Week 4 Flashcards
Carbs Energy Content
17.2 kJ/g
Protein Energy Content
17.2 kJ/g
Fat Energy Content
39 kJ/g
Respiratory Quotient (RQ)
Ratio of CO2 produced to Oxygen consumed by the body (used for BMR)
Carbs RQ
1
Fat RQ
0.7 (16/23)
Protein RQ
0.82 (2.5/3)
Whole Body RQ
~ 0.85
Total Energy Expenditure (TEE)
Net amount of Energy used by organism to maintain core physiological functions and to allow locomotion
Measuring energy expenditure indirectly
~ 21kJ/L of O2 are liberated
Basal Metabolic Rate
Energy expenditure at complete rest
Diet Induced Thermogenesis (DIT)
Increase in energy expenditure after eating due to GI motility
(8 - 15% of TEE)
TEE equation
TEE = BMR + DIT + EE
- measured in morning
Normal BMR values
- M: 7000 kJ /Day
- F: 6000 kJ /Day
Lateral Hypothalamic Area
“Hunger Center”
Stimulates eating
What nuclei control eating
- PVN
- Arcuate Nuc.
- Nucleus Accumbens (reward)
What external factors/drugs can enhance appetite
- Endogenous Cannabis
- Endogenous Opioids
Nicotine effect on appetite
Suppression of Apetite
I.C Ca2+
100 nM
E.C Ca2+
- Free: 1.1 - 1.4 mM
- Total: 2.2 - 2.8 mM
Types of Circulatory Ca2+
- Free ionized (45%, 1.0-1.3 mM)
- Protein bound (45%)
- Complexed with anions (~10%)
E.C PO4 3-
0.8 - 1.5 mM
Synthesis of PTH
1) Pre-pro-PTH (115a.a)
2) Pro-PTH (90a.a) in ER
3) PTH (84a.a) in secretory granules
Regulation of PTH secretion
- Ca-SR (sensing-R), GPCR, Gq
- Calcitriol, more intestinal abs.
- Plasma PO4 3- binds and decreases free Ca2+
What type of hormone is PTH
Peptide Hormone
(doesn’t require a BP for transport)
Half life of PTH
4 minutes
Target cells expressing PTH1R
- Kidney
- Bones
Kidney PTH1R
- Stimulation of Ca2+ reabsorption
- TAL & Distal tubule (ECaC)
How does PTH affect Pi absorption
PTH stimulates Endocytosis of Na/Pi symporter from Luminal side of Proximal tubules
Calcitriol specs.
- Steroid Hormone
- 1,25-dehydroxy-vitamin-D
Biosynthesis of Calcitriol SKIN
7-dehydroxycholesterol reacts with UV light in skin
= Cholecalciferol (D3/D2)
Biosynthesis of Calcitriol LIVER
Cholecalciferol reacts with 25-a-hydroxylase
= 2,5-hydroxy-vitamin-D
Biosynthesis of Calcitriol Kidney
2,5-hydroxy-vitamin-D
- 24-a-hydroxylase = 24,25-dehydroxy-vitamin-D
- 1-a-hydroxylase = 1,25-dehydroxy-vitamin-D
What forms the INACTIVE form of Vitamin D?
24-a-hydroxylase
= 24,25-dehydroxy-vitamin-D
What forms the ACTIVE form of Vitamin D?
1-a-hydroxylase
= 1,25-dehydroxy-vitamin-D
How is Calcitriol transported in blood
- Vitamin-D Binding Protein (DBP)
(needed since its a steroid)
Calcitriol Receptor
Nuclear Vitamin D receptor which forms a Heterodimer with the Retinoid X Receptor (RXR)
- Binds genes and alters expression
- More CaS-R & 24-a-hydroxylase
Target organs of Calcitriol
- GI (small intestines)
- Kidneys
- Bones (osteoblasts)
Vitamin D deficiency
Rickets
- De-mineralization of bones due to impaired Ca and Pi absorption
- Deformation of Bones
What synthesizes Calcitonin
C-cells of Thyroid gland
What type of hormone is Calcitonin
Peptide Hormone (32a.a)
Calcitonin Receptor
- Only on Osteoclasts
- Inhibits bone breakdown
Paget’s Disease
Abnormally high Osteoclast activity where Calcitonin is needed as a treatment (from salmon)
What can cause Hypocalcemia
- No PTH (thyroid / PT removal)
- No Vitamin-D
- Hyperventilation (causes albumin to bind 2 Ca instead of H)
Proteins secreted by Osteoblasts
- Collagen Type I
- Osteocalcin (Gla)
- Osteonectin
Catabolic Bone enzymes
- Collagenase
- Gelatinase
Osteoid formation duration
10 - 14 days
Bone mineralization duration
5 - 6 weeks
- Formation of Hydroxyapatite
Bone Nucleation
Hydroxyapetite formation and built into protein matrix to provide bone rigidity
What is needed for Osteocalst activation
- M-CSF
- RANKL
- IL-6
What is secreted into lacuna where Osteoclast is to help bone resorption
- TRAP (phosphatase)
- Protons (H+)
Bone Remodeling
1) Osteoclasts create micro-injuries with deep 20μm tunnels
2) Osteoblasts repair this damage
Effects of PTH & Calcitriol on Bone remodeling
- Act on Osteoblasts only
- RANKL & OPG secretion
RANK-L
- Binds RANK activating nuclear factor Kappa B on Osteoclasts
- Osteoclast activation
- RANKL is TNF
Osteoprotegnin (OPG)
Inhibits Osteoclasts
Glucocorticoids effect on Bone remodeling (cortisol & synth.)
Increase RANKL/OPG ratio of Osteoblasts
= Osteoclast activation
Estrogens effect on Bone remodeling
Opposite of GC
Decrease RANKL/OPG ratio of Osteoblasts
= Osteoclast inhibition
Inflammatory effect on Bone remodeling
Immune cells can express RANK-L leading to Osteoclast activation
Tumor Cells effects on Bone remodeling
Tumor cells can also express RANK-L leading to Osteoclast activation
