Physiology: Chapter 78 Insulin, Glucagon And Diabetes

Front 1

beta cells are primarily located where in the islets?

Back 1

in the center

Front 2

What is the role of amylin?

Back 2

decrease glucagon release and decrease appetite... increase insulin release as seen with the drug praminitide

Front 3

Why do chronic diabetics have tissue wasting?

Back 3

because insulin is needed to induce protein synthesis

Front 4

What is the half life of insulin? Where is insulin degraded and what is the enzyme?

Back 4

1) 6 min and cleared in 10-15 min because it is unbound
2) liver by insulinase

Front 5

The insulin receptor is composed of what? where does insulin bind? What happens in the cytoplasmic portion?

Back 5

1) 2 alpha and 2 beta subunits
2) binds alpha
3) beta subunits autophosphorylate

Front 6

Autophosphorylation of beta receptors is an example of an enzyme linked receptor. What are the downstream events that occur?

Back 6

tyrosine kinase activates insulin receptor substrates (IRS)

Front 7

What cells of the body do not have a high response to insulin?

Back 7

neurons and brain cells, kidney, retina, RBCs

Front 8

Under what conditions is insulin not needed to move glucose into cells?

Back 8

1) during exercise muscle becomes more permeable to glucose

Front 9

What enzyme does insulin inactivate that breaks down glycogen? What enzymes does it increase in the liver?

Back 9

1) liver phosphorylase which breaks down glycogen and phosphatase which dephosphorylates glucose
2) glucokinase and glycogen synthase

Front 10

What is the brains preferred energy source?

Back 10

glucose

Front 11

glucose below 20-50 cause what?

Back 11

hypoglycemic shock characterized by nervous irritabitability that leads to fainting, seizures, and coma

Front 12

glucose in adipocytes is converted to what/

Back 12

glycerol

Front 13

Where does most fatty acid synthesis promoted by insulin occur?

Back 13

in the liver and they are sent to adipose tissue for storage

Front 14

In order for fatty acids to be made acetyl-Coa must be made. What is its precursor? What enzymes need to be activated and how are they activated to make acetylCoa into fatty acids?

Back 14

1) pyruvate via glycolysis goes to acetylCoA
2) accumulation of citrate and isocitrate in the mitochondria activate acetyl-CoA carboxylase to carboxylate ACoA to form malonyl-CoA the first step in fatty acid synthesis

Front 15

What extracellular enzyme does insulin activate to help get fatty acids into cells?

Back 15

LPL

Front 16

What enzyme in adipose cells does insulin inhibit?

Back 16

hormone sensitive lipase

Front 17

Why do diabetics get arteriosclerosis?

Back 17

LPL is blocked and synthesis of adipocyte glycerol is blocked so that fatty acids accumulate in the blood

Front 18

How does the liver respond when fatty acid levels are high in the blood and insulin is deficient? What factors are released into the blood?

Back 18

1) it converts fatty acids to phospholipids and cholesterol and releases them to blood
2) beta oxidation increases which forms more ACoA. ACoA is condensed and forms acetoacetic acid which is relesased in blood

Front 19

What effect does the absence of insulin have on acetoacetic utilization?

Back 19

it decreases its use in peripheral tissues, this why it accumulates in the blood with long term absence of insulin

Front 20

What is acetoacetic acid converted to?

Back 20

acetone and beta-hydroxybutyric acid

Front 21

What amino acids does insulin strongly promote the uptake of?

Back 21

valine, leucine, isoleucine, tyrosine, phenylalanine

Front 22

What glucose receptor is on beta cells that allows glucose to be taken up? What happens when glucose enters beta cells?

Back 22

1) GLUT-2
2) glucokinase makes G6P and this inhibits ATP-sensitive K+ channels which causes depolarization and insulin release from stored vesicles

Front 23

In the presence of glucose what hormones can increase intracellular calcium and lead to insulin release?

Back 23

glucagon, GIP, Ach, gastrin, CCK, secretin, GH, cortisol

Front 24

What hormones inhibit insulin release? What is the effect of parasympathetic stim to beta cells? What does activation of beta receptors do?

Back 24

1) NE via alpha receptors and somatostatin
2) increases insulin release
3) increases insulin release

Front 25

What effect does leptin have on insulin?

Back 25

decreases it

Front 26

from a fasting state a person immediately consumes a soda. What does the release curve of insulin look like? what happens if they drink more?

Back 26

initially very high because there is a residual of preformed insulin; however this level declines over a few minutes as the stores are deplete but returns and new insulin is made

Front 27

Amino acids in general help increase the release of insulin from beta cells in conjunction with glucose (potentiators). What amino acids in particular are the best at this?

Back 27

arginine and lysine

Front 28

What effect do progesterone and estrogen have on insulin?

Back 28

increase its release

Front 29

Why do persistent high levels of the hormones that potentiate insulin release cause diabetes?

Back 29

beta cells become exhausted and cease functioning

Front 30

What hormones are released in response to hypoglycemia?

Back 30

GH and cortisol which promote fat utilization and glucose sparing

Front 31

How does epinephrines action differ from that of GH and cortisol?

Back 31

it increases blood levels of both glucose and fatty acids. It activates hormone sensitive lipase

Front 32

what else is glucagon known as?

Back 32

hyperglycemic hormone

Front 33

glucagon promotes the release of glucose. How?

Back 33

via adenylyl cyclase leading to activation of phosphorylase a which degrades glycogen to glucose-1-phosphate which is dephosphorylated and released to blood

Front 34

In high concentrations what can glucagon do besides its effects on glucose?

Back 34

1) increase heart strength
2) increase blood flow
3) enhance bile secretion
4) inhibit gastric acid secretion

Front 35

A high protein meal with little glucose does what?

Back 35

stimulates release of glucagon

Front 36

what is the relation of glucagon and insulin to protein intake?

Back 36

the same they are both increased

Front 37

During strenous exercise is glucagon high or low?

Back 37

very high

Front 38

What increases somatostatin?

Back 38

1) increased blood glucose
2) increased amino acids
3) increased fatty acids
4) GI hormones

Front 39

What are some of the effects of somatostatin?

Back 39

1) decreased glucagon and insulin
2) decreased motility of stomach, duodenum and gallbladder
3) decreased absorption and secretion in GI tract

Front 40

severe hypoglycemia activates what?

Back 40

sympathetic nervous system to release epi

Front 41

What are the longterm mechanisms for keeping glucose levels normal during fasting?

Back 41

elevated GH and cortisol. They increase fat consumption

Front 42

Where in the body is glucose the main source of energy?

Back 42

brain, retina, germinal epithelium of gonads, RBC

Front 43

When is the usual onset of type I diabetes?

Back 43

age 14

Front 44

When does glucose appear in the urine?

Back 44

at blood threshold (180mg/dL)

Front 45

Does hypertension precede or follow renal injury?

Back 45

follows

Front 46

How does a person breathe with ketoacidosis?

Back 46

fast and deep

Front 47

When does an acidotic coma occur?

Back 47

ph 7

Front 48

do blood cations increase or decrease in uncontrolled type I diabetes?

Back 48

decrease from osmotic diuresis. Note that Cl- also decreases

Front 49

What is asthenia? It is seen with polyphagia in what conditions?

Back 49

asthenia is lack of energy and they are seen in IDDM

Front 50

What conditions can predispose someone to NIDDM?

Back 50

1) PCOD because of increased androgens resulting in insulin resistance
2) mutations of PPAR gamma
3) hemachromatosis

Front 51

When blood glucose is between 50 and 70 what happens?

Back 51

sympathetic response lets you know you are hypoglycemic under 50 and you go into coma and seizures