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UVic BIOL 432 - Spring 2019 > Glucose Regulation > Flashcards

Glucose Regulation Flashcards

1
Q

Where in the body are glucagon receptors mainly expressed?

A

In the liver and kidneys.

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2
Q

On which human cells have insulin receptors been detected?

A

All cell types tested in the Human Protein Atlas.

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3
Q

What differentiates the effect of insulin on blood glucose from the effect of glucagon on blood glucose?

A

Insulin decreases blood glucose, while glucagon increases blood glucose.

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4
Q

Which blood glucose regulating hormones are released by the pancreatic islets?

A

Insulin, glucagon, and somatostatin.

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5
Q

Which blood glucose regulating hormones are secreted by the small intestine?

A

Glucagon-like-Peptide-1 (GLP-1) and Gastric Inhibitory Peptide (GIP) aka Glucose-dependent Insulinotropic Peptide.

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6
Q

What are 2 examples of incretins? What do they do?

A
  1. Glucagon-like-Peptide-1 (GLP-1)
  2. Gastric Inhibitory Peptide (GIP)
    Proteins that amplify the effects of insulin.
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7
Q

In the endocrine pancreas, which cells secrete insulin? Which cells secrete glucagon? Which cells secrete somatostatin? Where are all these cells located?

A

All in the Islets of langerhans.
(Inner) Insulin: β cells
(Outer) Glucagon: α cells
(Outer) Somatostatin: δ (delta) cells

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8
Q

What kind of feedback effects does insulin have on the islet cells?

A

Activates β cells, inhibits α cells.

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9
Q

What kind of feedback effect does glucagon have on the islet cells?

A

Activates α cells, β cells, and δ(delta) cells.

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10
Q

What kind of feedback effect does somatostatin have on the islet cells?

A

Inhibits α cells and β cells.

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11
Q

How are glucagon and GLP-1 similar? How are they different?

A

Similar: made from same precursor
Different: GLP-1 inhibits glucagon secretion and promotes insulin release + function

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12
Q

Describe the cause of hypoglycemia. What are some symptoms of this?

A

Blood sugar levels which are too low. Can cause loss of consciousness, brain damage, and even lethal coma.

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13
Q

Describe the cause of hyperglycemia. What are some symptoms of this?

A

Elevated blood sugar levels. Acts as a short-term appetite suppressant but can lead to diabetes mellitus: eye, kidney, heart disease + nerve damage.

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14
Q

How is diabetes mellitus brought about?

A

Either through a lack of insulin production (type 1) or development of insulin resistance (type 2).

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15
Q

How was supplemental insulin acquired for diabetics in the past? What about now?

A

Used to use pork or beef insulin, today use recombinant technology to make synthetic insulin.

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16
Q

Which 3 pathways are responsible for controlling insulin secretion in the pancreas?

A
  1. MAPK
  2. PKC
  3. PI3K
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17
Q

Why would insulin be stored in the pancreas?

A

Because it takes a while to make, so it’s important to have some on hand for instant release in response to food.

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18
Q

What ion is necessary for the release of insulin from the pancreas? What else is required?

A

Calcium and glucose stimulate the synthesis and release of insulin.

19
Q

How do pancreatic cells link blood glucose levels to insulin secretion?

A

By employing a glucose “sensor”: K+ channels coupled to metabolism which depolarizing the membrane, allowing entry of Ca2+ into the cell when glucose levels are high.

20
Q

How long does insulin last in the body once released? What gets rid of it?

A

Lasts 3-5 minutes in circulation before being degraded by insulinases in the liver, kidney (and placenta).

21
Q

Describe the 5 general steps of insulin release.

A
  1. Glucose enters the cell
  2. ATP + cAMP block K+ channel, cell depolarizes the cell. Incretins act.
  3. Ca2+ cannels open, Ca2+ enters the cell
  4. Ca2+ and cAMP/PKA cause insulin release
  5. cell repolarizes
22
Q

How do incretins GIP and GLP-1 act in the cell during the insulin-release process?

A

They increase intracellular cAMP/PKA, potentiating other steps.

23
Q

What 3 important growth factors utilize growth factor receptors/tyrosine kinase receptors?

A
  1. Insulin-like growth factor 1 (IGF-1)
  2. Insulin-like growth factor 2 (IGF-2)
  3. Insulin
24
Q

How did insulin and insulin-like growth factor (1 and 2) evolve?

A

Genes duplicated, allowing one copy to mutate without messing up the organism.

25
Q

What is the general purpose of a GLUT? Are they all the same?

A

To transport glucose into the cell. No, different cells and tissues have different types.

26
Q

What are the 3 main “storage” effects of insulin?

A

Promotes:

  1. Glucose storage as glycogen
  2. Triglycerides to store fat
  3. Protein synthesis to store amino acids
27
Q

What effect does insulin have on cell growth? What type of receptor does it target?

A

Increases cell growth by binding to growth factor receptor (tyrosine kinase receptor).

28
Q

What effect can insulin have on fetal growth?

A

Just know that it has an effect, but also can wildly affect size and gestation time of a baby.

29
Q

How does insulin regulate glucagon? What other regulatory effect does it have?

A

It can suppress glucagon transcription as well as upregulating itself.

30
Q

Describe the 4 steps of the insulin mitogenic pathway.

A
  1. Insulin binds to receptor (RTK)
  2. Receptor auphosphorylates
  3. MAPK signalling pathway activated
  4. Cell growth/gene expression
31
Q

Describe the 4 steps of the insulin metabolic pathway (4th is general, other cards are more in depth).

A
  1. Insulin binds to receptor (RTK)
  2. Receptor autophosphorylates
  3. PI3K/PKB signalling pathway activated
  4. Trigger glucose uptake by GLUT-4 and lipid/protein/glycogen synthesis
32
Q

What 2 pathways can be activated by insulin signalling (just the names)?

A
  1. Mitogenic

2. Metabolic

33
Q

What is the mechanism that allows PI3K/PKB signalling to trigger the uptake of glucose into the cell?

A

Triggers the translocation of GLUT-4 (stored in vesicles) to the membrane for glucose uptake.

34
Q

What is the alternate name for the PI3K/PKB pathway? What are all these abbreviations in full words?

A

The phosphoinositide-3-kinase / protein kinase B pathway can also be called the PI3K/Akt pathway. Akt in this context STILL MEANS protein kinase B (uuugggghhhh).

35
Q

What are the 2 effects of insulin activated PI3K/PKB signalling on the pancreas?

A
  1. Increased β cell growth

2. Increased insulin secretion.

36
Q

What are the 3 effects of insulin activated PI3K/PKB signalling on the liver?

A
  1. Increased glycogenesis.
  2. Decreased gluconeogenesis
  3. Decreased glycogenolysis.
37
Q

What are the 3 effects of insulin activated PI3K/PKB signalling on the muscles?

A
  1. Increased glucose transport
  2. Increased glycogenesis
  3. Increased protein synthesis
38
Q

What are the 4 effects of insulin activated PI3K/PKB signalling on the adipocytes?

A
  1. Increased glucose transport
  2. Increased protein synthesis
  3. Increased lipogenesis
  4. Decreased lipolysis
39
Q

What differentiates the binding of insulin to an insulin receptor from the binding of other growth factors to their receptor?

A

Insulin receptor is already a dimer, whereas other receptors form dimers upon ligand binding.

40
Q

In what order are the first 3 accessory proteins recruited to an insulin receptor?

A
  1. Insulin Receptor Substrate (IRS)
  2. GRB2 or PI3K with SH2/SH3 domains
  3. SOS
41
Q

What do SH3 proteins recognize?

A

Proline-rich regions.

42
Q

What do SH2 domains recognize?

A

Phosphorylated tyrosines.

43
Q

How are insulin receptors downregulated normally?

A

Internalization of receptors by endosomes, then fuse with lysosomes for degredation.

44
Q

How are insulin receptors downregulated if a person has chronic insuin?

A

Insulin receptor numbers are reduced (by inhibiting transcription).

UVic BIOL 432 - Spring 2019 (15 decks)

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