Introduction to Metabolism (L3-2) Flashcards
What are phase 1 and phase 2 of cellular respiration?
Phase 1 = Oxidation of fuels to produce NADH & FADH2
Phase 2 = Oxidative Phosphorylation produces ATP
What are the values of the dietary sources of energy? (Carbs, protein, Fat, EtOH)
Carbs / protein = 4 kcal/g
Fat = 9 kcal/g
EtOH = 7 kcal/g
Body fuel stores, in the body?
Adipose tissue (best bc low water content), glycogen and protein (worst)
Glucagon
Secreted from alpha cells
Stimulated by catecholamines (Epi/Norepi, dopamine)
Release leads to: \+ glycogenolysis \+ gluconeogenesis \+ lipolysis - liver glycolysis
Insulin
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
T/F: Insulin stimulates glucose uptake in muscle and adipose tissue only.
True!
Insulin synthesis
Synthesized as “preproinsulin;” “pre-“ is then removed in RER
Insulin release from beta cells
- Glucose enters cell and ATP is produced
- K+ channel closes, membrane depolarizes
- Calcium channels open, promoting fusion of vesicles
- Insulin is secreted
Glucagon signaling
Via GPCR
cAMP production increased by adenylate cyclase
Increases phosphorylation via PKA activation
Insulin signal transduction
Receptor Tyrosine kinase
Insulin Receptor Substrate (IRS) is phosphorylated
How does insulin inhibit glucagon?
cAMP is lowered and phosphatases are stimulated, that reverse PKA action
T/F: stress hormones are release by the brain in response to high blood glucose
False! Low blood glucose!
Also, the downstream effects of stress hormones counteract the action of insulin
Fxn of alpha-amylase and disaccharidases
A-A: Cleave alpha(1,4) bonds of starch and glycogen
Disaccharidases: cleave disaccharides into monosaccharides
Secondary active transporter of glucose and galactose?
SGLT 1
GLUT 2 transfers into circulation
Facilitative transporter of fructose?
GLUT 5
GLUT 2 transfers into circulation
Glucose-galactose malabsorption
AR dx, mutation in SGLT 1
tx = remove glu/galact from diet
Which transporter is the bidirectional GLUT transporter?
GLUT 2
GLUT characteristics?
Decreases the free energy of activation (like enzymes)
Allows glucose to cross membranes down its concentration gradient
GLUT 1
Found in RBCs and blood-brain barrier (CSF)
High affinity
GLUT 2
Bi-directional
Found in liver, kidney, pancreas; is low affinity, so only takes in glucose when concentrations are high
GLUT 3
Found in the brain
High affinity; major transporter in the CNS
GLUT 4
Is the only GLUT that is insulin-sensitive!
Found in adipose tissue, heart muscle and skeletal muscle
GLUT 5
Is a fructose transporter
Found in intestines, sperm
Mechanism of GLUT 4 insulin dependency?
- Insulin binds to its receptor
- Vesicles containing GLUT4 migrate to membrane
- Glucose passes through
GLUT 1 deficiency dx
AD dx
Infantile-onset epileptic encephalopathy
Dx’d by low glucose and presence of lactate in CSF
Fanconi-Bickel syndrome
AR dx of GLUT 2
Glucose cannot exit liver and kidneys, so hepatorenal glycogen accumulation occurs (glycogen storage dx type XI)
Hepatosplenomegaly
Why are C-peptides important, in insulin synthesis?
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.
