Metabolism 2

• • protein synthesis
  • amino acids -> proteins
  • lipogenesis
  • glycerol 3-phosphate and fatty acids -> triglyceride
  • glycogenesis
  • glucose -> glycogen

  absorptive state (actions in insulin)
• glucose -> CO2 + H2O + energy in most cells


  absorptive state (actions of insulin)
• excess glucose -> glycogen and fat (triglycerides) in liver

  • low fat foods NOT helping!


  absorptive state (actions of insulin)
• • proteolysis
  • proteins -> amino acids
  • lipolysis
  • triglyceride -> glycerol and fatty acids
  • glycogenolysis
  • glycogen -> glucose


  post-absorptive state (results of decreased insulin)
• fatty acids and ketones -> CO2 + H2O + energy in most cells

  • "glucose sparing" (for NS)


  post-absorptive state (results of decreased insulin)
• pyruvate, lactate, glycerol, and amino acids -> glucose in liver and kidney

  • gluconeogenesis (creation of new glucose)


  post-absorptive state (results of decreased insulin)
• secretion into duct and lumen


  exocrine portion of pancreas

  
• Islets of Langerhans


  endocrine portion of pancreas
• secrete insulin (peptide hormone)

  • anabolic/net storage
  • stimulates absorptive rxns
  • inhibits postabsorptive rxns

  beta cells
• secrete glucagon (peptide hormone)

  • catabolic/mobilization
  • stimulates postabsorptive state
  • inhibits absorptive state rxns


  alpha cells
• plasma glucose controls secretion

  • insulin is ___ _________ by the pituitary

  not regulated (no three gland cascade)

  
• increase in plasma insulin ->


  - ^ glucose uptake in adipocytes and muscle

  - ceases cessation of glucose output; net glucose uptake
• this also increases # of amino acid transporters

  • absorptive/net storage

  insulin
• this doesn't need insulin for glucose transport!

  • insulin-independent Glut-2 transporter


  the brain
• in exercising muscles, glucose transporters go to membrane _______ insulin stimulation

  without

  • why exercise helps improve conditions for type II diabetics
• mechanism of insulin action in muscle and fat cells

  • induce insertion of Glut-4
  • ^ ICF glucose
  • note membrane turnover, not permanent placement
  • increase in transport max is transient
  • this does NOT occur in renal epithelial cells
  • TM for nephron does not change

  
• the effect on insulin when ^ plasma glucose

  ^ insulin secretion from pancreatic islet beta cells
• the effect on insulin when ^ plasma amino acids

  ^ insulin secretion from pancreatic islet beta cells
• the effect on insulin when Incretins are present; e.g. GIP feed-forward


  ^ insulin secretion from pancreatic islet beta cells
• the effect on insulin when there's plasma epinephrine from sympathetic activity

  • fight or flight
  • mobilize fuel, not store, oppose insulin secretion

  decreased insulin secretion from the pancreatic islet beta cells
• the effect on insulin when ^ parasympathetic activity (Ach on M-AchR)

  • rest and digest
  • store fuel


  ^ insulin secretion from the pancreatic islet beta cells
• glucagon is ___ _________ by the pituitary

  • plasma glucose controls secretion


  not regulated
• glucose mobilizing

  • supported by other signals

  during post-absorptive state

  
• hypoglycemia


  low blood glucose
• epinephrine stimulates glycogenolysis in both liver and skeletal muscle, whereas glucagon does so only in the liver
• glucagon stimulates


  glycogenolysis and gluconeogenesis
• epinephrine stimulates


  glycogenolysis, gluconeogenesis, and lipolysis
• cortisol stimulates


  gluconeogenesis, lipolysis, and inhibition of glucose uptake by muscle cells and adipose tissue cells
• growth hormone stimulates


  gluconeogenesis, lipolysis, and inhibition of glucose uptake by muscle cells and adipose tissue cells
• redundancy in hormone regulation ensures fuel substrates are always available to burn
• insulin is unique; it stands alone in its role of glucose regulation

  it is the only hormone that protects against ______ plasma glucose

  excess
• at resting baseline, basal concentrations are permissive for stimulation of glucogenesis and lipolysis in the postabsorptive state


  effect of cortisol on organic metabolism
• during increasing stress, increased plasma concentrations cause:

  • increased protein catabolism
  • increased gluconeogenesis
  • decreased glucose uptake by muscle cells and adipose-tissue cells
  • increased triglyceride breakdown


  effect of cortisol on organic metabolism
• net result: increased plasma concentrations of amino acids, glucose, and free fatty acids


  effect of cortisol on organic metabolism