Unit 3 Day 19 Learning Objectives

pancreas tissues

acinar cells: smaller + dark pink

islet of langerhans: larger + light pink

islet of langerhans

alpha (A) cells

beta (B) cells

delta (D) cells

PP (F) cells → pancreatic polypeptide

insulin processed by

pre-pro insulin of DBCA chain

insulin structure

5 min half life

A chain: 21 aa residues + 1 intra disulfide bond

B chain: 30 aa

insulin receptor structure

2 alpha + 2 beta subunits

insulin receptor alpha structure

extracellular

ligand binding

disulfide bonds

• btw alphas

• btw alpha + beta

insulin receptor beta structure

transmembrane

transmits signal

RTK (receptor tyrosine kinase)

disulfide bonds

• btw alpha + beta

insulin receptor mechanism of action

insulin receptor substrate (IRS) binds alpha

transmits conformational change to beta

beta auto-phospholates = activate tyrosine kinase activity

phosphor. (activates) downstream: IRS → PI3K/Akt → GLUT4 expression on plasma membrane

OR

Grb2 → MAPK (ras, raf, mek, erk, elk, transcription)

insulin functions

glucose transport systems

glycogen synthesis

cell growth (proliferation)

glucagon structure

29 aa

species variation

from large precursor (processed diff. in diff. tissues)

• GLU: glucagon

• GLP: glucagon-like peptide

insulin affect on blood sugar

decreases

(allows glucose to move from blood into cells for energy)

glucagon affect on blood sugar

increases

insulin affect on the liver

promotes glucose storage as glycogen (glycogenesis)

inhibits glucose production (gluconeogenesis/glycogenolysis)

stims. fat synthesis (lipogenesis)

glucagon affect on the liver

stims. glycogenolysis (breaks down stored glycogen into glucose)

prom. fatty acid oxidation

reduces glucose production

insulin affect on adipose tiss.

prom. energy storage

reducing fat breakdown (lipolysis)

stims. glucose + fatty acid uptake from bloodstream

stims. lipogenesis

glucagon affect on adipose tiss.

increases lipolysis

triggers fatty acid release

reduces adipogenesis (fat cell prod.)

insulin affect on muscle

glucose uptake

glycogen storage

incr. aa

stims. protein synthesis

glucagon affect on muscle

prom. breakdown of skeletal muscle

release aa for gluconeogenesis

reduces protein synthesis

somatostatin produced by

delta (D) cells of pancreas

somatostatin function

inhibits alpha cells from secreting glucagon

inhibits beta cells from secreting insulin

somatostatin stimulated by

high plasma conc. of glucose, aa, + fatty acids

somatostatin function

modulates blood glucose

paracrine stim/inhibit?

alpha stims. beta

beta inhibits alpha

delta inhibits a + b

vagus nerve function

innervates pancreas to convey signals

vagus nerve parasympathetic NS pathway

acetylcholine (ACh) → beta cells → INS

vagus nerve sympathetic NS pathway

epinephrine → alpha cells → glucagon

metabolites

glucose

aa

fatty acids

thyroid as a regulator of CHO metabolism

T3-T4 stims glycogenolysis in liver + muscle

pituitary as a regulator of CHO metabolism

ACTH, GH, + TSH: stims glycogenolysis in liver + muscle

ACTH: adrenocorticotropic hormone

adrenal as a regulator of CHO metabolism

cortex → cortisol → liver gluconeogenesis

medulla → norepinephrine → liver glycogenolysis