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Amylin
slows gastric emptying
increase satiety
co-secreted with insulin and reduces glucagon
maybe a bone impact/calcitonin?
it is similar to calcitonin
Somatostatin
Inhibits both glucagon and insulin
Inhibits GH
“Brake” for secretion of other hormones
Exogenous treatment with SS for tumors, excess GH diorders, etc.
Pancreatic Polypeptide
Stimulated by CCK
Reduced by ghrelin
slows pancreatic secretions
Reduces appetite
Slows movement of food stomach to SI
Glucagon
When blood glucose is too low
Proglucagon cleaved into either
Glucagon+ (pancreas)
GLP-1+ (gut, brain, etc.)
Binds glucagon receptor an triggers glucose formation, glycogen breakdown
Mostly in liver
Insulin
When blood glucose is too high
Proinsulin is cleaved into insulin and C-peptide
Insulin secreted into blood to stimulate glucose uptake in target cells
C-peptide has no biological function, but is used to measure insulin
role of insulin in target tissue (not necessarily necessary to know i think)
Liver
Dec glucogeogenesis
Dec glycogenolysis
Muscle
Inc glucose uptake
Adipose
Dec lipolysis
Brain
Dec appetite
Mitochondria
Dec oxidative stress
Endothelium
Inc vasodilation
Lipids
Inc HDL
dec triglyceride
Large buoyant LDL
Kidney
dec gluconeogenesis
dec albuminuria
dec glomerulosclerosis
Coordination of blood glucose
Glucagon and insulin coordinate to maintain
blood glucose at appropriate range (72-100
mg/dL)
When blood glucose levels are high
(>100 mg/dL, hyperglycemia), insulin triggers
cells to take up glucose
When blood glucose is low (<72 mg/dL,
hypoglycemia), glucagon triggers release of
glucose (and glycogen)
A1C
Test to detect avg blood suagr level over 3 months
Tests glucose coating hemoglobin
High A1C = inc (sustained) blood glucose = inc risk of diabetes
prediabetes: 5.7-6.4%
Diabetes: 6.5%+
GLUT4
Insulin binding
P13K signaling triggers exocytosis of GLUT4 to cells membrane
High GLUT4 at membrane takes up glucose from blood along concentration gradient
What are the pancreatic islets called
Pancreatic islets