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Endo/Repro > 04a: Pancreas > Flashcards

04a: Pancreas Flashcards

1
Q

Body’s fuel sources. List them and star the largest/most efficient.

A
  1. Fat*
  2. CHO (Glycogen)
  3. Protein
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2
Q

T/F: Most tissues possess enzymatic apparatus to form free glucose from glycogen.

A

False - really only liver

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3
Q

T/F: Protein synthesis from AA occurs in all tissues.

A

True

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4
Q

Most AA released during protein breakdown are used for:

A

Gluconeogenesis (via liver)

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5
Q

T/F: Brain normally uses more Kcal/day than muscle.

A

False

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6
Q

T/F: Following meal, fuels used by muscle and liver vary, depending on meal’s composition.

A

True

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7
Q

T/F: During fed state, insulin and glucagon mediate many of the anabolic processes throughout the body.

A

True, but glucagon ONLY for processes in liver

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8
Q

Fed CHO state: what’s the liver doing with the glucose?

A
  1. E

2. Glycogen, protein, TAG synthesis

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9
Q

Fed CHO state: what’s the muscle doing with the glucose?

A
  1. E

2. Glycogen, protein synthesis

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10
Q

Fed CHO state: what’s the adipose doing with the glucose?

A
  1. E

2. TAG, protein synthesis

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11
Q

Fed protein state: the meal stimulates (insulin/glucagon) production and blood glucose levels (rise/fall/don’t change)

A

Both;

Glucagon prevents blood glucose from falling (due to insulin) since meal doesn’t have CHO

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12
Q

T/F: Brain gets no new E after a pure protein meal.

A

False - via gluconeogenesis in liver (from AA)

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13
Q

T/F: Muscle FA uptake increases during post-absorptive state.

A

True - taken from lipolysis; used for fuel

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14
Q

T/F: In brief starvation (3 days), muscle glycogen stores are deplete, but liver’s are not.

A

False - both deplete!

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15
Q

Muscle during brief starvation (3 days) (increases/decreases) use of FA for fuel. It also has increasing dependence on (X) fuel source from liver.

A

Decreases;

X = ketone bodies

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16
Q

In (brief/prolonged) starvation, muscle switches from (X) to (Y) utilization. (X) needs to be conserved for:

A

Prolonged;
X = ketone bodies
Y = FA

Brain

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17
Q

Exercising muscle: initially, (circulating/local)

(X) used as fuel. Then, switch to (circulating/local) (Y).

A

Local;
X = glycogen and TAG
Circulating
Y = FA

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18
Q

T/F: During severe exercise, muscles become increasingly dependent on FA.

A

False - glucose (more glucose-dependent fibers are recruited)

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19
Q

Exercise: the muscle’s recovery involves accelerated repletion of (X). Why is this high priority?

A

X = glycogen

So muscle is ready for any renewed demands

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20
Q

Exercise: during recovery, the muscle has enhanced sensitivity to which hormone? Why is this important?

A

Insulin (further promotes glucose uptake/glycogen formation)

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21
Q

Most, (X)%, of the pancreatic islet is composed of (A/B/D) cells, producing (Y).

A

X = 60
B
Y = insulin

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22
Q

(A/B/D) cells are primarily found in the center of the pancreatic islet. And (A/B/D) cells around the periphery. Which direction does blood flow?

A

B (insulin-secreting);
A (glucagon-secreting);

From center outwards

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23
Q

T/F: Blood flow through islet of Langerhans allows paracrine control of insulin by A (glucagon) cells.

A

False - vice versa

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24
Q

mRNA for insulin is translated initially into (X). Where does (X) go?

A

X = pre-proinsulin

Targeted (via pre- sequence) to ER

25
Q

Proinsulin is generated from (X) upon (Y) modification in which location?

A 
X = pre-proinsulin
Y = cleavage (of pre- sequence)

ER

26
Q

Pro-insulin structure: contains (X) chains of insulin, (as well as/except for) (Y).

A

X = A and B
As well as (in the middle);
Y = C-peptide

27
Q

Proinsulin becomes insulin upon (X) modification. The (Y) chains of insulin are linked by (Z).

A 
X = proteolytic cleavage (of C-peptide)
Y = A and B
Z = disulfide bridges
28
Q

Though it has no bio function, (X) is useful for measuring insulin secretion when (Y) are present.

A 
X = C-peptide (released in 1:1 ratio with insulin)
Y = Ab against insulin (ie. Type I dm)
29
Q

There’s greater insulin production following (oral/IV) glucose intake. This is due to the effect of (X), which originate from (Y).

A

Oral;
X = incretins (GLIP/GIP)
Y = endocrine cells in small bowel epithelium

30
Q

Catecholamines (stimulate/inhibit) insulin secretion.

A

Depends on receptor!

Alpha (inhibits insulin) dominates; but beta receptors stimulate insulin secretion

31
Q

Somatostatin (stimulates/inhibits) insulin secretion and (stimulates/inhibits) glucagon secretion.

A

Inhibits both

32
Q

ACh (stimulates/inhibits) insulin secretion.

A

Stimulates

33
Q

Serotonin (stimulates/inhibits) insulin secretion.

A

Inhibits

34
Q

Prostaglandin E (stimulates/inhibits) insulin secretion.

A

Inhibits

35
Q

Insulin secretion: high glucose extracellularly leads to its increase in (X) cell via entering through (Y) channel/ATPase/transporter.

A 
X = Beta
Y = GLUT-2 transporter
36
Q

Insulin secretion: Beta cell increase in glucose leads to (increase/decrease) (X) ratio, which (opens/closes) (Y).

A

Increase;
X = ATP/ADP
Closes
Y = ATP-sensitive K channel

37
Q

Insulin secretion: membrane (de/re/hyper)-polarizes due to (opening/closing) of (X). This leads to (opening/closing) of (Y) followed by (Z).

A 
Depolarizes;
Closing;
X = ATP-sensitive K channel;
Opening
Y = Ca channel
Z = exocytosis of insulin granules
38
Q

Insulin receptor is a (cytoplasmic/membrane) (X) protein with which subunit(s)?

A

Membrane;
X = RTK (transmembrane glycoprotein)

2 A and 2 B

39
Q

T/F: Both insulin and its receptor have subunits linked by disulfide bridges.

A

True

40
Q

Insulin receptor is mutated and can’t bind insulin. Which domain/subunit has gone awry?

A

Alpha

41
Q

(A/B) subunit of insulin receptor is trans-membrane protein that has role in (X) function.

A

B;

X = signal transduction

42
Q

Following auto-phosphorylation of insulin receptor, phosphorylation of (X) proteins begins insulin cascade.

A

X = docking (IRS-1/2)

IRS = insulin-receptor substrates

43
Q

The main mechanism for insulin clearance is:

A

Receptor-mediated endocytosis

44
Q

Glucose utilization by (X) tissues is determined, in large part, by that rate of transportation into cells.

A

X = muscle and adipose (GLUT-4 transporter)

45
Q

T/F: Glucose uptake into cell is rate-limiting step for its metabolism in all tissue.

A

False - not those with GLUT-2 receptors (ie. liver, beta-cells)

46
Q

GLUT (2/4) is a low affinity, (high/low) capacity transporter.

A

GLUT-2;

High capacity

47
Q

Insulin (increases/decreases) K movement into cells. The mechanism behind this is an (increase/decrease) in (X) activity.

A

Increases;
Increase;
X = Na/K ATPase

48
Q

Treating Type I diabetic with insulin: must be done with care to prevent (hyper/hypo)-kalemia.

A

Hypokalemia (insulin increases K uptake into cells)

49
Q

Three main factors stimulating glucagon secretion.

A
  1. Falling glucose levels
  2. Sympathetics
  3. Increase in free AA
50
Q

Glucagon has most of its effects in which tissue type?

A

Liver!!

51
Q

T/F: Most (80-90%) of glucagon is removed from blood on its first pass through the liver.

A

True

52
Q

T/F: Glucagon has no direct effect on glucose uptake by muscle.

A

True

53
Q

“Three polys” indicative of (X) disease. List them.

A

X = diabetes mellitus

  1. Polyuria
  2. Polydipsia
  3. Polyphagia
54
Q

T/F: In diabetes mellitus, both glucose and ketones appear in urine.

A

True

55
Q

Seriously affected, untreated type II DM: (hyper/hypo)-glycemia with (X) symptom can result in (ketotic/nonketotic) syndrome. This leads to coma and death.

A

Hyperglycemia;
X = dehydration

Nonketotic

56
Q

Type II DM: usually (low/high) likelihood of ketoacidosis because…

A

Low;

Small amount of insulin activity is sufficient to dampen ketone formation

57
Q

The classic “three pathys” of (X) disease. List them.

A

X = long-term DM

  1. Neuropathy
  2. Retinopathy
  3. Nephropathy
58
Q

T/F: More than half of all diabetics have some form of neuropathies.

A

True

Endo/Repro (15 decks)

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