Energy and Obesity Flashcards

1
Q

What is the respiratory quotient?

A

RQ=ratio of CO2 produced by a fuel (e.g. carbs/fat) to O2 used to burn the fuel

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2
Q

What fuel is used with a RQ = 1?

A

oxidizing carbs

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3
Q

What fuel is used with RQ= 0.7?

A

oxidizing fat

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4
Q

What fuel is used with RQ= 0.8?

A

oxidizing fats and carbs

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5
Q

What is the RQ for protein oxidation?

A

~0.81

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6
Q

What does an RQ > 1.1 indicate?

A

fat synthesis

RARE: if force-fed carbs all day

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7
Q

What are long term signals of body fat?

A

insulin and leptin

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8
Q

Short term signals of body fat

A

signals from gut: ghrelin, CCK, GLP-1, PYY, apoA IV

leptin modulates sensitivity to short therm signals (CCK)

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9
Q

What are adiposity signals?

A

leptin (from fat) and insulin (from pancreas)

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10
Q

What are satiation signals?

A

CCK, GLP-1, gastric distension

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11
Q

What are orexigenic signals? (tell you to eat eat eat)

A
ghrelin
orexin
galanin
MCH (melanin concentrating hormone)
GABY -gamma amino butyric acid
PYY NRY neuropeptide Y
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12
Q

What are anorexigenic signals? (tell you not to eat)

A
gastric distension
CCK
GLP-1 (glucagon like peptide 1)
insulin
leptin
lipid
protein/AAs
glucose
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13
Q

What are the effects of leptin?

A

Letpin –> (+) POMC –> catabolic response –> stop eating/increase expenditure

Leptins also takes away the inhibition PY neurons to inhibit appetite

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14
Q

What are the risk factors for weight gain?

A
  • relatively low RMR (body temp)
  • high RQ
  • high insulin sensitivity
  • low spontaneous physical activity
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15
Q

What happens?

Parabiosis: ob next to normal

A

ob shrinks

Why?
ob has no leptin
leptin from normal crosses over and restores body weight of ob

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16
Q

What happens?

Parabiosis: db next to norm

(note: db = agouti: blocked melanin formation which is involved in food intake)

A

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)

17
Q

What happens?

Parabiosis: ob next to db

A

Ob strinks

ob gets leptin from db but db still can’t respond

18
Q

What did we learn from ob/db parabiosis?

A

leptin produced by adiopose –> goes brain –> stim energy expenditure and decrease food intake

19
Q

Barker hypothesis

A

epigenitc changes: hypothesis to explain relationships btwn SGA and metabolic syndrome DM2

20
Q

What was learned from Fecal transplants betwn lean and obese twins into gnotobiotic (germ-free) mice?

A

Lean mouse donor: body mass composition did not change in recipient

Obese mouse donor: body mass composition of recipient increases

21
Q

Which appears to be dominant: obese twin fecal biome or lean twin fecal biome?

A

lean

put lean and obese together in a germ free it will end up looking like a lean

22
Q

What happened when…?

transplanted fecal material from lean and obese twins into gnotobiotic mice

A

mice repliacted phenotype (adiposity) of donor twin, but consumed equal amts of food

microbiota resembled donors

23
Q

What happened when…?

mixed two mice in common cage: one that received lean and one that received obese (keep in mind, mice eat poop)

A

“obese” mice housed with “lean” mice became leaner and microbiota reverted to “lean” pattern

germ free co-housed with both types became leaner

24
Q

UCP1

A

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

25
Q

Brown adipose tissue

A

many mito, lipid droplets, highly vascularized, beta3 adrenergic receptors

EXISTS FOR HEAT GENERATION (new born, hibernation)