Assuming proper experimental design, group A should be used as a baseline for "normal" glucose clearance rate. Any groups showing glucose levels higher than group A demonstrate impaired clearance.

Group A and group D show similar trends, with similar values for the initial and final blood glucose samples. This indicates that the injection was cleared from the blood completely over the 2-hour sample period.

Group B and C, however, show higher blood glucose levels after two hours than their initial levels, indicating that they were unable to completely clear the injected glucose from the blood during this period. Although, the glucose levels decrease after the injection, the glucose levels after two hours are still greatly elevated compared to fasting levels, suggesting a defect in glucose tolerance.

The investigators are measuring for a relationship between blood glucose level and genetic mutation. They must isolate the variation between samples to only the genetic mutation in order to get accurate results. Variation in weight will alter the blood volume and metabolism of glucose in the blood, resulting in an uncontrolled variable. The investigators needed to weigh the mice, and provide different injection amounts based on the different mouse weights. As the experiment currently stands, heavier mice will metabolize the glucose injection faster than lighter mice.

While it may be important to eventually analyze the Dia gene in females, they should not be included in the same study as males because males and females can have different rates of clearing blood glucose. The exclusion of females limits the data, but does not result in a design flaw. Similarly, sampling data every 15 minutes would give more data points (more information), but sampling every 30 minutes does not represent a design flaw. Finally, the mice need to be fasted to eliminate the possibility of a mouse eating shortly before the test, complicating the results. Injecting the mice before and after fasting would neither increase, nor decrease the validity of the results, and does not represent a design flaw.

Growth hormone (GH) causes increased calcium retention and stimulation of the immune system. It reduces liver uptake of glucose and increases lipolysis. Growth hormone also causes increased protein synthesis, muscle mass, bone mineralization, and gluconeogenesis. 

The following answer choices are all examples of anterior pituitary hormones, however, follicle-stimulating hormone (FSH) is the hormone that acts on Sertoli cells in the testes to nourish sperm and facilitate spermatogenesis.

Luteinizing hormone (LH) acts on the testes, but works on Leydig cells in producing testosterone. Adrenocorticotropic hormone (ACTH) and thyroid-stimulating hormone (TSH) do not act on the testes.

The parasympathetic nervous system is responsible for the "rest and digest" functions of the body. When digesting, the body will be storing nutrients, converting them to fat and glycogen in the liver and other tissues of the body. Insulin is responsible for the lowering of blood glucose levels and storing glucose as glycogen in the liver.

All the other hormone options would be seen when the body is active and under stress. Cortisol is triggered during long-term stress, while epinephrine is secreted in response to an immediate threat. Aldosterone is raised when water levels in the body are low, a sign of possible dehydration or drought.

When blood glucose is high, beta cells of the islets of Langerhans in the pancreas sense the high glucose and release insulin. Insulin binds to cells throughout the body and encourages production of additional glucose transporters on the cell surface in order to take up more glucose from the blood.

Glucagon, in contrast, is secreted when glucose levels are low and acts to prevent glucose uptake from the blood. It also stimulates gluconeogenesis and glycogenolysis.

When blood glucose is low, alpha cells of the islets of Langerhans in the pancreas sense the low glucose and release glucagon. Glucagon acts to prevent glucose uptake from the blood and stimulates gluconeogenesis and glycogenolysis in the liver.

In contrast, insulin binds to cells throughout the body when glucose levels are high. Insulin encourages production of additional glucose transporters on the cell surface in order to take up more glucose from the blood.

A decreased blood glucose level would cause growth hormone, glucagon, and cortisol release to protect from the effects of hypoglycemia. Growth hormone promotes cell replication, which indirectly stimulates other pathways to create free glucose. Glucagon increases glucose levels by stimulating gluconeogenesis in the liver and glycogen breakdown in the liver. Cortisol acts to increase free fatty acid levels and increases gluconeogenesis.

Insulin promotes glucose sequestration, further decreasing blood glucose.

Calcitonin, produced by the thyroid, decreases (or "tones down") the blood calcium level. Calcitonin decreases the amount of calcium in the blood by inhibiting the activity of osteoclasts, which break down bone and release calcium in the bloodstream. By inhibiting osteoclasts, calcitonin directly reduces the blood calcium level.

Parathyroid hormone, released by the parathyroid gland, increases the blood calcium level. Parathyroid hormone stimulates osteoclasts to break down bone and release calcium into the bloodstream. Insulin and glucagon are produced by the pancreas and are responsible for the regulation of blood glucose levels. Insulin lowers blood glucose and increases glycogen stores, while glucagon increases blood glucose by stimulating the conversion of glycogen to glucose in the liver. 

Significant amount of blood loss results in a sudden and large drop in blood pressure due to the decreased fluid volume in the body. To compensate for this change, the body will attempt to increase fluid retention. This is directly accomplished by increasing the level of ADH (anti-diuretic hormone) that allows reabsorption of water in the kidneys. Therefore, increased ADH level is the best response.