lecture 6- hormonal control

metabolic homeostasis

ensuring balance between cells and what they need that’s available

elevated blood glucose- postprandial state

pancreas releases insulin, glucose transported into cells, conversion of glucose into glycogen, normalized blood glucose 

low blood glucose- fasting state 

pancreas releases glucagon, breakdown of glycogen to glucose, increased gluconeogenesis, normalized blood glucose

high-carb meal: glucose

peak of blood glucose (~1h after meal), decrease with oxidation or storage, return to fasting state (80-100 mg/dL) by ~3h

high-carb meal: insulin

parallels blood glucose concentration, anabolic hormone, glucose high = insulin high

high-carb meal: glucagon

glucagon low = insulin high, reciprocal relationship, catabolic hormone

oxidation

utilized as an energy source in body cells, glycolysis (glucose becomes pyruvate), stimulated by insulin

glycogen synthesis

conversion of glucose to glycogen stores, stored in liver and muscle tissue, stimulated by insulin

fat synthesis

glucose to acetyl-CoA to palmitate, cytosol of liver, muscle, mammary gland, adipose tissue, protection against hyperglycemia, stimulated by insulin

glycogenolysis

the breakdown of glycogen stores

gluconeogenesis

conversion of non-carbohydrate sources to glucose, amino acids, glycerol, lactate, stimulated by glucagon

glycogenolysis- liver stores

used to maintain blood glucose concentration, stimulated by glucagon

glycogenolysis- muscle stores

used as an energy source within muscle, stimulated by intracellular signals (low ATP, contraction)

pancreatic release- beta cell

beta cell releases insulin decreasing blood sugar, stimulated by high blood glucose, some amino acids, inhibited by low blood glucose to increase protein synthesis 

insulin release from pancreatic β-cell

GLUT2 glucose transporter, glucokinase phosphorylated, glycolysis, pyrite, increase ATP, closes K+ channel, increase calcium, insulin released by exocytosis secretory vesicles 

increase blood glucose

insulin release, decrease lipolysis (fat breakdown), increase glycolysis, glycogen synthesis, fat synthesis, and protein syntheses 

pancreatic release- alpha cell

alpha cell releases glucagon which increases blood sugar, stimulated by low blood  glucose, some amino acids, inhibited by insulin

glucagon signaling (not in muscle cells)

transmembrane G protein-coupled receptor, expressed in the liver (high), kidneys, adrenal glands, adipose tissue, GI tract, and pancreas

glucagon binding

conformational change triggers GDP-GTP exchange, release of α subunit

activation of adenylate cyclase 

converts ATP to cAMP (2^nd messenger), increased PKA activity, phosphorylation leads to activation or inactivation of downstream targets

only insulin and glucagon

are synthesized and released in direct response to changing levels of fuels in the blood 

decrease blood glucose 

decrease glycolysis, increase glycogenolysis, gluconeogenesis, and lipolysis (fat breakdown)