A hormone that has its receptor located on the surface of a cell will be a peptide hormone, not a steroid hormone. A steroid hormone can diffuse through the cell membrane and will find its receptor inside of the cell. The only peptide hormone listed as an answer choice is oxytocin.

Peptide hormones are hydrophilic and polar, and therefore cannot diffuse across the cell membrane to find a receptor within the cell. That answer choice actually describes how non-polar, hydrophobic steroid hormones exhibit their effects.

While it is certainly possible that a peptide hormone could have the effect of feedback inhibition on another hormone, that does not describe how most peptide hormones initially exert their effects. Likewise, a peptide hormone could eventually result in a change in plasma osmolality of the blood, but that does not describe how most exert their effects.

When insulin acts on its receptor, it has the overarching function to begin storing energy. Insulin is released when the level of glucose in the blood is high. Thus, more glucose is taken into cells, as is fat. So breakdown of glycogen and breakdown into fatty acids would not occur in the presence of insulin - these processes imply that the body is in need of energy. Moreover, the GLUT4 transporters are the main method by which glucose is taken into cells when insulin is active, so there would be increased activity of these transporters.

In this question, we're asked to determine a set of metabolic pathways that would be activated by insulin.

Firstly, let's recall what the primary function of insulin is. After consuming a meal, digestion and absorption allows for the increase in blood glucose levels and fatty acid levels. To help regulate this, insulin is secreted from the pancreas.

Insulin's function is to reduce blood sugar levels by allowing cells to absorb glucose through their plasma membranes via glucose transporters. Because cells are now taking up more glucose and thus now have a surplus of it, some of that glucose is used to produce energy via glycolysis. Additionally, excess glucose absorbed in the liver can be converted into glycogen via glycogenesis.

As for fats, insulin helps in the formation of fatty acids as opposed to their degradation. This is because after consuming a meal, a large amount of energy is available in the form of macromolecules absorbed via the breakdown of food. So rather than using stored fatty acids to supply energy, the body takes this opportunity to synthesize new fatty acids for storage.

Dipeptidyl peptidase-4 (DPP4) curbs the amount of insulin that is released in response to increased glucose. Activating DPP4 would not increase the insulin secretion. Increased ATP concentration would increase the amount of insulin released because it would activate active transporters. Inhibiting potassium channels would slow the termination of the action potential, allowing insulin to be secreted for longer. Increasing glucose in the bloodstream would activate more pancreatic cells to release insulin.

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).