Introduction to Metabolism (L3-2) Flashcards Preview

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Flashcards in Introduction to Metabolism (L3-2) Deck (27)
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1
Q

What are phase 1 and phase 2 of cellular respiration?

A

Phase 1 = Oxidation of fuels to produce NADH & FADH2

Phase 2 = Oxidative Phosphorylation produces ATP

2
Q

What are the values of the dietary sources of energy? (Carbs, protein, Fat, EtOH)

A

Carbs / protein = 4 kcal/g

Fat = 9 kcal/g

EtOH = 7 kcal/g

3
Q

Body fuel stores, in the body?

A

Adipose tissue (best bc low water content), glycogen and protein (worst)

4
Q

Glucagon

A

Secreted from alpha cells

Stimulated by catecholamines (Epi/Norepi, dopamine)

Release leads to:
\+ glycogenolysis
\+ gluconeogenesis
\+ lipolysis
- liver glycolysis
5
Q

Insulin

A

Released from beta cells

Increased metabolism of glucose and storage

Release leads to energy storage and growth via:
\+ glycogen synthesis
\+ fatty acid synthesis
\+ triglyceride synthesis
\+ liver glycolysis
6
Q

T/F: Insulin stimulates glucose uptake in muscle and adipose tissue only.

A

True!

7
Q

Insulin synthesis

A

Synthesized as “preproinsulin;” “pre-“ is then removed in RER

8
Q

Insulin release from beta cells

A
  1. Glucose enters cell and ATP is produced
  2. K+ channel closes, membrane depolarizes
  3. Calcium channels open, promoting fusion of vesicles
  4. Insulin is secreted
9
Q

Glucagon signaling

A

Via GPCR

cAMP production increased by adenylate cyclase

Increases phosphorylation via PKA activation

10
Q

Insulin signal transduction

A

Receptor Tyrosine kinase

Insulin Receptor Substrate (IRS) is phosphorylated

11
Q

How does insulin inhibit glucagon?

A

cAMP is lowered and phosphatases are stimulated, that reverse PKA action

12
Q

T/F: stress hormones are release by the brain in response to high blood glucose

A

False! Low blood glucose!

Also, the downstream effects of stress hormones counteract the action of insulin

13
Q

Fxn of alpha-amylase and disaccharidases

A

A-A: Cleave alpha(1,4) bonds of starch and glycogen

Disaccharidases: cleave disaccharides into monosaccharides

14
Q

Secondary active transporter of glucose and galactose?

A

SGLT 1

GLUT 2 transfers into circulation

15
Q

Facilitative transporter of fructose?

A

GLUT 5

GLUT 2 transfers into circulation

16
Q

Glucose-galactose malabsorption

A

AR dx, mutation in SGLT 1

tx = remove glu/galact from diet

17
Q

Which transporter is the bidirectional GLUT transporter?

A

GLUT 2

18
Q

GLUT characteristics?

A

Decreases the free energy of activation (like enzymes)

Allows glucose to cross membranes down its concentration gradient

19
Q

GLUT 1

A

Found in RBCs and blood-brain barrier (CSF)

High affinity

20
Q

GLUT 2

A

Bi-directional

Found in liver, kidney, pancreas; is low affinity, so only takes in glucose when concentrations are high

21
Q

GLUT 3

A

Found in the brain

High affinity; major transporter in the CNS

22
Q

GLUT 4

A

Is the only GLUT that is insulin-sensitive!

Found in adipose tissue, heart muscle and skeletal muscle

23
Q

GLUT 5

A

Is a fructose transporter

Found in intestines, sperm

24
Q

Mechanism of GLUT 4 insulin dependency?

A
  1. Insulin binds to its receptor
  2. Vesicles containing GLUT4 migrate to membrane
  3. Glucose passes through
25
Q

GLUT 1 deficiency dx

A

AD dx

Infantile-onset epileptic encephalopathy

Dx’d by low glucose and presence of lactate in CSF

26
Q

Fanconi-Bickel syndrome

A

AR dx of GLUT 2

Glucose cannot exit liver and kidneys, so hepatorenal glycogen accumulation occurs (glycogen storage dx type XI)

Hepatosplenomegaly

27
Q

Why are C-peptides important, in insulin synthesis?

A

C peptide levels in the blood can be measured to assess insulin production (ie. they can be used to distinguish Type I (no insulin) from Type II (high insulin) Diabetes). Patients who are administered insulin for the treatment of Type I Diabetes will not have C peptide in the blood, but will have active insulin (from the injections). So assays of C Peptide levels can be a more reliable measure of endogenous insulin production, than an direct measurement of insulin itself.