Introduction to Metabolism (L3-2)

Question 1

What are phase 1 and phase 2 of cellular respiration?

Answer 1

Phase 1 = Oxidation of fuels to produce NADH & FADH2

Phase 2 = Oxidative Phosphorylation produces ATP

Question 2

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

Answer 2

Carbs / protein = 4 kcal/g

Fat = 9 kcal/g

EtOH = 7 kcal/g

Question 3

Body fuel stores, in the body?

Answer 3

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

Question 4

Glucagon

Answer 4

Secreted from alpha cells

Stimulated by catecholamines (Epi/Norepi, dopamine)

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

Question 5

Insulin

Answer 5

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

Question 6

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

Answer 6

True!

Question 7

Insulin synthesis

Answer 7

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

Question 8

Insulin release from beta cells

Answer 8

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

Question 9

Glucagon signaling

Answer 9

Via GPCR

cAMP production increased by adenylate cyclase

Increases phosphorylation via PKA activation

Question 10

Insulin signal transduction

Answer 10

Receptor Tyrosine kinase

Insulin Receptor Substrate (IRS) is phosphorylated

Question 11

How does insulin inhibit glucagon?

Answer 11

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

Question 12

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

Answer 12

False! Low blood glucose!

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

Question 13

Fxn of alpha-amylase and disaccharidases

Answer 13

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

Disaccharidases: cleave disaccharides into monosaccharides

Question 14

Secondary active transporter of glucose and galactose?

Answer 14

SGLT 1

GLUT 2 transfers into circulation

Question 15

Facilitative transporter of fructose?

Answer 15

GLUT 5

GLUT 2 transfers into circulation

Question 16

Glucose-galactose malabsorption

Answer 16

AR dx, mutation in SGLT 1

tx = remove glu/galact from diet

Question 17

Which transporter is the bidirectional GLUT transporter?

Answer 17

GLUT 2

Question 18

GLUT characteristics?

Answer 18

Decreases the free energy of activation (like enzymes)

Allows glucose to cross membranes down its concentration gradient

Question 19

GLUT 1

Answer 19

Found in RBCs and blood-brain barrier (CSF)

High affinity

Question 20

GLUT 2

Answer 20

Bi-directional

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

Question 21

GLUT 3

Answer 21

Found in the brain

High affinity; major transporter in the CNS

Question 22

GLUT 4

Answer 22

Is the only GLUT that is insulin-sensitive!

Found in adipose tissue, heart muscle and skeletal muscle

Question 23

GLUT 5

Answer 23

Is a fructose transporter

Found in intestines, sperm

Question 24

Mechanism of GLUT 4 insulin dependency?

Answer 24

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

Question 25

GLUT 1 deficiency dx

Answer 25

AD dx

Infantile-onset epileptic encephalopathy

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

Question 26

Fanconi-Bickel syndrome

Answer 26

AR dx of GLUT 2

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

Hepatosplenomegaly

Question 27

Why are C-peptides important, in insulin synthesis?

Answer 27

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.