When an a meal is consumed, the digestive system is stimulated. This causes the release of secretin and cholecystokinin, hormones that are involved in digestion. Once glucose is in the bloodstream, it interacts with beta cells and causes the release of insulin. Insulin enters the bloodstream and stimulates widespread expression of the GLUT-4 receptor. Glucagon, on the other hand, counters the effects of insulin in a negative feedback loop and would not be expected to increase after a meal is consumed.

If the lack of a certain hormone can cause high calcium levels, that means the hormone acts to lower plasma calcium when it is present. Only one of the choices, calcitonin, decreases blood calcium. Parathyroid hormone (PTH) and calcitriol increase plasma calcium levels. Aldosterone and glucagon are unrelated to calcium regulation—aldosterone regulates kidney activity to increase blood pressure and glucagon increases blood sugar levels.

Of all the choices, the only one released by the anterior pituitary is TSH (thyroid-stimulating hormone). Glucagon is released from the pancreas, parathyroid hormone is released from the parathyroid glands, melatonin comes from the pineal gland, and atrial natriuretic hormone is a heart hormone.

Calcitonin lowers plasma calcium, while parathyroid hormone (PTH) increases it. Insulin and glucagon are responsible for blood glucose, not calcium.

The polysaccharides from the meal will be digested down into glucose by various enzymes in the digestive track. That glucose will be absorbed in the small intestine and travel into the bloodstream. This increase in blood glucose will cause a release of insulin to allow for tissue to take up the glucose and use it for energy. In this individual's blood, we would expect insulin to be higher than normal.

Conversely, when little blood glucose is present, glucagon is released to break down glycogen and fat into glucose that is needed for energy. Gastrin, while also involved in digestion, is closely linked to the release of hydrochloric acid, which activates pepsin to digest proteins. Gastrin is not linked to the digestion of carbohydrates and polysaccharides.

Oxytocin is not involved in digestion.

Aldosterone is a mineralcorticoid, meaning that it is released by the adrenal cortex, not the anterior pituitary.

Mineralcorticoids are also steroids, and are able to cross the cell membrane due to their lipophilic nature. Both aldosterone and antidiuretic hormone (ADH) increase blood volume by acting on different regions of the nephrons in the kidney. Finally, angiotensin-converting enzyme (ACE) inhibitors do decrease the secretion of aldosterone, since aldosterone is activated by the renin-angiotensin system and the inhibitors block a vital conversion step in this chain.

Progesterone is responsible for maintaining the uterine environment during pregnancy. In contrast, estrogen is responsible for the development of female secondary sex characteristics, and luteinizing hormone and follicle-stimulating hormone help stimulate follicle growth, ovulation, and estrogen production.

Estrogen is produced by the combination of luteinizing hormone and follicle-stimulating hormone in the ovaries. Estrogen is responsible for causing the luteinizing hormone surge through positive feedback (one of the only examples of positive feedback in endocrine biology) and the growth of the female sex organs.

Progesterone is responsible for preparing and maintaining the uterus for pregnancy.

Growth hormone is secreted by the anterior pituitary and is responsible for increased metabolism and cell growth. Growth hormone increases glucose and free fatty acid levels in the blood, increasing substrates for metabolism for other cells in the body.

Under normal conditions, spermatogenesis is somewhat inhibited. Follicle-stimulating hormone, luteinizing hormone, and testosterone can act to overcome this inhibition and promote sperm development. Testosterone, however, is produced in the testes, not the anterior pituitary.