Pancreatic function and carb metabolism

Question 1

alpha cells

Answer 1

glucagon

Question 2

Beta cells

Answer 2

insulin, proinsulin, C peptide, amylin

most numerous of all cells

Question 3

delta cells

Answer 3

somatostatin

Question 4

F cells (PP cells)

Answer 4

pancreatic polypeptide

Question 5

Humoral communication

Answer 5

blood supply runs from center of the islet to the periphery
hormonal products in the blood can influence hormonal release from other cells
Glucagon stimulates insulin
insulin inhibits glucagon
somatostatin inhibits Ins and glucagon

Question 6

cell-cell communication

Answer 6

islet cells are connected by gap and tight junctional structures

regulates both insulin and glucagon secretion

Question 7

Neural communication

Answer 7

Ach increases insulin secretion
B-adrenergic stimulates insulin
A-adrenergic inhibits insulin

therefore sympathetic stimulation via celiac nn inhibits insulin secretion
PSNS stimulation thru vagus nn increases insulin release

Question 8

Fasting state

Answer 8

less insulin

lipids mobilized, AAs mobilized to be used in oxidation, ketogenesis and GNG

Question 9

Feeding state

Answer 9

increased ins
less mobilization of endogenous food stores
increased carb, lipid, and AA uptake
gluconeogenesis

Question 10

substances that can stimulate insulin release

Answer 10

glucose
galactose
mannose 
some AAs (arg, leu) 
keto acids
fructose 
depolarization of islet cell 
glucagon

Question 11

7 steps for insulin release

Answer 11

1) glucose enters thru GLUT2
2) Glycolysis—>increase ATP, ATP/ADH, NADH/NAD
3) increase in ATP closes K_ATP channel
4) Cell depolarizes
5) ACtivation of V-gated Ca channels
6) increased Ca influx –>increased Ca release from ER
7) activation of calmodulin which causes mobilization and release of insulin from vesicles

Question 12

exercise and insulin

Answer 12

alpha adrenergic inhibition of insulin secretion is key in preventing hypoglycemia

(exercising muscle use blood glucose, even when levels are low, so if insulin is on board, it would take up an excessive amount of glucose) also there would be no hepatic GNG, lipolysis, FA release etc

Question 13

enteric factors

Answer 13

aka incretins
augment B cell response to an oral glucose stimulus (explain why the amt of insulin released after an oral dose of ins is greater than after the same IV dose)

CCK
GLP-1
GIP

Question 14

Glycogen synthesis

Answer 14

stimulated by insulin (via GK and glycogen synthase and inhibition of glycogen phosphorylase

Question 15

Insulin effects on the liver

Answer 15

(+):
Glycogen synthesis 
glycolysis 
lipogenesis 
protein synthesis 

(-)
gluconeogenesis 
glycogenolysis 
lipolysis 
protein degradation

Question 16

Glucagon’s effects on the liver

Answer 16

release is stimulated by proteins

stimulates glycogenolysis, gluconeogenesis, ketogenesis

Question 17

Type I diabetes

Answer 17

autoimmune destruction of Beta cells in teh pancreas 
loss of insulin 
preservation of glucagon 
elevated blood glucose 
osmotic diuresis 
ketoacidosis

Question 18

Type II diabetes

Answer 18

resistance to the actions of insulin
less likely to have severe ketoacidosis bc SOME of the insulin is still recognized

associated with HTN, Ob, high LDL and TGs

predicated by metabolic syndrome and insulin resistance