Pancreas Physiology

Question 1

Storage of energy sources

Answer 1

Skeletal Muscle and Liver –> glycogen (enough to last ~12 hrs)
Adipose tissue -> triglycerides
Brain –> NO STORAGE

Question 2

Fasting State

Answer 2

• brain likes/prefers glucose –> when not available, it uses ketone bodies which are a product of FFA beta oxidation –> they are converted to acetyl-CoA to produce energy in TCA cycle
• TAG stores break down to form FFA and glycerol
• liver increases gluconeogenesis and glycogenolysis
• muscle induces proteolysis to increase AA for gluconeogenesis

Question 3

Insulin’s effects

Answer 3

• inhibits breakdown of fat/adipose tissue by inhibiting the intracellular lipases that hydrolyze TAG
• promotes accumulation of TAG in fat cells by facilitating entry of glucose into adipocytes

Question 4

Fed State

Answer 4

INSULIN dominates

- increase glucose oxidation, glycogen synthesis, fat synthesis, protein synthesis

Question 5

Fasted State

Answer 5

GLUCAGON dominates

- increases glycogenolysis, gluconeogenesis, ketogenesis

Question 6

Innervation of islet of Langerhans

Answer 6

Sympathetic –> inhibit insulin and amylin (fight/flight)

Parasympathetic -> activate insulin secretion

Question 7

Feedback mechanisms on insulin

Answer 7

Resulting change in plasma glucose (either up/down) will negatively feedback on insulin or glucagon

• decrease in glucose = inhibit insulin
• increase in glucose = inhibit glucagon

Question 8

Insulin and C-peptide

Answer 8

insulin is composed of 2 chains with a C-chain attached

• when insulin is cleaved into active form, C-peptide is also released with it
• way to measure endogenous insulin production

Question 9

Amylin

Answer 9

co-packaged and co-secreted with insulin in 1:1 ratio

• very short half-life
• inhibits glucagon secretion, induces satiety

Question 10

Glucagon

Answer 10

produced by alpha cells, synthesized from a proglucagon molecule

• increased by hypoglycemia, inhibited by amylin
• increases with sympathetic and parasympathetic stimulation
• GPCR –> Gsalpha –> increase cAMP –> increase PKA

Question 11

Somatostatin

Answer 11

delta-cells produce it, triggered by increased insulin

- SST inhibits insulin, glucagon, and ghrelin

Question 12

Ghrelin

Answer 12

hunger hormone, increases during fasting

- promotes glucagon secretion and inhibits insulin and SST

Question 13

Incretins

Answer 13

promote insulin release after eating –> during intestinal phase

• GLP-1 = stimulates insulin in high glucose situations
  
  • secreted by intestinal L cells = part of proglucagon molecule
  • degraded by dipeptidyl peptidase-4
• GIP = produced by K cells

Question 14

“Incretin Effect”

Answer 14

oral glucose has “normal” response by insulin
IV glucose barely raises insulin levels
- indicates importance of incretins

Question 15

GLUT 1 transporter

Answer 15

most cells

Question 16

GLUT 2 transporter

Answer 16

liver, beta cells, kidney, hypothalamus, intestine

- activated by insulin

Question 17

GLUT 3 transporter

Answer 17

neurons, placenta, testes

Question 18

GLUT 4 transporter

Answer 18

skeletal and cardiac muscle, fat

- ACTIVATED BY INSULIN

Question 19

GLUT 5 transporter

Answer 19

mucosal surfaces in small intestine

- primarily fructose carrier

Question 20

Pancreatic Beta Cell

Answer 20

cholinergic stimulation increases secretion of insulin
adrenergic stimulation decreases secretion of insulin
GLP-1 and GIP stimulate release of Ca, which induces insulin release