Insulin & Glucagon - CB Flashcards
What do beta cells produce?
insulin
What do alpha cells produce?
glucagon
What do delta cells produce?
somatostatin
What do F cells produce?
Pancreastic polypeptide
What does pancreatic polypeptide do?
inhibits gallbladder contractions and pancreatic enzyme secretions
what does glucagon do?
a catabolic hormone. mobilizes energy stores
What does insulin do?
anabolic activities, energy storage
What does somatostatin do?
inhibits insulin,glucagon, gastrin, all gut hormones, and gastric acid release
Describe glucagons post translational processing. Where is it degraded?
160 AA pre-proglucagon → glucagon + glicentin, glicentin-like peptide, GLP1 and GLP2
liver (80%) and kidneys
What stimulates glucagon secretion?
hypoglycemia, increase in arginine and alanine (indicative of protein degradation), exercise, stress
What inhibits glucagon secretion?
- somatostatin
- insulin
- hyperglycemia
What is the primary target organ of glucagon? What proceses does it trigger?
Liver
Glycogen lysis, gluconeogen., liplysis
What effect does glucagon have in adipose tissue?
decreased glycolysis, increased lipoysis
Describe the processing of proinsulin?
- insulin synthesized in preproinsulin form, packed into Golgi and then into granules along with endopeptidase with trypsin-like activity → proinsulin and endopeptidase are secreted together. secretory granules contain Zn, which joins insulin molecules into hexamers
- proinsulin cleaved into → insulin and C peptide
- C peptide no known biological activity, but used to quantitate endogenous insulin production in patients receiving exogenous insulin
- crystalline Zn-insulin is basic preparation used to treat diabetes mellitus
What is the half life of insulin? where is it degraded?
insulin half life ~5-8 minutes and degraded by insulinase in liver, kidney, other tissues
How is insulin secretion regulated?
glucose stimulates the release, mediated by calcium influx
- fast component/early stage of insulin release occurs ~10 minutes of food ingestion, peaks at ~30-45 minutes
- first peak of insulin is likely release of stored insulin - fast component falls within 10 minutes
- if stimulus for insulin secretion maintained, release increases gradually during next hour
- later rise in insulin = late phase, likely due to release of newly formed insulin
decribe the phasic response of insulin after feeding.
- incretins give advance notice of feeding and stimulate insulin secretion
- oral glucose yields more insulin than does IV glucose due to prediction of rise
- CCK and GIP both enhance insulin secretion
- GLP1 similarly increases insulin during feeding - Cephalic phase – gastric acid secretion and small rise in plasma insulin mediated by vagus nerve
- intestinal phase – increased glucose from absorption = primary stimulus for insulin secretion
What affect does epinephrine binding to beta adrenergic cells have on insulin?
stimulates secretion
What affect does norepinephrine binding to alpha adrenergic cells have on insulin?
inhibits secretion (this mechanism prodominates) prevents hypoglycemia during excercise
What effects does insulin have in the liver?
promotes: glycogen syn, glycolysis, lipogenesis, protein syn
inhibits: glycogenlysis, fat oxidation, gluconeogen., ketogenesis, protein breakdown
What effects does insulin have in the muscle?
glucose uptake by GLUT4, promotes glycogenesis, glycolysis, lipgenesis, protein syn
inhibits: protein degradation
What effects does insulin have in the adipocytes?
insulin stimulates glucose uptake via GLU4
- also increases glycolysis, producing a-glycerophosphate in turn increasing esterification of fats
- stimulates synthesis of LPL which moves to surface of endothelium and releases fatty acids from chylomicrons and VLDL
What are orexigenic factors?
neurotransmitters like NPY increasing feeding
What are anorexigenic factors>
neurotransmitters inhibiting feeding like CRH (corticol tropin releasing hormone), GLP1 (glucagon like peptide), a-MSH (alpha-melanocyte stimulating hormone), cocaine-and-amphetamine related transcript (CART)
