Hormones and Neurotransmitters - Biochemistry

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.

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.

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.

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.

Phentolamine is an alpha-antagonist. Propranolol is an beta-agonist. Epinephrine/adrenaline is the methylated form of norepinephrine/noradrenaline.

Insulin is secreted in response to high blood glucose levels, which increases cell uptake of glucose. Glycogen has the opposite effect - it stimulates glycogenolysis and lipolysis to release glucose into the bloodstream during times of fasting/starvation.

Epinephrine and glucagon are examples of hormones that affect G protein-coupled receptors like adenylate cyclase and increase levels of cAMP. The other hormones listed affect receptor tyrosine kinases and non-receptor tyrosine kinases.

Elevated arginine leads to an increase in secretion of insulin, not decreased. GIP, CCK and closing of the voltage gated potassium channels lead to an increase in secretion of insulin.

Ketone bodies, which include acetoacetate, beta-hydroxybutyrate, and acetone, are produced by the liver in the fasting state by beta-oxidation of fatty acids. They are then released into the blood stream, where they can be used as alternative energy sources for other organs, such as muscle, kidney, and brain. Apoprotein B is one of the proteins that hold lipoproteins together. Beta-carotene is a vitamin with antioxidant properties.

Epinephrine first binds to an adrenergic receptor. The activated receptor works via a G protein, and so GDP is exchanged for GTP and the protein is activated. This then causes activation of adenylate cyclase and subsequent conversion of ATP to cAMP. cAMP acts upon protein kinase A and several other effector molecules. Diacylglycerol and IP3 are second messengers that are uninvolved in this process.

Erythropoietin is a glycoprotein hormone produced in the kidney that stimulates the production of red blood cells in the bone marrow.

Glucagon is a short peptide hormone involved in triggering signal cascades in response to low blood glucose. Biotin, also known as vitamin B7, is a cofactor in fatty acid synthesis. Pyridoxal phosphate, the activated form of vitamin B6, is a cofactor in transamination reactions, among others. Epinephrine is a steroid hormone involved in the fight or flight response.