Biochem 43

3-6 minutes

Beta cells inhibit alpha cells through endocrine mechanisms and alpha cells inhibit beta through paracrine mechanisms

Long arm of chromosome 3

SS-14, inhibits the release of growth hormone.

prosomatostatin, SS-28. 7-10 times more potent in inhibiting GH release then SS-14

sulfonylurea drug that increases insulin secretion and pancreatic somatostatin, SS-28.

glucose, arginine, and leucine. Similar to what causes the release of Insulin

glucogon, vasoactive intestinal peptide, cholecystikinin. NOT insulin.

inhibitory heterotrimeric G protein receptors. As a result cAMP is inhibited and PKA inactivated.

Carcinoid tumor

3 minutes.

Somatostatin variant with a half life of 110 minutes.

It inhibits the secretion of a lot of hormones.

Treat GH secreting neoplasm

GH secreting tumor before closure of long bone growth centers.

excess GH chronically secretes after the closure of long bone growth plates

GH receptor antagonist

GH

chromosome 17

somatotrophs located in the lateral area of the anterior pituitary

GH

glucose causes the release somatostatin which in turn suppresses GH release

low glucose, increase in AA, sleep, exercise, stress

contributes to cell multiplication and differentiation. Leads to skeletal muscle and visceral growth.

Somatocrinin

Increase cAMP and calcium-calmudulin stimulation.

liver derived IGF-1, Increase in glucose

Arginine

GHRH, estrogens, Alpha agonists, Beta antagonists, Dopamine agonists, K infusion, Seritonin precursers.

somatostatin, progesterone, Alpha antagonists, beta agonists, dopamine antagonists, GH and IGF-1

starnation, anorexia, ectopic GHRH production, acromegaly, chronic renal failure, hypoglycemia.

obesity hypo and hyper thyroidism

fatty acids

it make FFA available to tissues to use as energy so glucose and amino acids are available for growth

DM

secretion of IGF-1, increase gluconeogenisis, Increase glycogen synthesis. The glycerol from lypolisis is used for gluconeogenisis.

growth

lipolysis. GH increases the sensitivity of the adipose tissues to the actions of catecholamines and decreases its lipogenic response to insulin. Impairs the glucose uptake by post-receptor insulin inhibition.

decreased glucose uptake, increased protein synthesis. The increases FFA are prefferentially used for fuel by the mucle suppressing the glucose uptake. AA uptake is increased for protein synthesis.

The receptor is bound to a tyrosine kinase that activates the JAK/STat cascade which results in the activation of transcription factors and increased mitogenic response.

IGFs

causes the same response as insulin but are more potents in there growth promotion.

development of colon, breast, prostate, and lung cancer.

IGF 1 is regulated by GH and IGF 2 from hepatic production is independent of GH control

tyrosine

AP arrives at the terminal end of the neuron and causes release of Ach which bind to nicotinic receptors on the adrenal medulla, this casues an influx of calcium and the release of epi and norepi from the chromaffin granules.

they are counter-regulatory hormones that have metabolic effects directed toward mobilizing fulels from storage for oxidation to meet the increased energy requirements of acute and chronic stress.

sleep, cold, pain, emotions, hemorrhage, exercise, hypoglycemia, infection, trauma, toxins

Ach and serotonin

paraventricular nucleus of the hypothalmus

conversion of cholesterol to pregnenolone by cholesterol dismutase. ACTH binds to a Gs receptor which stimulates adenyl cyclase, the increased cAMP activates protein kinase A which phosphorolates cholesterol dismutase.

on ACTH levels and CRH levels. During times of severe stress high cortisol levels are overridden by stress induced activity on the hypothalamus.

inhibit

cushings disease is excess cortisol due to a ACTH secreting tumor. Cushings syndrome is increase in cortisol by an adrenal cortical tumor

GC cause lipolysis and muscle breakdown to supply substrates for gluconeogenisis. GC also promote the storage of said glucose as glycogen. During times of stress this stored glycogen is released by epinephrine. Epinephrin acts as the acute alarm system

The catabolic effect of GC causes the breakdown of elastin which weakens the skin and allows it to stretch and subcutaneous tissues become torn.

due to thinning of the skin as well as cortisol induced increase in bone marrow production RBCs

trapping of blood iodine in the thyroid acinar cells. Oxidation of the iodine. Iodination of tyrosyl residues on thyroglobulin to form iodotyrosines. coupling of monoiodothyronine and diiodothyronine to for T3 and T4. Proteolytic cleavage of thyroglobulin to release free T3 and T4.

lipolysis activated by GC breaks down peripheral adipose tissue but GC also stimulate hunger this increase in food intake can cause central obesity and buffalo hump.

the pump is activated by TSH but the amount of iodine uptake is controlled by intercellular iodine concentrations.

located on the apical border of the acinar cell and oxidises the iodide forming iodium.

iodide is added to an organic compound

able to store large amounts of thyroblobulin within its colloid space.

T4 is 7 days and T3 is 1.5 days. T3 is the more active compound and T4 is eventially turned into T3. T3 has a lower affinity for thyroxine binding globulin so it is released faster.

in the thyrotropic cells of the anterior pituitary

occurs in a circadian rhythm, a surge beginning late in the afternoon and peaking before the onset of sleep. TSH is also secreted in intervals of 2-6 hours between peaks.

stimulates every aspect of thyroid hormone production

increases glycolysis and cholesterol synthesis, the cholesterol in used in the increased conversion to bile salts. Increase in the B adreonergic receptor action of gluconeogenic and glycogenolytic actions of epi

amplifies the beta adronergic effects of epinephrine on lypolysis.

Increases glucose uptake and stimulates protein synthesis. The B adrenergic effects increases the glycogenlysis.

needed for optimum insulin release

causes the release of norepinephrine.

the increase in NE release causes action potentials and the increased cellular permablity of Na and K. The increase in intercellular Na is toxic to the cell and activates Na/K ATPases to pump the Na out of the cell. At normal times the Na/K ATPase activity accounts for 20% of heat production. Increase in thyroid hormone increases these pumps and increases heat production.

DM caused by increased degradation and clearance of insulin along with the increased demand for insulin. Pt will rarely develop significant DM

Regulate the availability of substrates used for fuel oxidation

secreted by the M cells of the proximal small bowel increases secretion of gastric and peptic enzymes.

reduces gastric emptying and slows intestinal motility

inhibit gastrin secretion

both sympathetic and parasympathetic

increased by vagus nerve and suppressed by sympathetic stimulation.

high protein of low glucose will cause secretion

give patient oral load of glucose and measure GH levels. They should fall in a normal patient.

resorts fuel so that it can be rapidly available for fight of flight

25% for Dm, 33% for impaired glucose tolerance. At physiology levels GH along with cortisol have permissive effects on insulin release that are intended to act like a brake to any negative effects of GH.

enzyme linked immunosorbent assay. Plate is bound with Ig specific for the hormone. The hormone bonds to Ig1. floating Ig2 binds to the hormone, Ig3 is specific for Ig2. Ig3 has and attached enzyme that is activated by binding Ig2 and the enzyme produces a measurable product.

Monoclonal antibodies are produced to a hormone. They are mixed with serum form pt of unknown hormone concentration and a solution of radiolabled hormone of known concentration. The amount of labeled hormone that becomes bound is measured and teh amount of hormone in the patients serum is extrapolated from this measurement.