(#10) Pancreas

Summary of pancreas hormones
+ adrenal cortex

Blood supply + drainage of adrenal glands

Action of aldosterone

@ Aldosterone acts on renal tubes

1) ↑ Na resorption (water comes w/ it)
(ENaC) (renal -> interstitium)
-> ↑ water retention
-> ↑ BV & BP

2) K+ & H+ excretion
(as Na+ IN, exchanged for K+ and H+ OUT)
(NaK+) (interstitium -> blood)

Action of cortisol

Cortisol release: (mainly want ↑ energy)

1) enhance metabolism (breakdown protein, lipids, gluconeogenesis)
2) immune system suppressed
3) anti-inflammatory (corticosteroid cream)
4) vasoconstriction to increase BP

Adrenal cortex produces what hormones & where

Adrenal medulla produces what hormones and where?

Aldosterone = glomerulosa

Cortisol = fasciularis

NE/Epinephrine = chromaffin cells of medulla

Aldosterone activates due to:

Cortisol activates due to:

1) kidney senses DROP in Na/K+

2) stress + circadian rhythm

Blood supply + drainage of pancreas

What’s the histology of pancreas?

Pancreatic ACNI = exocrine

Pancreatic ISLET OF LANGERHANS = endocrine (what were interested in)

Whats the difference b/w GLUT 2 & GLUT 4?

g2 = liver = insulin INDEPENDENT
- liver will uptake glucose regardless of whether insulin is there or not

g4 = muscle = insulin DEPENDENT
- only uptake glucose if insulin binds to insulin receptor (*not only, but it greatly enhances glucose uptake)

What are the different types of diabetes?

What are symptoms of diabetes?

1) Type 1 (insulin dependent)
- loss of beta cells → no insulin produced → can’t call for glut 4 transporters

2) Type 2 (insulin independent)
- low levels of insulin production
OR
- insenstivity of insulin receptors (affinity not there)
(decreased senstivity to urine)

3) Poly = excessive
- polyuria = peeing too much
- polydipsia = excessive thirst
- polyphagia = excessive eating (glucose not entering cell → eat more)

Overall effect of insulin:

Insulin binds to insulin receptor of target cell:

1) Limit fuel synthesis via inhibit:
- gluconeogenesis (don’t need to create glucose)
- glycogenolysis (don’t need to breakdown glycogen for glucose)
- lipolysis (don’t need to breakdown fats for glucose)

2) Increase fuel storage:
- glycogenesis (muscle: glucose -> glycogen)
- lipogenesis (liver: glucose -> fats)

3) Main = ↑ # of glut4 transporters to PM -> glucose INTO cell

Due to:
Too HIGH blood glucose (hyperglycemia)
- parasympathetic (vagus) (eat too much)

Overall effect of glucagon:

Glucagon binds to glucagon receptor (primarily in liver)

1) Breakdown fuel storage
- gluconeogenesis (create glucose baby)
- glycogenolysis (breakdown glycogen for glucose YO)
- lipolysis (breakdown fatty acid + glycerol)
(glycerol = fluconeogenesis; FA = fuel for cardiac myocyte + neurons)

Due to:
Too LOW blood glucose (hypoglycemia)
- sympathetic (exercise) (need ATP)