1.Hypercalcemia is a condition in which you have too much calcium in your blood. Calcium performs important functions, such as helping to keep your bones healthy. However, too much of it can cause problems. Hypercalcemia makes it hard for calcium to do its job. Your body manages the calcium level in your blood through parathyroid hormone (PTH) and another hormone called calcitonin. Normally, PTH increases when the level of calcium in your blood falls and decreases when your calcium level rises. Your body also makes calcitonin when your calcium level gets too high. When you have hypercalcemia, your body is unable to regulate your calcium level as it normally would. The three main organs that regulate calcium levels in your blood are the small intestine, the bones, and the kidney. The small intestine is the site where dietary calcium is absorbed. Importantly, efficient absorption of calcium in the small intestine is dependent on expression of a calcium-binding protein in epithelial cells. The Bone serves as a vast reservoir of calcium. Stimulating net reabsorption of bone mineral releases calcium and phosphate into blood, and suppressing this effect allows calcium to be deposited in bone. The kidney is critically important in calcium homeostasis. Under normal blood calcium concentrations, almost all of the calcium that enters glomerular filtrate is reabsorbed from the tubular system back into blood, which preserves blood calcium levels. If tubular reabsorption of calcium decreases, calcium is lost by excretion into urine.
Do we have to include the hormones that effect it too?

2. How might over-secretion of insulin, which results in an exaggerated response to rising hypoglycemia be related to insulin resistance? In many people with type 2 diabetes who have insulin resistance, the lipolytic effects of epinephrine outweigh the effects of insulin on adipose tissue. Plasma free fatty acids increase in response to hypoglycemia in type 2 diabetes but do not in type 1 diabetes. Epinephrine secretion during hypoglycemia may therefore have a greater protective effect in insulin-resistant patients by promoting metabolic substrate release rather than storage. Epinephrine also stimulates release of glucose from the kidney, and, in people who have a deficient