Type I diabetes occurs when the body is incapable of producing insulin, so after a meal it is necessary to inject it. Because insulin isn't being produced, the signal cascade following insulin secretion never occurs. Without insulin, when blood glucose is high it isn't taken up by the muscle cells. Glucagon release is still occurring, so fatty acids are being oxidized to provide energy. This depletes the supply of triacylglycerol. Ketone production is in fact too high in people with type I diabetes, leading to ketoacidosis, an acidification of the blood from excess ketone bodies. Glycogen synthesis would not be triggered, as glucagon would still be triggering glycogen breakdown.

The correct answer is glucagon. Epinephrine does stimulate the breakdown of glycogen and lipids, but it is an amino acid derivative, not a polypeptide. The rest are all polypeptide hormones, but with different functions. Somatostatin inhibits the release of insulin and glucagon from the pancreas. Insulin has the opposite effect of glucagon, reducing blood sugar levels by stimulating the synthesis of glycogen and fat. Ghrelin stimulates appetite.

All steroid hormones are derived from cholesterol, which is a lipid molecule with three six-membered rings and one one-membered ring; it is thus tetracyclic.

Since steroid hormones are derived from cholesterol, they are all lipid-soluble and diffuse across the plasma membrane of both their target and their secretory cells. Since they are able to diffuse through the phospholipid bilayer, their receptors are either cytoplasmic or nuclear. Also, they must be synthesized on-demand since they can't be stored in vesicles; the membrane would be unable to contain them. All hormones travel to their target tissues via the blood. Neurotransmitters are the signal molecules that are are released into the synaptic cleft.

Steroid hormones are nonpolar and hydrophobic, whereas peptide hormones are polar and hydrophilic. This means that the steroid hormones cannot dissolve in water but peptide hormones can dissolve in water. Since they are minimally soluble in water, steroid hormones are carried by special transporters in the blood.

Steroid hormones are nonpolar molecules that are synthesized from a cholesterol molecule. Recall that cholesterol is a four membered hydrocarbon ring structure; therefore, steroid hormones are synthesized from a molecule with four rings. Gonads, or sex organs, and adrenal glands are the two main sources of steroid hormones. Gonads produce several sex hormones (such as estrogen, progesterone, and testosterone) that are involved in male and female reproduction. Adrenal glands produce aldosterone, cortisol, and a few inactive sex hormones that are activated in the gonads. Aldosterone is involved in regulation of sodium reabsorption in kidneys and cortisol is involved in metabolism. Recall that steroid hormones can traverse the hydrophobic interior of membranes. This applies for both plasma and nuclear membranes; therefore, steroid hormones can have receptors inside the cytoplasm or nucleoplasm (inside the nucleus).

The question states that the synthesized hormone is soluble in water; therefore, this must be a polar molecule. The hormone involved in regulation of sodium reabsorption in kidneys is aldosterone. This is a steroid hormone that is synthesized by the adrenal glands. Since the hormone in the question is polar, it cannot be aldosterone. Recall that structure determines function. Thus, if the structures of these two hormones differ significantly, their functions will also differ significantly. Note that steroid hormones are nonpolar and will not dissolve in water. 

Steroids do have a common cyclic skeleton, but they are not only present in animal tissue; they can be found in plants as well. This cyclic skeleton has a four-ring structure, but they are not aromatic rings. The progesterone receptor is found inside cells, although recent research has also confirmed its presence on plasma membranes. Aldosterone is a mineralocorticoid, not a glucocorticoid, which is indeed secreted by the adrenal gland.

If a person is deficient in 21-hydroxlyase, the steroid pathway converting progesterone to deoxycorticosterone will be unable to continue.  Therefore, the final product of that pathway, aldosterone, will not be made.  Aldosterone acts to retain salt, and so a lack of aldosterone causes significant salt loss in patients deficient in 21-hydroxlyase.  

Steroid hormones, not peptide hormones, travel through the cell membrane and into the nucleus to directly affect transcription of DNA. The only answer choice that is a steroid hormone is cortisol.

For this question, we're being asked to identify the rate-limiting step for the creation of steroid hormones. Remember, the rate-limiting step refers to the slowest step of the overall process.

First, it's important to remember that all of the steroid hormones are initially derived from cholesterol. The pathway leading to the biosynthesis of cholesterol is very long and complex, but does not represent the rate-limiting step for steroid hormone production.

Cholesterol is either obtained from the diet, or made in the cytosol of cells. Once here, the cholesterol needs to be translocated into the mitochondrial matrix for further processing. The enzyme StAR (steroid acute regulatory protein) is able to bind cholesterol and, through a poorly understood mechanism, it is able to carry it across the hydrophilic intermembrane space as well as both mitochondrial membranes. Once inside the matrix, an enzyme of the electron transport chain called cholesterol side chain cleavage enzyme () cleaves the side chain of cholesterol to produce the new compound called pregnenolone. Pregnenolone, in turn, is able to be converted into any of the other steroid hormones depending on the enzymes present.

It turns out that the rate-limiting step of this is the translocation of cholesterol into the matrix by StAR.