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NUTR 4210 > Leptin and Adiponectin > Flashcards

Leptin and Adiponectin Flashcards

1
Q

what is the only adipokine to decrease with obesity

A

adiponectin

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2
Q

what does the co-culture experiment show

A

Co-incubation study = incubate 2 cell types together
- Muscle cells, culture and grow it (from rectus abdominis)
- Fat depot is mammary = from breast (representative depot of visceral fat) more realistic compared to going deep to get the viscera

- Let mix and make contact or make layers with a fine screen between, stopping physical mending 

- If they coincubation, after 48hrs if you then isolate muscle cells and give an insulin challenges, and look you see impairment
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3
Q

two ways that fat cells increase

A

hypertrophy or new cells

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4
Q

what way is worse increase size or quantity

A

size

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5
Q

why is an increase in visceral adipose cell size bad

A

we hit a threshold due to certain size and we create a stress response sending out cytokines and peptides that recruit immune cells (macrophages)

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6
Q

what do the macrophages change (altered secretory profile)

A

Pro-inflammatory response
- increased TNF, resistin, IL6, IL8 and FA
- decrease in adiponectin
Causes problems with insulin response over all and now the muscle is unable to clear glucose

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7
Q

what do toll like receptors do

A

triggers immune response when FA bind

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8
Q

what did the removal of VF but not subcutaneous fat from aging/diabetic rats show

A

as the rats aged they became more insulin resistant
- VF removal saw an increase in glucose clearance similar to that of caloric restriction
- sub-Q fat removal was only similar to the sham group (less than young)

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9
Q

what is lipoatrophy

A

absence of peripheral adipose tissue
- associated with severe insulin reisstance

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10
Q

why is the absence of peripheral adipose tissue a bad thing

A

we are still consuming fat so it is converted and then needs to be stored which is in tissue instead like heart and liver

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11
Q

what does the study done where they transplanted AT from either a normal or leptin deficient mouse into a lipoatrophic mouse show

A

lipoatrophic mice = elevated bld glucose, insulin, TG-insulin resistant, liver TG

Transplanted with wildtype AT = improvement (decrease in all and more insulin sensitive)

Transplanted with no leptin = no improvement

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12
Q

leptin =

A

the anti obesity hormone

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13
Q

t or f leptin has both central and peripheral effects

A

true

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14
Q

what positive correlations does leptin have

A

positive correlation to adiposity and BMI

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15
Q

what are the central effects of leptin

A

decrease NPY and appetite
increase SNS activity

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16
Q

leptin stimulates

A

FA oxidation in muscle

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17
Q

how does leptin increase FA oxidation

A

activates AMPK
- AMPK detects the disturbance in energy charge (increase ATP)

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18
Q

what happens when AMPK is activated

A

ACC produces malonyl CoA
- puts a break on the carnitine system
- malonyl CoA is an inhibitor of this
= AMPK deactivates this so there is less malonyl CoA = less of a break = more fat in

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19
Q

the important peripheral role of leptin is to prevent

A

lipotoxicity in non-adipocytes

  • increase AMPK and PGC1a = increases FA oxidation and mitochondrial content
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20
Q

what does an increase in HSL (ERK) and lipolysis do to lipid content

A

decreases it
(leptin turns on the HSL = fat breakdown)

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21
Q

how does leptin correct a HF diet (insulin resistance)

A

leptin increases insulin stimulated glucose uptake
- increases IRS-1, insulin stimulated PI3Kinase activity, Akt phosphorylation, plasma membrane and total GLUT4

decreases = muscle lipid content (TG, DAG, ceramides)

22
Q

how is adiponectin related to obesity and insulin resistance

A

inversely

23
Q

adiponectin functions much like leptin as it increases

A

AMPK/FA oxidation
mitochondrial biogenesis
restores insulin stimulated glucose uptake in HF fed rodents

24
Q

Adiponectin gene therapy ____ mice from a HF High sucrose diet

A

protects
- improves glucose tolerance and lose fat mass

25
Q

skeletal muscle becomes _____ to the ability of leptin and adiponectin to stimulate FA oxidation

A

resistant

(observed in obese humans)

26
Q

is leptin and adiponectin resistance inducible and how

A

yes via HF diets (modifiable by lifestyle)

27
Q

what does early leptin/Ad resistance do

A

decrease fat oxidation/increase storage
and insulin resistance

28
Q

when do we first observe Ad resistance in a mouse HF diet

A

only 3 days in

29
Q

when are Plasma membrane FA transporters increased in a HF diet in mice

A

2 weeks

30
Q

when are reactive muscle lipids increased in a HF diet in mice

A

by 2 weeks

31
Q

when do we see a decrease in insulin response in a HF diet

A

between 2-4 weeks

32
Q

does Ad and leptin resistance occur slowly or rapidly

and before or after impaired insulin response

A

occurs rapidly and prior to

33
Q

how can you prevent Lep/Ad resistance

A

via diet and exercise
- treadmill training prevents leptin resistance
- fish oil supplementation prevents diet induced leptin and Ad resistance in muscle

34
Q

Does an improvement in leptin and Ad response precede improvements in muscle insulin response

A

we see restoration of FA oxidation response and improvement of insulin response following

35
Q

what does the study show in the trying to reverse leptin resistance (HF diet + 4 weeks treadmill maintaining diet)

A

insulin response recovers with 1 week of exercise
- this corresponds to a decrease in muscle ceramide content

leptin response was restored AFTER the reduction in muscle lipids and improved insulin response

36
Q

Restoration of adiponectin response

A

we have failed to see this through 2 weeks of exercise or fish oil supplementation even though those DO reverse insulin resistance

37
Q

explain how FFA are related to inflammation

A

JNK SOCS3
TLR4
IkKB and NFkB increasing in nucleus

38
Q

_____ signs of inflammation after 3d of HF feeding

A

No

39
Q

what happened when aspirin was given as a supplementation with the HF diet

A

it didn’t prevent anything (decrease inflammation if that was the cause) it actually reduced adiponectin response

40
Q

Adiponectin and leptin resistance are neither _________ prior to the recovery of insulin response

A

REVERSABLE

41
Q

what was the hypothesis that said leptin and Ad resistance was

A

PROTECTIVE

42
Q

how would Lep and Ad be protective

A

prevent lipid overload into teh mitochondria
deportonated FA
ROS production

43
Q

how long does it take for the increase of ROS production due to excessive FA in MITO

A

little as 3 days on HF diet

44
Q

what do ROS activate

A

stress kinases and impairs insulin signalling

45
Q

the hypothesis for ROS production and ad/lep resistance

A

ROS production impairs the ability of Leptin and Ad to stimulate mitochondrial FA uptake and oxidation

46
Q

what did they use for the study design to prove their new hypothesis

A

used a control diet plus antioxidant (N-acetylcysteine)
and HF diet
and HF diet + N-a

47
Q

what is glutathione (GSH)

A

a cellular redox buffer = index of the oxidative state (GSSG = oxidized GSH)

48
Q

HF diet _____ oxidative state in oxidative muscle

A

increases

49
Q

what findings were seen in the soleus with the inclusion of antioxidant

A

does not protect against HF diet induced Ad resistance

50
Q

what findings were seen in the EDL with antioxidant

A

Ad resistance develops with a HF diet even though oxidative status was unaffected

51
Q

do ROS acutely/directly impair Ad-stimulated FA oxidation

A

no H2O2 doesn’t impair the ability of Ad to stimulate FA oxidation
= hypothesis = wrong

NUTR 4210 (3 decks)

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