glucagon. Directions to carry the glucagon kit with them at all times should be given. Patient compliance in this regard is variable to non-adherence so must be encouraged repeatedly.

an inert, volatile gas,

insulin, or malfunction of glucose-sensing or insulin delivery equipment,

diabetes prevention program (DPP) data. (if you say DPP, student might think you are referring to data with dipeptidyl peptidase (DPP) and DPP-4 inhibitors and look for DPP data!)

Oral glucose tolerance test (OGTT) at 2h postprandial

The production of NADH from ethanol metabolism inhibits gluconeogenesis.

autophosphorylate on tyrosine residues.

before

"peak,"

corrected. Furthermore, once blood glucose level decreases during management of DKA, glucose may be administered along with insulin to avoid hypoglycemia as the patient is rehydrated and the electrolyte balance is returned to normal.

"regular"

delete "used"

ketone bodies. ("ketones" and "ketone bodies" are inexact names, but as they are used in the literature and clinic, we should probably keep using these terms. However, for the written word, it is better to say "ketone bodies" than just "ketones." Not all ketone bodies are actual ketones (acetone and acetoacetate are ketones, beta-hydroxybutyrate is not a ketone).

ketone body

The increase in two of the ketone bodies, acetoacetate and beta-hydroxybutyrate, leads to acidemia.

GLP-1

plasma renal threshold

eu-glycemic, if word must be split over 2 lines. (Maybe this can't be controlled in Pressbooks?)

by the rise in ATP after

patients

recommends

Delete? I think this was referring to a figure that was removed. Fig 4 in this chapter discusses sulfonylurea.

States

resistance,

This is a repeat of a sentence used at the beginning of the DM section. Delete.

ability of the pancreas

the insulin receptor,

insulin receptor signaling pathways.

metanephrines (including the clinical analytes metanephrine and normetanephrine, derived from epinephrine and norepinephrine, respectively).

blood glucose.

Cushing

cholecystokinin (CCK)

generating glucose, (the term "gluconeogenesis" is reserved specifically for using substrates like amino acids, glycerol, pyruvate/lactate in the gluconeogenesis pathway and is not used to refer the generation of increased glucose from breakdown of glycogen.)

catabolism

counter-regulatory effects on insulin action.

hyper-

production via glycogenolysis

transmembrane

phosphorylation

insulin secretory granules.

In the second phase, the undocked insulin secretory granules are part of the reserve pool and are mobilized for exocytosis and release of their contents, while additional insulin is synthesized in the beta cell. This second phase has a lower rate of insulin release and can last for an hour or more.

phases. The first phase, which is the immediate post-meal response, begins within two minutes of nutrient ingestion. Insulin secretory granules docked to the beta cell plasma membrane are readily available to be released in this first phase.

It is a polypeptide synthesized in the beta cells of the pancreas. Proinsulin is folded in the rough endoplasmic reticulum (RER) where disulfide bonds form. Proinsulin is transported to the Golgi and then to immature secretory granules where most of the proinsulin is cleaved to form A and B chains held together by disulfide bonds, and the C-peptide is released. Mature "insulin secretory granules" fuse with the plasma membrane, and mature insulin, C-peptide and a small amount of proinsulin is released outside the cell.

glucagon. Directions to carry the glucagon kit with them at all times should be given. Patient compliance in this regard is variable to non-adherent so must be encouraged repeatedly.

before

"regular"

delete "used"

"peak,"

corrected. Furthermore, once blood glucose level decreases during management of DKA, glucose may be administered along with insulin to avoid hypoglycemia as the patient is rehydrated and the electrolyte balance is returned to normal.

ketone bodies. ("ketones" and "ketone bodies" are inexact names, but as they are used in the literature and clinic, we should probably keep using these terms. However, for the written word, it is better to say "ketone bodies" than just "ketones." Not all ketone bodies are actual ketones (acetone and acetoacetate are ketones, beta-hydroxybutyrate is not a ketone).

a volatile gas,

ketone body

The increase in two of the ketone bodies, acetoacetate and beta-hydroxybutyrate, leads to acidemia.

insulin, or glucose-sensing or insulin delivery equipment malfunction,

plasma renal threshold

GLP-1

patients

eu-glycemic, if word must be split over 2 lines. (Maybe this can't be controlled in Pressbooks?)

by the rise in ATP after

DPP data.

at 2h postprandial

Delete? I think this was referring to a figure that was removed. Fig 4 in this chapter discusses sulfonylurea.

ability of the pancreas

recommends

States

insulin receptor signaling pathways.

This is a repeat of a sentence used at the beginning of the DM section. Delete.

resistance,

the insulin receptor,

metanephrines (including the clinical analytes metanephrine and normetanephrine, derived from epinephrine and norepinephrine, respectively).

Cushing

cholecystokinin (CCK)

catabolism

blood glucose.

counter-regulatory effects on insulin action.

generating glucose, (the term "gluconeogenesis" is reserved specifically for using substrates like amino acids, glycerol, pyruvate/lactate in the gluconeogenesis pathway and is not used to refer the generation of increased glucose from breakdown of glycogen.)

Fig 10 does not show methimazole inhibiting TPO (on the follicular cell apical membrane facing the colloid) which is the drug target. This detail would connect this discussion with the one illustrated in Figure 5. If Figure 5 is redrawn as suggested, Fig 10 could also be redrawn, as it is based on Figure 5 information.

same comment as earlier- TPO is located on the apical membrane of the follicular cell, facing the colloid. This figure 14 is also based on Figure 5, so if Fig 5 is changed, Figs 10 and 14 could also be changed.

T4. Because of the similarity between TSH and a hormone that increases in pregnancy (human chorionic gonadotropin, hCG), a temporary gestational hyperthyroidism may develop with increasing hCG levels during pregnancy causing a thyrotoxicosis (discussed below).

autoimmune destruction of the anterior pituitary (hypophysis) (autoimmune lymphocytic hypophysitis)

and also

regulates the uptake of iodide via the sodium/iodide symporter, resulting in reduced organification and synthesis of thyroid hormone, a phenomenon known as the Wolff-Chaikoff effect.

a monoiodo- or diiodotyrosine side chain to DIT residues within thyroglobulin, to form a T3 or T4 residue in thyroglobulin, respectively. (These are not really T3 and T4 molecules until released from thyroglobulin via proteolysis).

pendrin mentioned below

the colloid fluid, an acellular, amorphous gel-like colloid that changes its density depending on the activity of the thyroid. The colloid portion of the thyroid contains nascent….

While methimazole and propylthiouracil (PTU) both block thyroid hormone synthesis by inhibiting the PTO enzyme, PTU also inhibits peripheral T4 deiodination to active T3 so is used when a significant reduction in circulating thyroid hormone is required, as in a thyroid storm.

to be consistent with text, change to "Graves' disease" and add "gestational thyrotoxicosis" to the other causes of hyperthyroidism

remove space

problem,

paragraph duplicates Table 3. Remove.

(T4)

hyper- and

...globulin, a carrier protein that binds to thyroid hormone in the blood.

reciprocal

"nuclear receptor" superfamily

iodide

and other inactive metabolites

as

anterior pituitary

iodide transport via pendrin protein,

"thyroglobulin by the apical plasma membrane protein thyroid peroxidase (TPO)," (Figure 5 is incorrect because TPO is on the plasma membrane, so it probably should be redrawn. However if it isn't redrawn, adding the above phrase may help with confusion over its location. If the figure 5 is redrawn, pendrin can be added on the membrane where iodide (add a negative charge on iodide I-) crosses the membrane to the colloid.)

intracellular

heterodimeric receptor

iodinated thyroglobulin with the newly formed T4 and T3 residues.

Thyroglobulin is synthesized in the thyroid follicular cells and moved via exocytosis to the colloid space where it is stored. Iodide is moved from the follicular cell to the colloid via the anion transporter protein Pendrin. (Mutations in the pendrin gene can cause Pendred syndrome, with deficiencies in hearing and thyroid function).

(DIT) within thyroglobulin.

remain part of the thyroglobulin protein at this point.

iodinated

a sodium gradient resulting from the action of a

calcium and phosphate

catabolism

catabolism

catabolism

"then causes negative or positive feedback ..."

such as during pregnancy, while

Receptors activating the JAK-STAT pathway

and the cell surface receptors that activate the JAK-STAT pathway.

vitamin D, and they bind intracellular receptors in the "nuclear receptor" family.

onset. The rate of clearance of a steroid hormone also affects the total concentration of the hormone in the cell.

(also commonly called "tropic" hormone)

one would

stimulating hormone produced by the pituitary,

absence or underdevelopment of the parathyroid glands

XRH

XH,

are present predominantly in the adrenal glands and gonads.

"mostly bound" The small percentage of unbound, free hormones are the active form.

anterior pituitary

binds

anterior pituitary

anterior pituitary

polypeptide

measure serum ACTH

catecholamines are not peptide hormones but are derived from an amino acid (tyrosine). Remove catecholamines from this sentence.

(< 0.005% of general population). Acquired nephrogenic DI may present in patients on long term lithium therapy, e.g., for bipolar disorder.

(ADH) action. (Adding the word "action" covers ADH deficiency in pituitary DI as well as nephrogenic DI from vasopressin receptor (AVPR2) deficiency, and aquaporin (AQP2) deficiency.)

(aka, antidiuretic hormone, ADH)

with insulin in an "insulin tolerance test." (later in the chapter, this test is referred to in name, so the name should be given here.)

that

(TRH)

as discussed

change to: "so prolactin may be elevated in primary hypothyroidism if the lack of thyroid hormone feedback inhibition causes elevated TRH." (They didn't have thyroid yet, so the connection between low TH causing high TRH needs to be made here for them.)

GH levels

Add: "Over-the-counter growth hormone may be used by body builders and athletes with the intention of increasing muscle mass; however the efficacy and long term effects are controversial." (Reword as you wish if you want to include this application- probably good for them to know people use this OTC, but I don't know if there is good data for its value.)

used

pituitary tumor

GH levels

glucose

as shown in the bottom image.

glucose

explain what "TH" is on the graph. Maybe enlarge figure a bit to make it easier to see.

are

comma within quotes

their

period within quotes

they require

is this the prevalence in the US or world-wide?

GLUT4 translocation to the plasma membrane.

glucose

Stimulates melanin synthesis and other functions

glucose

remove semi-colon

glucose

adrenocorticotropin hormone (ACTH)

(termed releasing hormones (RH) or release inhibiting hormones (RIH))

Releases ACTH (adrenocorticotropin hormone/corticotropin), beta-endorphin, alpha-melanocyte stimulating hormone, and beta-lipotropin )

(aka growth hormone release inhibiting hormone, GHRIH)

hormones (just to be consistent with naming - they are referred to as peptide hormones later)

releases

GH excess can cause high blood glucose (hyperglycemia), insulin resistance and diabetes mellitus.

thyrotropin releasing hormone (TRH)

It would be easier to see the text if you enlarge this figure.

I will test out

spell check

This disorder occurs in three phases

receive

Each BMD standard deviation from the mean

negative 2.5 (Or put negative sign on same line as 2.5)

diagnose

"fragility fracture."

osteoprotegerin (OPG) (in case someone is reading this section without the previous ones)

bone mineral density (BMD)

greater than 4g (? - just saw this in another resource)

adenylate cyclase

increased

The volume depletion and increased bicarbonate reabsorption

Among other effects, hypercalcemia causes vasoconstriction and inhibition of the Na/K/2Cl channels in the nephron ascending loop of Henle, thereby decreasing water reabsorption in the descending loop of Henle. This results in hypovolemia and the consequent decrease in the GFR.

also called calcium-alkali syndrome,

serum calcium, low serum PTH,

Although inherited mutations in the menin tumor suppressor gene in MEN1 are recessive, the chance that an individual will acquire a somatic mutation in the other menin allele during their lifetime is so high that this inheritance is considered "autosomal dominant." (This "Two-hit hypothesis" for cancer predisposition syndromes was discussed in your previous genetics sessions.) Consequently, all three MEN syndromes (MEN1, MEN2A, MEN2B) are considered to be inherited via an autosomal dominant inheritance pattern.

dominant mutations in the RET proto-oncogene

MEN is a term used to describe three syndromes associated with certain hormone-producing neoplasms.

recessive mutation

D (calcitriol),

25-OH-vitamin D (calcidiol)

vitamin D (cholecalciferol)

add space before Circulating

1,25-(OH)2-vitamin D (calcitriol) Consider using "calcitriol" and "calcidiol" throughout the discussion to make clear that calcidiol is the most abundant form in serum and calcitriol is the active form of Vit D. These terms make it easier to read than the others. Also, these are the terms used in Fig 3.

calcitriol, the

25-OH-vitamin D (calcidiol or calcifediol)