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Flashcards in Pancreas Physiology Deck (20):
1

Storage of energy sources

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

2

Fasting State

- 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

3

Insulin's effects

- 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

4

Fed State

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

5

Fasted State

GLUCAGON dominates
- increases glycogenolysis, gluconeogenesis, ketogenesis

6

Innervation of islet of Langerhans

Sympathetic --> inhibit insulin and amylin (fight/flight)
Parasympathetic -> activate insulin secretion

7

Feedback mechanisms on insulin

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

8

Insulin and C-peptide

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

9

Amylin

co-packaged and co-secreted with insulin in 1:1 ratio
- very short half-life
- inhibits glucagon secretion, induces satiety

10

Glucagon

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

11

Somatostatin

delta-cells produce it, triggered by increased insulin
- SST inhibits insulin, glucagon, and ghrelin

12

Ghrelin

hunger hormone, increases during fasting
- promotes glucagon secretion and inhibits insulin and SST

13

Incretins

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

14

"Incretin Effect"

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

15

GLUT 1 transporter

most cells

16

GLUT 2 transporter

liver, beta cells, kidney, hypothalamus, intestine
- activated by insulin

17

GLUT 3 transporter

neurons, placenta, testes

18

GLUT 4 transporter

skeletal and cardiac muscle, fat
- ACTIVATED BY INSULIN

19

GLUT 5 transporter

mucosal surfaces in small intestine
- primarily fructose carrier

20

Pancreatic Beta Cell

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