Random high yield things from Bessesen lectures Flashcards

1
Q

In what way is gluconeogenesis different from glycolysis?

A
  • It runs in reverse

- Goes from pyruvate –> oxaloacetate –> PEP instead of straight backwards

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2
Q

Kids who can’t burn fat via TCA cycle present as what?

A

Hyperglycemia

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3
Q

What tissue is most important source of glucose in blood?

A

Liver & Kidney because have G6P-ase (enzyme). Liver > Kidney

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4
Q

What pathway level is responsible for a diabetic increased glucose level?

A

Gluconeogenesis

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5
Q

What is the source of the carbons that make the glucose that is in a fasting diabetic’s blood?

A

Lactate from RBCs

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6
Q

If a baby can’t sleep through the night, what is happening?

A

He is fasting and gets a neurologic problem. Depends upon his liver to produce glucose for his brain.

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7
Q

Tissues and glycogen

A

Muscle - its own use

Liver - whole body

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8
Q

Where does the glycogen pathway start and end?

A

Starts at glycogen

Ends at glucose-6-P (which goes on to glucose)

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9
Q

Explain coordinate regulation of glycogen

A

You are either going to make glycogen or break it down, you won’t do both together

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10
Q

UDP is a ___ form of glucose

A

high energy

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11
Q

What is function of branched structure of glycogen

A
  1. Rapid mobilization to glucose

2. Rapid storage as glycogen

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12
Q

What serves as a protein anchor to start glycogen chain?

A

Glycogenin

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13
Q

Which enzymes are critical for glycogen formation?

A

Glycogen synthase; only gives linear 1-4 structure. You need a branching enzyme (4:6 transferase) that counts 5 glucoses in to make a 1-6 bond for the branch.

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14
Q

Contrast the functions of glycogen in the liver vs. muscle

A
  1. Liver -> has glucose-6-phosphatase and can therefore turn it into glucose for the blood. 400g, doesn’t last you very long
  2. Muscle - does not have the G6P enzyme, so it ends up using glycogen (via G6P input into glycolysis) for energy
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15
Q

Key steps of glycogen (forward and backward pathway)

A
  1. Forward to glycogen: Glycogen synthase from UDP-glucose –> Glycogen
    Branching enzyme as well.
  2. Backward to G6P: Glycogenphosphorylase for Glycogen –> Glucose 1-P
    Debranching enzyme as well.
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16
Q

In the liver, what things inhibit glycogen breakdown?

A
  1. Glucose
  2. ATP
  3. G6P
17
Q

In the muscle, what things inhibit & stimulate glycogen breakdown?

A
  1. G6P - inhibit
  2. ATP - inhibit

These are indicators of exercise, which should stimulate breakdown

  1. Ca++ - stimulate
  2. AMP - stimulate
18
Q

Covalent modifiers of glycogen phosphorylase

A
  1. Glucagon phosphorylates glycogen phosphorylase via phosphorylation of glycogen phosphorylase kinase –> glycogen breakdown
  2. Insulin dephosphorylates glycogen phosphorylase kinase and glycogen phosphorylase (by glycogen phosphorylase kinase)
19
Q

When is glycogen phosphorylase kinase active? What is its role?

A

Active when it is phosphorylated

Role: put a phosphate group on glycogen phosphorylase to make it active

20
Q

Catabolic vs. Anabolic

A

Catabolic: associated with energy
Anabolic: associated with structure & function

21
Q

2 functions of HMP Shunt

A
  1. Make NADPH (for synthesis of lipids)

2. 5-C skeleton (ribose sugars) for nucleotide synthesis

22
Q

Young patient comes in, treated for a UTI with a sulfa drug. They were jaundiced at birth and now have increased retic count, indirect bili, and free Hgb. What is the most likely cause of her problem? Why?

A

She is G6PD deficient
Gets a hemolytic anemia because it is necessary for the regeneration of NADP+ from glutathione reductase. Cannot relive the oxidant stress of drugs without G6PD.

23
Q

How can you distinguish between insulin you give someone and the insulin they make?

A

Measure C-peptide as this is the molecule of endogenous insulin production

24
Q

Actions of insulin

A
  1. Increase glucose uptake into muscle
  2. Increase glycogen synthesis
  3. Mitogen
  4. Na+ and H20 retention
  5. Inhibits lipolysis
  6. Inhibits ketogenesis
  7. Changes blood flow
25
Q

GLP-1

A
  1. Product of proglucagon gene from intestinal L-cells
  2. Release is rapid in response to meals
  3. Potent insulinotropic hormone (requires glucose to stimulate insulin secretion, this just potentiates it)
  4. Impaired glucose tolerance and T2D manifest with lower plasma GLP-1 than controls
26
Q

3 hormones playing a role in T2D

A
  1. Relative insulin deficiency
  2. Relative glucagon excess
  3. Relative GLP-1 deficiency