Physio Final - Pancreas & Diabetes

Front 1

What does each type of cell in the islet of langerhans produce?

Back 1

alpha: glucagon
beta: insulin
delta: somatostatin
PP: pancreatic polypeptide

Front 2

what type of bonds connect the alpha and beta chains of insulin?

Back 2

disulfide bridges

Front 3

What cleavage is made to proinsulin, at what branch point, to make it bioactive?

Back 3

C-peptide is cleaved out at Lys-Arg and Arg-Arg to form disulfide bridges and make it active.

Front 4

What does the GLUT2 transporter do?

Back 4

TAKES UP GLUCOSE, then converted to pyruvate,

- stimulates calcium uptake
- stimulates INSULIN release

Front 5

Where is insulin stored and what is it associated with?

Back 5

Stored in granules with ZINC

Front 6

What does Phospholipase C do, and what activates it?

Back 6

cAMP activates it.
Phospholipase C increased PKC activity and increased calcium levels.

Front 7

How does potassium play a role in insulin release?

What is DIAZOXIDE?

Back 7

It opens potassium channels on the beta cells.

Diabetes treatment that forces the potassium channels on beta cells open to force insulin release.

Front 8

What is the biochemical breakdown of insulin receptors?

Back 8

- They are a Tyrosine Kinase
- They have 2 alpha and 2 beta subunits
- alpha subunit binds insulin with its CYSTEINE rich domain

Front 9

What is Leptin?

Back 9

Thin. Made in adipocytes.
- regulates satiety, reduces appetite
- excessive body fat can result as a result of leptin not working.

reduced insulin and leptin in diabetes type II don't control appetite, which is why they become obese.

Front 10

Describe the following reversible metabolic conversions:

1) glycogenolysis
2) glycogenesis
3) gluconeogenesis
4) lipogenesis
5) lipolysis

Back 10

1) glycogenolysis: glycogen to glucose
2) glycogenesis: glucose to glycogen
3) gluconeogenesis: amino acids to glucose
4) lipogenesis: glucose to fats
5) lipolysis: fats to FFA and glycerol

Front 11

What are insulin's effects on the liver?

Back 11

ANABOLIC

1) increases glycogenesis
2) metabolizes glucose
3) inhibits glucose release
4) inhibits AA uptake / gluconeogenesis
5) inhibits ketogenesis

insulin talking to the liver: why make de novo glucose or use ketones when u have fresh glucose?

Front 12

What target tissues does insulin work on?

Back 12

Liver, Muscle, Adipose

Front 13

What is the effect of insulin on muscle tissue?

Back 13

ANABOLIC - builds muscle by taking up glucose, and also stimulates the Adipose tissue to take up glucose and make fat (Lipogenesis).

Insulin overall: take up glucose for fuel, as well as sequester it into fats.

Front 14

INSULIN = STORAGE

Back 14

INSULIN = STORAGE

Front 15

Does cardiac muscle prefer ketones or sugars?

Back 15

Ketone bodies. In diabetes there is a shift to ketones.

Front 16

What is the major action of glucagon?

Back 16

To mobilize sugar out of storage.

Front 17

What type of receptor does glucagon use?

Back 17

G protein, adenylate cyclase, cAMP, PKA, phosphorylates

Front 18

What are glucagon's effects on the liver?

Back 18

1) starvation hormone
2) stimulates hyperglycemia - breaks glycogen into glucose to make sugar available
3) important in prolonged exercise
4) upregulates glycogen phosphorylase (breaks it down)
5) decreases glycogen synthase (stop making glycogen!)
6) increases liver conversion of AA to glucose

Front 19

What does glucagon do to the muscle?

Back 19

NOTHING! It only works on the liver!

Front 20

Does glucagon response go on forever?

Back 20

No, only for 30 mins because of hepatocyte autoregulation from HYPERGLYCEMIA created by glucagon, inhibits itself.

Front 21

What are 2 diagnostic factors for diabetes?

Back 21

High blood glucose

Reduced glucose tolerance (blood glucose falls fast, flushes into urine)

Front 22

Where does all this glucose go if it isn't tolerated?

Back 22

It gets filtered and dumped by the kidney

Front 23

What happens to muscle and fat in the absence of insulin?

Back 23

Muscle and fat stores get broken down.

Front 24

Describe these treatments"
1) sulfonylurea
2) meglitinides
3) biguanides / metformin
4) TZDs / glitazones
5) alpha glucosidase inhibitors
6) injectable drugs

Back 24

all are treatment for diabetes.

INCREASE INSULIN OUTPUT: sulfonylureas (glipizide), meglitinides (repaglinide)

DECREASE LIVER GLUCOSE PRODUCTION / INCREASE INSULIN SENSITIVITY: biguanides (metformin/glucophage), TZDs (avandia / azones)

DESCREASE STARCH BREAKDOWN and ABSORPTION: alpha-glucosidase inhibitors (acarbose/precose/meglitol)

and give them insulin...
or synthetic amylin (pramlintide, synergistic effect with insulin), incretin (exanetide)

Front 25

What is insulin's effects on muscle and fat storage?

Back 25

Insulin decreases muscle anabolism (decreased build-up)

Increases lipolysis (increased free FFA in blood, lowers body fat)

Front 26

What type of fuel source does cardiac tissue prefer?

Back 26

Cardiac muscle prefers ketone bodies. Insulin lowers ketoacids

Front 27

Why is there neovascularization in the retina for diabetics?

Back 27

Clogged arteries give oxygen starved retinal cells. The cells then secrete VEGF to proliferate the capillaries, the leaky caps break and scar the retina.

Front 28

How does sulfonylurea increase insulin output from the cell?

Back 28

It closes the K+ channel and allows for depolarization.