Parathyroid hormone (PTH) does not enhance absorption of vitamin D through the skin.

It does, however, act independently on the bones, kidneys, and gut, to increase blood calcium. Interestingly, cancer cells in various types of cancers (breast and lung) can secrete parathyroid hormone-related protein (PTHrP), which acts similarly to PTH and can cause hypercalcemia (high serum calcium) in cancer patients.

Insulin functions to decrease blood glucose levels, causing cells to take up glucose from the blood. If someone takes too much insulin it would result in hypoglycemia, or decreased blood glucose levels. Insulin has no effect on calcium levels. Glucose is rarely found in the urine and can be a sign of extremely high blood glucose levels, or hyperglycemia.

This question requires knowledge of the negative feedback loop between the anterior pituitary hormones (FSH and LH) and the sex hormones (estrogen and progesterone). Prior to menopause, FSH and LH production is inhibited by estrogen production in the ovaries. When ovarian estrogen production decreases, during menopause, FSH and LH levels increase uninhibited.

Aldosterone functions to make the collecting duct and distal convoluted tubule in the kidneys to make them more permeable to Na+, Cl–, K+, and H+. When Na+ and Cl– are reabsorbed, water follows them into the blood, thus increasing total blood volume and raising blood pressure.

An increase in aldosterone will cause an increase in sodium reabsoption, an increase in blood osmolarity, an increase in antidiuretic hormone (ADH) release, an increase in water reabsoption, and an increase in blood volume.

Addison's disease is a disorder in which the adrenal cortex is unable to be stimulated by adrenocorticotropic hormone (ACTH). The adrenal cortex is responsible for the secretion of aldosterone and cortisol. Aldosterone is responsible for the increased reabsorption of sodium and increased excretion of potassium, leading to water retention. This process helps raise the blood pressure. Since aldosterone is not being adequately produced in a patient with Addison's disease, the patient's blood pressure will be lower than normal.

Estrogen is a very versatile hormone that regulates several biological processes, including structural roles (such as increasing fat stores and developing female reproductive organs) and reproductive roles (such as promoting ovulation and preparing the uterine lining to support a fertilized egg). In order for estrogen to have such diverse effects, it enters the cell and binds to the estrogen receptor. The estrogen-receptor complex translocates to the nucleus and binds to hormone response elements (also call estrogen response elements) to activate target gene expression. Finally, although estrogen plays a role in the differentiation and formation of the milk duct system, following birth estrogen levels are dramatically reduced because high levels of estrogen inhibit lactation.

Water moves to regions where solute concentrations are high. Because the kidney is unable to reabsorb the filtrate glucose, the urine has a high osmolarity and will draw water into the collecting duct to balance solute concentrations. The water that was part of the filtered blood volume is usually reabsorbed, but instead will be excreted. This excess loss of water will lead to decreased blood volume.

When blood glucose levels are high, the body seeks to store this additional glucose as glycogen and fat. Glycogen is stored in a process called glycogenesis, which is mainly performed in the liver. Fat can also be produced by running glycolysis and using the acetyl-CoA products to create long-chain fatty acids. Glycogenesis is stimulated by insulin action.

In contrast, when glucose is low glycogenolysis, beta-oxidation, and gluconeogenesis all occur in order to restore glucose levels. Glycogenolysis is the break down of glycogen to produce glucose. Beta-oxidation is used to produce ketone bodies as alternative energy. Gluconeogenesis is the process of making glucose from non-carbohydrates.

The thyroid hormones, T3 (triiodothyronine) and T4 (tetraiodothyronine), are synthesized and released from the thyroid gland after stimulation by thyroid-stimulating hormone (TSH) from the anterior pituitary. These two hormones serve to increase the basal metabolic rate in humans.

Cortisol secretion is stimulated by adrenocorticotropic hormone (ACTH) from the anterior pituitary, while sodium excretion is increased by atrial natriuretic hormone from the cardiomyocytes.