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.

Calcitonin generally antagonizes the effect of parathyroid hormone (PTH). When the c-cells of the thyroid sense a high calcium level, they will secrete calcitonin. Calcitonin then serves to inhibit osteoclasts and stimulate osteoblasts, promoting osteogenesis and sequestration of blood calcium into the bone matrix.

In contrast, parathyroid hormone stimulated osteoclasts and inhibits osteoblasts, causing degeneration of the bone matrix and increase in blood calcium levels.

Human chorionic gonadotropin is a water-soluble hormone that is secreted from the placenta, and stimulates the corpus luteum to grow and release estrogen and progesterone. It is vital for the maintenance of the uterine environment for the fetus to grow and develop.

Luteinizing hormone and follicle-stimulating hormone regulate ovulation and the menstrual cycle, while testosterone is responsible for development of male secondary sex characteristics.

Testosterone is produced by the Leydig cells of the testes after stimulation by luteinizing hormone. Testosterone is responsible for the development of male secondary sexual characteristics such as deeper voices, increased muscle mass, testicular development, and pubic hair. 

Adrenocorticotropic hormone promotes release of cortisol in response to prolonged stressors, and estrogen is responsible for the development of sexondary sex characteristics in females.

There are three main classes of hormones: peptide hormones, steroid hormones, and tyrosine-derivatives. Peptide hormones act by binding to plasma membrane receptors. They are large and polar, preventing them from crossing the plasma membrane. Steroid hormones and tyrosine-derivatives, on the other hand, are lipid soluble and are able to cross through the plasma membrane and bind to receptors in the cytosol.

We know from the base of the question that this drug has similar chemical properties to testosterone. Testosterone is a steroid hormone; thus, our drug likely acts in a similar manner to steroid hormones by crossing the membrane and entering the cell to elicit its effects.

None of the groups have a pre-injection blood glucose level greater than 120mg/dL, indicating that none of the groups have diabetes.

Groups B and C, however, have elevated final blood glucose levels after the glucose challenge, indicating that these groups have glucose intolerance.

The mice need to be fasted to control for consuming meals at irregular times. For example, if one mouse ate shortly before the test, it would have higher blood glucose levels than a mouse that did not, which would complicate the results. Fasting ensures that the mice have a controlled base blood glucose level before the injection.

Because the mice are injected with glucose, the mice do not need to orally consume the glucose for the test. While low blood glucose after a fast will also lower insulin levels, the insulin levels are never measured in the experiment and would not be a good explanation for fasting the mice.

The total amount of pancreatic insulin is affected by the number of beta cells and the amount of insulin produced by each beta cell; therefore, an increase or reduction of pancreatic insulin cannot be used to distinguish the two possibilities. Insulin levels in the pancreas could be reduced due to lower cell numbers or due to less production from a large number of cells. There is no way to differentiate these two causes.

Measuring the mass of beta cells, and to an extent calculating the amount of beta cell death, can determine if there are fewer beta cells in the pancreas. Additionally, using an equal number of beta cells and measuring insulin secretion can determine if beta cell function is impaired.