Energy and Obesity Flashcards
What is the respiratory quotient?
RQ=ratio of CO2 produced by a fuel (e.g. carbs/fat) to O2 used to burn the fuel
What fuel is used with a RQ = 1?
oxidizing carbs
What fuel is used with RQ= 0.7?
oxidizing fat
What fuel is used with RQ= 0.8?
oxidizing fats and carbs
What is the RQ for protein oxidation?
~0.81
What does an RQ > 1.1 indicate?
fat synthesis
RARE: if force-fed carbs all day
What are long term signals of body fat?
insulin and leptin
Short term signals of body fat
signals from gut: ghrelin, CCK, GLP-1, PYY, apoA IV
leptin modulates sensitivity to short therm signals (CCK)
What are adiposity signals?
leptin (from fat) and insulin (from pancreas)
What are satiation signals?
CCK, GLP-1, gastric distension
What are orexigenic signals? (tell you to eat eat eat)
ghrelin orexin galanin MCH (melanin concentrating hormone) GABY -gamma amino butyric acid PYY NRY neuropeptide Y
What are anorexigenic signals? (tell you not to eat)
gastric distension CCK GLP-1 (glucagon like peptide 1) insulin leptin lipid protein/AAs glucose
What are the effects of leptin?
Letpin –> (+) POMC –> catabolic response –> stop eating/increase expenditure
Leptins also takes away the inhibition PY neurons to inhibit appetite
What are the risk factors for weight gain?
- relatively low RMR (body temp)
- high RQ
- high insulin sensitivity
- low spontaneous physical activity
What happens?
Parabiosis: ob next to normal
ob shrinks
Why?
ob has no leptin
leptin from normal crosses over and restores body weight of ob
What happens?
Parabiosis: db next to norm
(note: db = agouti: blocked melanin formation which is involved in food intake)
norm shrinks
Why?
db has LOTs of leptin but faulty receptor for leptin in brain
next to the normal, the overproduced (compensated) leptin from db crosses over to norm and inhibits food/increases expenditure of normal)
What happens?
Parabiosis: ob next to db
Ob strinks
ob gets leptin from db but db still can’t respond
What did we learn from ob/db parabiosis?
leptin produced by adiopose –> goes brain –> stim energy expenditure and decrease food intake
Barker hypothesis
epigenitc changes: hypothesis to explain relationships btwn SGA and metabolic syndrome DM2
What was learned from Fecal transplants betwn lean and obese twins into gnotobiotic (germ-free) mice?
Lean mouse donor: body mass composition did not change in recipient
Obese mouse donor: body mass composition of recipient increases
Which appears to be dominant: obese twin fecal biome or lean twin fecal biome?
lean
put lean and obese together in a germ free it will end up looking like a lean
What happened when…?
transplanted fecal material from lean and obese twins into gnotobiotic mice
mice repliacted phenotype (adiposity) of donor twin, but consumed equal amts of food
microbiota resembled donors
What happened when…?
mixed two mice in common cage: one that received lean and one that received obese (keep in mind, mice eat poop)
“obese” mice housed with “lean” mice became leaner and microbiota reverted to “lean” pattern
germ free co-housed with both types became leaner
UCP1
brings protons back into mitochondria w/o making ATP, but you DO make a lot of heat
-in intact cells, UCP1 is constantly inhibited by ATP in cytosol
-IF COLD:
NE stimulates lipolysis of lipid droplet to release FFA which stimulate UCP1 (overtake ATP’s normal inhibition of UCP1) –> heat and uncoupling of
