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Physiology Block III > Pancreatic Endocrinology & States > Flashcards

Pancreatic Endocrinology & States Flashcards

1
Q

What are the 2 most important hormones in respect to absorptive and post-absorptive states?

A

Insulin, Glucagon

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2
Q

Insulin is released by:

A

Beta cells of pancreas

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3
Q

Glucagon is released by:

A

Alpha cells of pancreas

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4
Q

Glucose in blood stimulates which hormone?

A

Insulin, a spike is insulin follows a peak in glucose, and a decrease in glucagon

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5
Q

Secretion of Insulin (increases or decreases) during the absorptive state.

A

INCREASES

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6
Q

What 2 main effects does insulin have?

A

Metabolic (CHO, lipid and protein synthesis)

Growth-promoting (DNA synthesis, cell division)

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7
Q

What do the tissues do in order to keep the uptake of glucose coming in?

A

By changing it into storage forms. Glycogen in muscle and liver

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8
Q

Besides glycogen formation, what other forms can glucose be stored in?

A

In triglycerides, done in liver and adipocytes

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9
Q

What’s the only tissue type to uptake AA in Addition to glucose?

A

MUSCLE

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10
Q

The liver can form TG but doesn’t want to store it, where’s the only place that TG are stored?

A

Adipocytes

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11
Q

In a fasted state with LOW INSULIN and HIGH GLUCAGON what happens in MUSCLE tissue?

A

DECREASE glucose uptake, BREAKDOWN of glycogen + Proteins, RELEASE AA, UPTAKE FA and utilization

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12
Q

In a FASTED state with LOW INSULIN and HIGH GLUCAGON what happens in ADIPOCYTES?

A

DECREASE glucose uptake, BREAKDOWN of TG -> FA and glycerol

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13
Q

In a FASTED state with LOW INSULIN and HIGH GLUCAGON what happens in LIVER?

A

RELEASE glucose, SYNTHESIS of ketones

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14
Q

In a fasted state, why is it essential to MAINTAIN GLUCOSE levels?

A

the brain, if don’t then COMA

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15
Q

What effect does insulin have on Glucose transporters?

A

Bind of insulin triggers second messenger system to cause VESICLES that contain GLUT4 to fuse with PM and increase glucose uptake

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16
Q

What happens to GLUT4 transporters when insulin decrease?

A

Then endocytose back into vesicle form

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17
Q

Beside just increasing glucose in the cell, Insulin also increases GLYCOGEN FORMATION in the muscle cells how?

A

by stimulating the key enzyme, GLYCOGEN SYNTHASE.

and inhibiting the enzyme that breaks glycogen down, GLYCOGEN PHOSPHORYLASE

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18
Q

How does insulin increase PROTEIN SYNTHESIS in the muscle?

A

AA transport into cell, stimulating ribosomal enzymes, inhibit enzymes that break proteins down

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19
Q

In order for glucose to be stored in adipocytes, what has to happen to it?

A

Needs to go through partial glycolysis and then join with a FA to make a TG

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20
Q

Since the Liver does not store TG, how does it send it to the adipocytes for storage?

A

With VLDL

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21
Q

How are TG exited from the GI tract?

A

Endocytosis in a CHYLOMICRON

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22
Q

When the chylomicron arrives at the APIDOCYTES, what has to happen to it for it to be absorbed?

A

LIPOPROTEIN LIPASE must break it down in to FA to diffuse across membrane

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23
Q

What are the potential fates of AA in the liver?

A

Excreted as urea in urine, Form FA, metabolized to water and CO2

24
Q

Beside plasma concentrations of glucose, what else causes the release of insulin?

A

PARASYMPATHETIC ANS on muscarinic receptors on beta cells

25
Q

How do the beta cells respond to high levels of glucose to release insulin INSIDE the cell?

A

More glucose inside –> More ATP via Krebs–> closes K channels –> Ca open and influx Ca –> work as second messenger to dock Insulin vesicles –> exocytose and RELEASE

26
Q

How does sympathetic ANS effect insulin levels?

A

Releases Epinephrine which INHIBITS insulin release

27
Q

How does Gluose-dependednt insulin peptide (GIP) effect insulin levels?

A

STIMULATES secretion

28
Q

Where does Amylin come from and what does it do?

A

Released WITH insulin by BETA cells but goes to BRAIN to tell it it’s in a fed state

29
Q

What else increased intracellular Ca and thus second messages to increase insulin secretion?

A

CCK and ACh

30
Q

What decreases intracellular cAMP to DECREASE secretion?

A

Epi, Somatostatin, glucagon

31
Q

During moderate exercise, what do we expect to see in in plasma glucose, glucagon and insulin levels?

A

glucagon INCREASE (moving into a fasting state), Glucose + Insulin DECREASE

32
Q

If brain can’t have glucose what’s a substitute fuel?Who makes it?

A

Ketones synthesized in the liver as response to high glucagon levels

33
Q

Glycogen in the muscle can be broken down into 2 fates depending on if Oxygen is present or not.

A

with O2 –> Pyruvate, w/o O2 –> Lactate

34
Q

Gluconeogenesis is performed where?

A

Liver & Kidneys

35
Q

Who sends things to the liver for gluconeogenesis and what do they send?

A

Muscle –> lactate/pyruvate + AA, Adipose –> glycerol

36
Q

FA from the adipose goes into circulation to be burned by other tissues or it can go back to the liver for formation of what?

A

KETONES

37
Q

The overall effect of GLUCAGON is to INCREASE plasma concentration of ______ and __________.

A

glucose, ketones

38
Q

Which is a stronger signal - the ABSENCE of INSULIN or the PRESENCE of GLUCAGON?

A

Insulin is always the stronger signal, whether it’s present or not

39
Q

T/F. sympathetic NS increase EPINEPHRINE secretion?

A

FALSE. EPI comes from Adrenal medulla

40
Q

In addition to alpha cells, EPINEPHRINE also STIMULATES:

A

Glycogenolysis in liver and muscle, and Gluconeogenesis in liver and kidney, and lipolysis in adipocytes.

41
Q

How does EPI have all these effects?

A

By turning UP and DOWN enzyme systems

42
Q

What effect does EPINEPHRINE have on SYNTHETASE?

A

Inhibition!

43
Q

What effect does EPINEPHRINE Have on Phosphatase?

A

STIMULATE! (adrenergic input INCREASES CATABOLISM INSIDE)

44
Q

T/F. Cortisol secretion fluctuates depending on his in fed or non-fed state.

A

FALSE

45
Q

What happens in a fasting state if cortisol deficient?

A

Hypoglycemia, serious enough to interfere with brain function

46
Q

Cortisol has similar effects as:

A

Epinephrine & Growth Hormone

47
Q

How do cortisol and GH effect glucose transporters?

A

Inhibit the second messenger system so fewer GLUT4 are inserted in the membrane and glucose stays HIGH OUTSIDE

48
Q

What 4 hormones all work in synergy to OPPOSE INSULIN?

A
  1. Glucagon
  2. Epinephrine
  3. Cortisol
  4. Growth Hormone
49
Q

how do the 2 types of DIABETES differ?

A

Type 1 –> NO RELEASE of INSULIN, Type 2 –> Problem in RECEPTOR BINDING

50
Q

what’s the result of no release of insulin?

A

No Glut4 –> HIGH levels of glucose in blood –> high glucose in urine and formation of KETONES –> impaired brain function, coma, death

51
Q

What’s an effective treatment of Diabetes?

A

Type 1 –> Insulin, Type 2 –> Metformin

52
Q 
Which of the following hormones are associated with appetite? 
A. leptin
B. Ghrelin
C. Insulin
D. Neuropeptide Y (NPY)
E. All of the above
A

E

53
Q

Wheres does leptin come from?

A

Adipose tissue, released in proportion of how much fat is in storage

54
Q

So, if you have lots of TG stored in adipose tissue, what is your leptin release like?

A

Increased to DECREASE appetite

55
Q

How does leptin reduce food intake?

A

Acts on hypothalamus by inhibiting release of NPY

56
Q

What effect does leptin have on metabolic rate?

A

INCREASES it

57
Q

T/F. Both leptin and insulin are transported across the brain-barrier.

A

TRUE - as well as amylin and glucagon

Physiology Block III (8 decks)

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