Insulin, Glucagon Dphy3

Front 1

1. Contrast the endocrine with the exocrine portions of the pancreas and know which cells secrete insulin, which secrete glucagon and which somatostatin

Back 1

Endocrine Islets of Langerhans: alpha-glucagon; beta-insulin; delta-somatostatin; pancreatic polypeptide (somatostatin inhibitor)-PP cells; Exocrine: acini secrete bicarbonate into duodenum

Front 2

What is somatostatin and how does it work?

Back 2

PARACRINE somatostatin inhibits Growth hormone, INHIBITS insulin, and glucagon, decreasing GI absorption [somatostain = body static = no growth]

Front 3

What stimulates PP

Back 3

hypoglycemia

Front 4

Which insulin subunit has a long halflife in blood so it's a good marker for panc function?

Back 4

C peptide

Front 5

2. List the effects of insulin on carbohydrate metabolism.

Back 5

1. Liver uptake, storage, use of glucose; 2. Glucose metabolism in muscles; 3. Glucose conversion to FA; 4. inhibit gluconeogenesis

Front 6

3. Describe the effects of insulin in promoting glucose metabolism in muscle.

Back 6

insulin increases permeability of glc into muscle cells; cells preferentially use it instead of fat

Front 7

4. Describe the mechanism by which insulin facilitates glucose uptake by liver cells.

Back 7

1. Insulin INACTIVATES Glycogen Phosphorylase, prevent glycogen breakdown; 2. Glucokinase phosphorylates glucose after entering liver, preventing it from leaving liver; 3. Glycogen synthase activity increases

Front 8

5. Recognize the major enzyme systems stimulated by insulin. (5)

Back 8

Glucogen synthase, glucokinase, pyruvate kinase, lipoprotein lipase, PFK [PK, PFK, LL, GK, GS]

Front 9

5.5 Enzymes inhibited by insulin

Back 9

Phosphorylase, Hormone sensitive lipase, glucose-6-phosphatase, pyruvate carboxylase

Front 10

6. Describe the steps required to release glycogen from the liver between meals.

Back 10

low insulin means high phosphorylase activity, releasing free glucose

Front 11

7. Describe the effect of insulin on glucose utilization by brain tissue and the significance of hypoglycemia.

Back 11

Brain cells are ALWAYS permeable to glucose so insulin doesnt play a role in uptake. BUT if blood/glc drops (20-50 mg/dL), then brain cant get enough glc - faint, seizures, coma

Front 12

8. Describe how insulin promotes fat storage.

Back 12

insulin means glucose will be metabolized and so FA get stored instead. Also, promotes FA synth, stored in adipose; LIPOPROTEIN LIPASE is activated, bringing FA into adipose; HORMONE-SENSITIVE LIPASE INACTIVATED with INSULIN so FA not broken down and glc is taken up, making glycerol to fuel FA synth

Front 13

9. Describe how the lack of insulin causes increases in plasma free fatty acids.

Back 13

HORMONE-SENSITIVE LIPASE is activated when insulin levels drop, so FA are released in minutes

Front 14

10. Describe why atherosclerosis often develops rapidly in uncontrolled diabetics.

Back 14

HSL means fats get released into blood, that also means more cholesterol

Front 15

11. Describe the mechanism of development of ketosis from lack of insulin.

Back 15

Without insulin, cells wont take up glucose and resort to smashing FAs for energy. Byproducts of FA metabolism are ketone bodies

Front 16

12. Describe the effects of insulin on amino acids and protein, and the effects of a lack of insulin on protein metabolism.

Back 16

increase glucose uptake, incrase fat storage, decrease fat release, increase protein syn, tissue growth, decrease muscle breakdwon

Front 17

14. Describe the role of insulin in switching from carbohydrate to lipid metabolism.

Back 17

turns off HSL

Front 18

15. Describe how glucagon produces hyperglycemia.

Back 18

gluconeogenesis, glycogenolysis

Front 19

16. Describe the control of glucagon secretion

Back 19

hypoglycemia

Front 20

17. List the 4 major mechanisms for regulation of blood glucose.

Back 20

1. Liver (glycogen storage); 2. Insulin/glucagon; 3. Epinephrine; 4. GH and Cortisol cause increased blood glc

Front 21

18. Describe the importance of blood glucose regulation. Recognize the normal fasting and postprandial blood glucose levels

Back 21

glucose postprandial = 120-140mg/dL; normal=100-110

Front 22

2 key signs of high blood sugar (no insulin)

Back 22

kussnaul breathing (deep/rapid); acetone breath

Front 23

19. Describe why diabetic patients lose glucose in the urine, why they get dehydrated and why they can become acidotic.

Back 23

osmotic effect - water gets pulled in to follow glc, causing polyuria

Front 24

20. Describe the various forms of treatment for diabetics.

Back 24

weight, diet, exercise; sufonoureas (inc. incsulin), metformin, acarbose, prandin, thiazoolindindiones (insulin receptor sensitivity)

Front 25

21. Describe the complications of diabetes which necessitate special precautions in dental treatments of affected patients. (Lecture)

Back 25

more detnal prbs - perio, caries, bone loss, infection

Front 26

22. Describe why larger than normal doses of insulin are required in diabetic coma.

Back 26

to bring down blood glc since levels have goten so out of control

Front 27

23. Describe the mechanism of development of "insulin shock."

Back 27

panc tumor; overmedication of insulin

Front 28

Which cells make somatostatin in panc

Back 28

delta cell (10%)

Front 29

What organelle makes proinsulin into mature insulin

Back 29

golgi apparatus

Front 30

Example of insulin effects

Back 30

inhibition of PEP carboxykinase transcription so you get inhibition of gluconeogenesis

Front 31

TF Brain glucose uptake is INDEPENDENT of insulin

Back 31

TRUE

Front 32

Insulin promotes glucose conversion to what structures?

Back 32

fatty acids

Front 33

TF inuslin is lipolytic

Back 33

false - antilipolytic

Front 34

If insulin is antilipolytic, why would a LACK of insulin INCREASE FA?

Back 34

No insulin means no fat storage mechanism, which then activates hormone sensitive lipase, hydrolyzing triglycerides. This then activates liver synthesis of phospholipids and cholesterol (which then cause atherosclerosis)

Front 35

discovery of insulin

Back 35

banting and best, 1920s, macleod

Front 36

Effect of lack of insulin on protein metabolism

Back 36

increases portein catabolism/wasting; increased AA metabolism and urea formation

Front 37

In addition to blood gluocse, what else can increase insulin secretion?

Back 37

amino acids

Front 38

at what blood/glc level is insulin secreted

Back 38

>100 mg/dl

Front 39

What drug type stimulates insulin secretion

Back 39

sulfonylureas

Front 40

function of sulfonylureas

Back 40

inhibit Katp channels and stimulate insulin secretion (depol of beta cells causes influx of ca2+, stimulating insulin secretion)

Front 41

4 things that can cause a decrease in insulin secretion

Back 41

1. Leptin; 2. alpha-adrenergic activity; 3. Somatostatin; 4. Fasting

Front 42

Increase in insulin has what effect on fat utilizaiton?

Back 42

decreases fat utilization

Front 43

Increase in insulin has what effect on fat storage?

Back 43

increases fat storage

Front 44

alpha chains are intracellular or extracellular

Back 44

extracellular

Front 45

TF beta chains of insulin receptor - extracellular

Back 45

false - span membrane

Front 46

when does hypoglycemic shock develop (mg/dl)

Back 46

20-50 mg/dL

Front 47

Insulin will breakdown fat or increase FA synthesis?

Back 47

FA synth: increases triglyceride formation for FA storage

Front 48

Insulin will cause protein breakdown or synth?

Back 48

synth - INSULIN MAKES YOU CENTRALLY FAT/STRONG

Front 49

which phase of insulin secretion is defective in type II diabetes - phase 1 or phase 2?

Back 49

phase 1 is defective in type II

Front 50

effect of leptin on insulin secretion

Back 50

leptin decreases insulin secretion

Front 51

alpha-adrenergic activity increases or decreases insulin secretion

Back 51

decrease insulin secretion

Front 52

alpha-adrenergic stimulaiton sitmulates or inhibits glucagon secretion

Back 52

inhibits glucagon secretion

Front 53

Effect of ACh, beta-adrenergic stimulation on insulin secretion

Back 53

increases insulin secretion

Front 54

leptin function

Back 54

stops you from getting fat by telling you when you're full [i've "lept" my plate of food and leapt away from the table because im full]

Front 55

effect of somatostatin on insulin secretion

Back 55

decreases insulin secretion

Front 56

5 things that decrease insulin secretion

Back 56

1. Somatostatin; 2. alpha-adrenergic; 3. Leptin; 4. blood glc; 5. Fasting [FLABS decrease insulin secretion, that's why theyre so fat]

Front 57

At 200 mg/dL, how much of an increase in insulin secretion do we see as compared to at 100mg/dL

Back 57

10x more insulin secreted at higher levels, meaning system is very robust and not linear

Front 58

Epi increases or decreases lipolysis

Back 58

increases lipolysis via HSL

Front 59

glucagon receptor eventually acts on

Back 59

adenyl cyclase (AC)

Front 60

enzyme required to convert pyruvate to PEP

Back 60

PEP Carboxykinase

Front 61

what does lipoprotein lipase do (insulin effect?)

Back 61

cleaves off the protein part so you just have the fat which can then enter the adipose (stim. by insulin)

Front 62

% pop with DM

Back 62

10% (26 million ppl)