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HL22015 physiology > Nutrition health and exercise 2 > Flashcards

Nutrition health and exercise 2 Flashcards

1
Q

Why do differences in GI arise?

A

Gross matrix structure (different sized oats–> smaller oats are ground up so increased SA so more digestion), cell wall present/absent

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2
Q

Second meal effect?

A

Thing eaten can affect digestion of foods eaten after it

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3
Q

What does a slower glucose appearance do to insulin response?

A

Reduces it

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4
Q

How can foods with different exogenous glucose appearance rate result in similar blood glucose concentrations?

A

Foods that are digested faster (and so would cause a higher glucose appearance rate) cause a larger increase in insulin conc so the higher glucose conc is then buffered

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5
Q

Why do rapidly and slightly slowly digestible starches result in a similar (moderate to high) glycaemic response?

A

Rapidly causes a high insulin response which cancels out the higher glucose and leads to a similar glycaemic response

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6
Q

What kind of starch foods leads to a low glycaemic response?

A

Very slowly digestable starch

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7
Q

Exercise interaction with GI?

A

Low GI combined with exercise can improve glucose control (via insulin)

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8
Q

How to study positive energy balance effect on metabolic control?

A

Have one group who overate (150% of normal) and were sedentary while the other group overate but did enough exercise to offset the extra 50% calories

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9
Q

Effect of flux on insulinemia independent of energy balance?

A

Exaggerated insulin response (bad as less sensitive to insulin) is only seen in non-exercise group even though both groups were eating 150% of what they normally would

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10
Q

Effect of quantity of fat ingested on triglyceride response?

A

If a meal has more fat (and all else is equal) there is a higher plasma triglyceride concentration

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11
Q

In the fasted state, where do triglycerides come from?

A

Liver

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12
Q

How are triglycerides generally transported when fasted?

A

VLDLs

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13
Q

What are VLDLs cleared by?

A

Adipose tissue and muscle

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14
Q

What does adipose tissue and muscle have that allows them to digest lipids?

A

Lipoprotein lipase

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15
Q

What does lipoprotein lipase break triglycerides into?

A

Non esterified fatty acids and glycerol

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16
Q

Fate of fatty acids in adipose tissue?

A

Storage

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17
Q

Fate of fatty acids in muscle?

A

Oxidation

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18
Q

What kind of triglyceride enters circulation in the fed state?

A

Chylomicron triglycerides

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19
Q

What competes for clearance with VLDL in the fed state?

A

Chylomicrons

20
Q

Which type of fat storage does LPL have the higher affinity for?

A

Chylomicrons so it will preferentially clear those

21
Q

What happens as a result of eating fats?

A

Increase in VLDL conc in blood

22
Q

Why does eating fat increase VLDL blood conc?

A

Chylomicrons are preferentially cleared

23
Q

Effect of insulin on VLDLs?

A

It directly suppresses the output of VLDL from the liver (reduced triglyceride appearance in circulation), also indirectly suppress VLDL appearance as it suppresses adipose tissue lipolysis (fewer FAs to incorporate in VLDLs)

24
Q

Effect of insulin on LPL in adipose tissue?

A

Stimulated it–> more storage

25
Q

Effect of insulin on LPL in muscle?

A

Inhibits it, so less oxidation

26
Q

Effect of high sugar diet on triglyceride clearance?

A

Can reduce triglyceride clearance so when eating fats the fats are cleared at a lower rate

27
Q

Clearance rate of fats on a lower carb diet compared to a higher carb diet?

A

Lower carb diet results in faster triglyceride clearance

28
Q

Effect of high carb diet on fatty acid fate?

A

High carb diet leads to a lower dietary fat oxidation

29
Q

Why should free sugars not exceed 5% of total dietary intake?

A

Free sugars can cause dental issues, and a higher energy intake

30
Q

Example of free sugar?

A

Sugar in apple juice is a free sugar, sugar in an apple is not (as matrix has been altered)

31
Q

Main difference in glucose and fructose metabolism in liver?

A

Fructose is two step metabolism, glucose is one step metabolism

32
Q

Glucose metabolism in liver?

A

Glucose–> glucose-6-phosphate–>G1P–>UDP glucose–> glycogen

33
Q

Why does fructose have a two step metabolism whereas glucose has a 1 step metabolism?

A

Fructose is not oxidised as fructose, it needs to be converted to other things before it can be used by peripheral tissues

34
Q

What can the liver convert fructose into?

A

Glucose, lactate or triglycerides

35
Q

What do high fructose diets increase the production of?

A

Fats

36
Q

What is denovolipogenesis?

A

The production of fats from non-fat sources

37
Q

Triglyceride response to glucose compared to fructose?

A

Fructose leads to a larger triglyceride response than the same amount of glucose

38
Q

VLDL and chylomicron response to glucose compared to fructose?

A

higher in response to fructose than glucose

39
Q

Why is the circulatory TAG response higher to fructose than glucose?

A

Fructose stimulates denovo lipogenesis

40
Q

How does fructose increase denovolipogenesis?

A

It can be the substrate and the signal, and it can saturate liver glycogen stores

41
Q

How is fructose the substrate for denovo lipogenesis?

A

It provides the fuel–> it can be converted into palmitate (fats)

42
Q

How is fructose the signal for denovo lipogenesis?

A

It stimulates glucose, AAs to be converted into fat

43
Q

How much fructose is converted to fat?

A

Not much

44
Q

More important role for fructose in denovo lipogenesis?

A

It is more important as a signal than as a substrate

45
Q

How does fructose saturating liver glycogen stores mean it can stimulate denovo lipogenesis?

A

Higher glycogen conc in the liver causes carbohydrates to be converted into fats instead of more glycogen

46
Q

Exercise effect on fructose denovolipogenesis?

A

Exercise reduces fructose induced de novo lipogenesis

HL22015 physiology (17 decks)

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