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CVD > Polyphenol 2 > Flashcards

Polyphenol 2 Flashcards

1
Q

Describe GI diets?

A
  • Low GI diets reduce fasting blood glucose + glycated protein
  • Low GI diets reduce risk of T2DM and CVD
  • Low GI better at controlling glucose + insulin
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2
Q

What happens if you give 25g vs 100g glucose?

A

don’t increase Cmax by 8x as much
o With glucose, body trying to regulate glucose in the blood tightly
o Even with 200g of glucose in a healthy person the blood glucose doesn’t increase that much
o This is because of insulin
 Released  cells in body take up glucose

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3
Q

What does this mean for insulin?

A

Cmax does increase

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4
Q

What does an obese person without impaired glucose tolerance (IGT) experience?

A

less controlled blood glucose but still close to normal

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5
Q

What does IGT mean?

A

sign of pre-diabetes
o Blood glucose = goes up much longer and comes down much more slowly
o Insulin = requires much more as person is becoming insulin resistant

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6
Q

What occurs with T2DM?

A

o Blood glucose = starts at higher level, increases much more and takes longer to decrease
o Insulin = not as high as IGT. Still elevated.

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7
Q

What occurs in a healthy person?

A

o Insulin = low level required

o Obese = needs a bit more but still decreases well

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8
Q

How do different sugars affect blood glucose differently?

A

Have different GI
Glucose gives highest AUC (peaks highest takes longest to fall)
Sucrose second highest AUC (peaks second highest, quick to fall)
Fructose peaks least almost level

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9
Q

Why was fructose considered to be healthiest?

A

because lowest AUC but o But goes through different biochemical pathway
excess intake –> more likely to get deposits of fat on liver = major risk factor for T2DM

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10
Q

What would real time plasma glucose in volunteers look like in healthy vs diabetic?

A

Diabetic glucose levels dysregulated, can go down + up to abnormal levels

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11
Q

What is the main contributor to glucose in the blood?

A

Starch

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12
Q

How is starch digested?

A

a-amylase in SI – degrades starch into maltose (too big, no specific transporters)

a-glucosidase (attached to surface of enterocyte) – degrades maltose to glucose

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13
Q

How is the digested starch (glucose) moved into blood?

A

By SGLT1 or GLUT2

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14
Q

How does SGLT1 work?

A

depends on Na availability. Takes glucose in active process into enterocyte. Good for abs when sugar conc is low

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15
Q

How does GLUT2 work?

A

for higher glucose concs (e.g. sugary food or starchy):

High conc stimulates movement for GLUT2 from inside of enterocyte to surface (basolateral membrane) so it can aid absorption

This is how body regulates intake

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16
Q

How is sucrose absorbed?

A
  • Sucrase (brush border) digests sucrose  glucose + fructose
  • Lots of sucrase on brush border – so quite efficient process
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17
Q

How is fructose absorbed?

A
  • Passive diffusion by GLUT5 into enterocyte
  • GLUT5 on basolateral membrane  blood
  • Not particularly well regulated
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18
Q

How is lactose absorbed?

A
  • LPH breaks down  galactose + glucose

* Galactose = in by same pathway as glucose

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19
Q

What have animal studies shown?

A

some polyphenols affect OGTT
o oGTT = (oral glucose tolerance test) = amount of glucose in blood after meal
o this is due to effects on digestive enzymes and sugar transporters

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20
Q

What can polyphenols inhibit?

A

o Sucrose, a-amylase, a-glucosidase, SGLT1, GLUT2
o Don’t completely block activity – just compete with substrate to slow transport down
o Means sugars + polyphenols eaten together slows sugar absorption

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21
Q

What is acarbose?

A

o Drug given to diabetics
o Slows down rate of sugar absorption
o Acts on a-amylase + a-glucosidase – strongly inhibits them
o So reduced amount of sugar getting into blood (lowers Cmax)
o Acarbose is large so isn’t absorbed or hydrolysed

22
Q

What can polyphenols do related to acarbose?

A

o Can also inhibit similarly
o But weaker, more subtle effects
o We consumer polyphenols everyday so have continuous effect

23
Q

What is the problem of acarbose?

A

symptoms of lactose intolerance (fermentation of sugars by microflora)

24
Q

What happens in T2DM patients?

A

Body thinks not enough sugar –> upregulates enzymes/transporters involved in sugar abs (to increase amount/rate of abs)

25
Q

What is the study into acarbose?

A

o 118 people – acarbose for 3 years  risk reduction for diabetes 6%
o Post -load plasma glucose was down by 1.16mmol/L
o No effect on insulin secretion and sensitivity

26
Q

What did a Cochrane meta analysis regarding acarbose find?

A

o Acarbose reduced post-prandial hyperglycemia
o Decreased incidence of diabetes by 36%
o Improved flow-mediated vasodilation
o Reduced progression of intima media thickness

27
Q

What did meta-analysis on T2DM patients find?

A

o Acarbose treatment associated with 64% lower rate of myocardial infarction
o 35% less cardiovascular events

28
Q

What was found when giving people bread and fruit puree and green tea?

A

Has basically as large an effect as acarbose

29
Q

How might beetroot juice be involved?

A

Beetroot juice is lowering blood glucose response in healthy volunteers is partly due to alpha-glucosidase inhibition

30
Q

What are consequences of high blood sugar?

A
  • High glucose –> high ROS in cells
  • –> insulin resistance and mitochondrial dysfunction = key features in T2DM
  • This is why in healthy people, the body tries to keep levels low
31
Q

When polyphenols circulate in blood, they have a key role in regulating?

A

o BP
o General CV health
o Fitness (elasticity) of vessels

32
Q

How are endothelial cells affected by poor diet?

A

o Exposed to high glucose post prandially FIRST = major problem site for high glucose
o So high glucose known to lead to endothelial dysfunction
o Also site which sees any polyphenols abs into blood first
o Consequently are what can lead to CVD

33
Q

What are blood vessels like in healthy people?

A

Open and flexible

34
Q

What does endothelial dysfunction cause?

A

biochemically damaged  can lead to atherosclerosis

35
Q

What is key in this?

A

endothelium communicating with smooth muscle

Smooth muscle controls BP

36
Q

What is a key part of response of smooth muscles?

A

NO

37
Q

What does eNOS in endothelial cells cause?

A

–> NO –> vasodilation –> lower BP

38
Q

What does NADPH oxidase cause?

A

NADPH oxidase –> produces O* –> reacts with NO –> peroxynitrite
= less NO = vasoconstriction

39
Q

What does superoxide dismutase do?

A

converts O* –> H2O2
o So doesn’t reduce NO
o So considered protective of endo cells

40
Q

What does xanthine oxidase do?

A

converts hypoxanthine –> uric acid + produces O*
o Purine catabolism pathways
o Diet high in certain types of meat (contain lots of purines which go by XO pathway) –> higher activity of XO –> more O* (bad)
o Uric acid itself in the blood is also risk factor for T2DM + CVD

41
Q

What is the inflammatory pathway?

A

COX2 converts Arachidonic
Acid to PGH2 = pro-inflammatory, can convert to thromboxane A2 (platelet aggregation) and can also lead to vasoconstriction

42
Q

What is NFkB?

A

pro-inflammatory genes –> inflammation

Inflammation = risk factors for CVD + T2DM

43
Q

What can some polyphenols do in these mechanisms?

A

o Some can interact with COX2 and XO

44
Q

What can quercetin (sulphate derivative) do?

A

Taken into endo cells by OAT1 and OATP4C1 transporters

Can slow down XO and COX2

Reduces amount of O* –> increased NO –> vasodilation

Reduces amount of PGH made by COX2 –> less vasoconstriction/inflammation

Study on humans given quercetin showed lower levels of uric acid in blood

45
Q

How can EC help?

A

can inhibit NADPH oxidase  reduced O*, increased NO, increase vasodilation

46
Q

How can hesperitin help?

A

increase/induce eNOS = more NO = more vasodilation.

Can inhibit NFkB  decrease inflammation = decrease vasoconstriction

47
Q

What is the study on hesperidin?

A
  • 24 healthy overweight men
  • RC crossover study
  • 3 x 4wk periods
  • 500ml orange juice, control drink plus hesperidin or control drink plus placebo – daily
  • Diastolic BP = sig lower after orange juice or hesperidin cf placebo
  • Significantly improved postprandial microvascular endothelial function at peak of plasma hesperitin conc
48
Q

What might high levels of glucose do?

A

may enhance endothelial dysfunction

49
Q

How might this work?

A

May enhance NADPH oxidase:

Increase O3*–> Reduce NO –> Less vasodilation

50
Q

Polyphenol can reduce glucose absorption, what does this mean?

A

they can therefore indirectly reduce the effect of glucose on endo cells

o Less glucose in blood = NADPH isn’t as activated

51
Q

What is the double effect of polyphenols?

A

o Direct effect on enzymes in the gut

o Indirectly by reducing glucose in blood

52
Q

What is the difference between flavonols and flavanols?

A

They are both subgroups of flavonoids.
The basic structure is different, flavonols have the ketone group which is absent in the flavanol (or flavan-3-ol) group.
Both groups can be hydroxylated in different positions.
Prominent members of flavonol group is quercetin, of the flavanol group it is catechins.

CVD (12 decks)

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