The pituitary (hypophysis) is formed from two embryonic sources. The adenohypophysis is derived from the oral ectodermof Rathke’s pouch and is regulated through a hypophyseal portal system carrying factors that stimulate or inhibit secretion. The anterior pituitary contains acidophils, which produce prolactin and growth hormone (GH), and basophils that produce luteinizing hormone (LH), follicle-stimulating hormone (FSH),thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), and melanocyte-stimulating hormone (MSH).
The neurohypophysis is derived from the floor of the diencephalon and consists of astrocyte-like glial cells (pituicytes) and expanded terminals of nerve fibers originating in the hypothalamus. The neurohypophysis contains the hormones vasopressin and oxytocin, which are synthesized primarily in the supraoptic and paraventricular nuclei respectively.
The adrenal gland consists of two parts. The adrenal cortex, derived from intermediate mesoderm, and covered by a connective tissue capsule, consists of three zones: the zona glomerulosa produces aldosterone (a mineralocorticoid) and is regulated primarily by angiotensin II; the zona fasciculata and zona reticularis produce glucocorticoids (e.g., cortisol) and weak androgens and are regulated primarily by ACTH. The adrenal medulla, derived from the neural crest, synthesizes epinephrine and norepinephrine. Most of the blood that reaches the adrenal medulla has passed through the adrenal cortex and contains glucocorticoids that regulate the norepinephrine/epinephrine balance in the adrenal medulla through regulation of phenylethanolamine-Nmethyl-transferase. The fetal adrenal cortex functions to produce dehydroepiadrosterone, an androgen that is transported to the placenta where it serves as a precursor of estrogen.
There are a number of adrenal hormonal disorders. Congenital virilizing adrenal hyperplasia results from the deficiency of an enzyme required for cortisol production. The result is elevated ACTH and secretion of dehydroepiandrosterone from the fetal cortex causing masculinization (virilizing) of the female genitalia. The fetal adrenal cortex is a key component of the fetal-placental unit. Hypercortisolism or Cushing’s syndrome is five times more common in women than men. Cushing’s syndrome may be caused by a tumor in the corticotrophs of the anterior pituitary (Cushing’s disease), an adrenal adenoma, or administration of exogenous glucocorticoids. Addison’s disease is primary chronic adrenal insufficiency and is most often caused by autoimmune mechanisms leading to atrophy of the adrenal cortex. Elevated ACTH levels lead to hyperpigmentation especially in exposed areas of the skin or at pressure points such as the elbows and knuckles.
The thyroid gland is characterized by an extracellular hormone precursor (iodinated thyroglobulin) stored in its follicles. The follicular cells endocytose the storage product to form the thyroid hormones [triiodothyronine (T3) and thyroxine (T4)]. Scattered between the follicular cells are “C” cells (parafollicular cells), which secrete calcitonin, a hormone that reduces blood calcium levels. Diseases of the thyroid include Hashimoto’s thyroiditis, an autoimmune disease, in which autoantibodies to thyroglobulin and thyroid peroxidase (antimicrosomal antibodies) are produced.
Binding of antibodies to those molecules interferes with their uptake and function respectively. Infiltrating T cells and autoantibodies destroy the thyroid follicular cells resulting in hypothyroidism. In Hashimoto’s thyroiditis autoantibodies are also produced to the thyroidstimulating hormone (TSH) receptor. In that case, the autoantibody recognizes an epitope which results in blocking the activity of TSH. In contrast, in Graves’ disease autoantibodies are produced to the TSH receptor, but they are long-acting thyroid stimulating (LATS) antibodies.
The result is unregulated activation of the receptor and overproduction of thyroid hormones (hyperthyroidism). The parathyroid gland consists primarily of chief cells that secrete parathyroid hormone (PTH) that increases blood calcium levels by stimulating ruffled border activity in osteoclasts and decreasing renal Ca++ excretion and increasing intestinal absorption. The pineal gland contains pinealocytes that secrete melatonin and is innervated by postganglionic sympathetic fibers. Darkness stimulates the production of melatonin in the pineal.
The pancreas is both an exocrine and endocrine gland. Endocrine cells of the pancreatic islets secrete primarily insulin and glucagon, hormones that regulate blood sugar by lowering and increasing gluocse respectively.
Blood entering the islets bypasses the peripherally located glucagonsecreting cells to reach the more centrally-located insulin-producing beta cells. Blood leaving the beta cells contains insulin that influences glucagon secretion from the alpha cells. Blood leaving the islets travels to the surrounding exocrine pancreas and influences secretion from the acini. In type I diabetes mellitus formerly known as insulin-dependent diabetes mellitus (IDDM) an autoimmune reaction results in destruction of beta cells and the absence of insulin. Type II diabetes, formerly known as non-insulin-dependent diabetes, is the most common form of diabetes mellitus. Type II diabetes can occur at any age and is reaching epidemic proportions in the United States.
Type II diabetes begins with insulin resistance, a condition in which adipocytes, muscle cells, and hepatocytes cannot efficiently use insulin because of a decrease in insulin receptors or defective glucose transporter function. The beta cells are overworked and eventually lose their ability to secrete enough insulin in response to meals. Individuals who are overweight and inactive have an increased chance of developing type II diabetes. Scattered through several organ systems (e.g., digestive and respiratory systems) are enteroendocrine cells, which synthesize peptide hormones for local regulation.