cortisol will suppress all of the this—anti-inflammatory and immunosuppression.
vi. Under stimulation of ACTH; part of a negative feedback loop. The cortisol levels, once they are sufficiently
high, will feedback back to the pituitary to say “stop producing this” and ACTH will decrease--modulated not
just by hormones but by actual levels of cortisol in the blood.
XLI.
Steroid Hormone synthesis [S41]
a. Steroid hormones are made on demand—accumulate lipid cholesterols (LDL is the source) and will store this.
b. Takes signaling and binding of the ACTH to the receptor to activate the synthesis pathway; as soon as the
steroids are made, they are directly secreted.
c. At no point are the steroids stored—immediately secreted.
XLII.
Steroid hormone [S42]
a. Steroid hormones are lipophilic, go through the plasma membrane and get to the nucleus.
b. Most will bind cytocysolic or nuclear receptors and activate gene transcription.
c. These steroid hormones will not give an immediate effect; you get more of a long term effect—you are turning
on genes and modulating what the cell is going to do—anyone one on steroid therapy, you don’t just want to
immediately take them off of the steroids—want to slowly take them off.
i. If you are giving someone steroids, this whole natural process is down regulated so if you immediately
remove the supply, you will go out of whack for a while because you are really altering how the cells are
acting.
XLIII. Zone Reticularis [S43]
a. Also under ACTH control.
Endocrinology: 8:00-9:00 am
Scribe: Maggie Law
Friday, November 6, 200
Proof: Ashley Hollady
Dr. Cotlin
Thyroid, Parathyroid, and Adrenal Glands
Page 6 of 7
b. Primary hormones are androstenedione and dehydoepiandrosterone (DHEA)
c. Both have a weak masculizing (I think she made this word up) effect; the cells don’t tend to have as much lipid
as the other two.
XLIV. Hormones of the ZR [S44]
a. The hormones secreted from the zona reticularis are almost negligible or insignificant relative to the androgens
that are produced by the reproductive organs.
b. At some low level, they do produce androgens, but a small fraction relative to what’s produced in the male
testes.
XLV. Histology [S45]
a. Picture of the glomerulosa, fasciculata, and reticularis
b. If you look up close, you can see the spacing and see how fatty they look—look like puffy and fatty cells.
c. The fasciculata is the really thick band you see—the wide space you see is reflective of the lipid droplets
XLVI. Histology [S46]
a. In this area you can see lots of spaces—all the sinusoids; lots of blood flow.
b. They radiate along the cords of the fasciculata into longitudinal sinusoids that parallel.
XLVII. Feedback mechanism of ACTH and glucocorticoid secretion [S47]
a. Reminder of the feedback loops at the pituitary level and the hypothalamus level.
b. Hypothalamus is what is stimulating the anterior pituitary.
XLVIII. Clinical Correlations of Adrenal Cortex [S48]
a. Addison’s Disease
i. Decreased secretion of adrenocorticoids—often an immune process.
ii. Systems include: weight loss, muscle weakness, low blood pressure.
b. Cushing’s Disease
i. Increase in adrencorticoids.
ii. These people gain weight, leading to obesity. People on steroid therapy tend to gain weight and they look
really full in the face—increased cortisol will have this effect.
XLIX. Effects of decreased or increased stimulation on the structure of adrenal cortex [S49]
a. These tissues can hypertrophy and hypotrophy depending on stimulation.
b. In times of decreased stimulation, it will almost look atrophied—all the layers will kind of shrink.
c. Under conditions of stress and increased stimulation, the gland can really hypertrophy—all the cells can
proliferate and expand in response to the body.
d. Someone receiving cortisol will have the cells down regulate, because if you have an exogenous source, you
don’t need to make your own and will sometimes see atrophy.
L. The Adrenal Medulla [S50]
a. Has a neural crest origin—functions in a sense of a modified ganglion.
b. Two populations of cells
i. Has chromaffin cells--cells that are producing adrenaline and nor-adrenaline.
c. The sympathetic ganglion cells are the neural cells that are actually stimulating secreting.
LI. Structure of the Adrenal Medulla [S51]
a. The cells are located in the center of the adrenal gland and surrounding the central medullary vein.
LII. Suprarenal Medulla [S52]
a. There are a lot of capillaries in the medulla.
b. Histologically, you can’t identify Chromaffin cells.
c. Chromaffin cells secrete catchacholamines.
d. The medulla has its own blood supply.
LIII. Chromaffin Cells [S53]
a. Secretion—2 populations—epi and NE; almost like sympathetic cells with no axons and dendrites—a kind of
neural, secretory cell.
b. Their stimulation of release is directly by innervation and stimulation of preganglionic splanchnic nerves.
c. No hormones control cells of adrenal medulla—they are under nerve stimulation completely!
LIV.
EM of the Adrenal Medulla [S54]
a. 2 populations of cells
i. The high density vesicles represent nor-epinephrine.
ii. The low density represents the epinephrine granules.
LV. Adrenal Medullary Cell Function [S55]
a. These molecules can be stored; this is a regulatory, secretory pathway.
b. The precursor is tyrosine; the cell makes this—tyrosine, dopa, dopamine to either epinephrine or norepinephrine.
c. These granules are going to be sitting there underneath the plasma membrane ready to go.
Endocrinology: 8:00-9:00 am
Scribe: Maggie Law
Friday, November 6, 200
Proof: Ashley Hollady
Dr. Cotlin
Thyroid, Parathyroid, and Adrenal Glands
Page 7 of 7
d. Once they get nerve stimulation, the signal transduction pathway will release the molecule.
e. These are stored granules just waiting to secrete and have a very immediate effect.
LVI.
Secretion from Chromaffin Cells [S56]
a. The molecules are produced in the fight for flight stage—want immediate reaction.
b. Chain of reaction is preganglionic cells synapse with the Chromaffin cells.
c. Then membrane depolarization occurs which will result in opening of Ca channels.
d. Ca will influx in and that will stimulate the release of the molecules.
e. Epinephrine is secreted in response to a pain stimulus where as nor-epinephrine is more to an emotion stimuli.
f. The effects are immediate and are flight or flight.
g. Direct blood supply, direct nerve stimulation, and direct secretion of these molecules into the blood stream.
h. Increase oxygen consumption (let’s say you have been startled and need to run), you will increased the oxygen
consumption so you can have that going on.
i. Usually also have increased heat production to keep the body warm and to up regulate activity, mobilized fat for
energy—in times of fight or flight, you need to have more energy.
j. The whole take home is you want to increase alertness, increase heart rate and increase glucoses release (ATP
release from a fat source)—breaking down glucose will give a more immediate ATP boost than mobilizing fats,
but for a long term situation, you would want to mobilize fat as well.
A pneumonic device shared with me by another student to help use remember the layers of the adrenal cortex:
It gets sweeter as you go in (GFR)--- (glomerulosa, fasciculata, and reticularis) ---salt (aldosterone), sugar
(glucocorticoid), sex (androgens)