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Physiology of Exercise and Health > Blood Lipids, Post-prandial Metabolism > Flashcards

Blood Lipids, Post-prandial Metabolism Flashcards

1
Q

What is the relationship between muscle triglyceride and glycogen synthase activity and insulin sensitivity?

A
  • Negative linear relationship (Phillips et al 1996)

- The more intramuscular triglyceride, the lower the insulin sensitivity

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2
Q

How much intramuscular triglyceride do trained, untrained lean, and untrained obese people have, in order of least to most ?

A

-Lean, Obese and Trained (Amati et al 2011)

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3
Q

If trained individuals have the highest intramuscular triglyceride, what is their typical insulin sensitivity and what does this say about the relationship between intramuscular triglyceride and insulin sensitivity?

A

-Very high insulin sensitivity, even with high intramuscular triglyceride, which suggests exercise or training status can offset the effects

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4
Q

What is the fat that is the vast majority of dietary lipids and adipose tissue?

A

-Triacylglycerol

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5
Q

What is a cholesterol? How much is found in the body pool? Where is it found? Where is it used?

A
  • A sterol/’fat like compound’
  • Total body pool of 140g
  • Synthesised endogenously, and consumed in diet (1g per day)
  • Essential component of cell membranes
  • Precursor to steroid hormones
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6
Q

Does dietary cholesterol impact cholesterol concentration?

A

-No

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7
Q

What impacts the rate of endogenous cholesterol production/breakdown?

A
  • Saturated fat increases cholesterol production

- Exercise increases cholesterol breakdown

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8
Q

What factors can impact the degree to which saturated fat impacts cholesterol/TC:HDL ratio/LDL levels?

A
  • Genetics
  • Obesity/Insulin Sensitivity
  • Hypertriglyceridemia
  • Sex
  • Concomitant dietary cholesterol intake
  • The type of food in which they are contained (e.g. cheese vs butter vs milk)
  • Genetic variance
  • Baseline LDL concentrations
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9
Q

What may impact the degree to which reducing saturated fat intake will have an impact on your TC:HDL ratio?

A
  • What it is replaced with.
  • Replacing with high GI carbs increases plasma triglyceride
  • Replacing with unsaturated fats improves TC:HDL ratio/TDL:HDL ratio.
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10
Q

Cholesterol is a lipid, and lipids are hydrophobic, so how are they transported around the body?

A

Via Lipoproteins

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11
Q

How are Triglycerides transported around the circulation?

A

Via lipoproteins

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12
Q

How is glycerol transported around the circulation?

A

Directly in the blood

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13
Q

How are free fatty acids transported around the circulation?

A

Associated with albumin

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14
Q

What is the structure of a lipoprotein?

A
  • Apoprotein which dips into the core of the structure to anchor it all together
  • An outer layer which is made of phospholipids and unesterified cholesterol
  • A core filled with TAG
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15
Q

What are the main categories of lipoprotein?

A
  • HDL
  • LDL
  • VLDL
  • Chylomicron
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16
Q

What is the comparative composition of HDL, VLDL and LDL?

A
  • HDL: High in protein and phospholipid, low in cholesterol and almost no TAG
  • LDL: High in cholesterol, low in protein and phospholipid, some TAG
  • VLDL: Very high TAG, low cholesterol, very low protein and phospholipid
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17
Q

What is the composition of chylomicron lipoproteins?

A

-80-90% TAG, with the rest mostly equally spread between phospholipid, cholesterol, and protein

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18
Q

What are chylomicrons?

A

Lipoproteins that deliver dietary fat from the small intestine to the muscle or adipose tissue

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19
Q

What impact does insulin have on VLDL?

A
  • Suppresses VLDL production by the liver, and suppresses fat metabolism from adipose tissue, so less is sent to the liver to even be made into VLDL
  • Stimulates uptake of VLDL/LDL into the adipose and suppresses intake into the muscle, by impacting the activity of Lipoprotein lipase
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20
Q

How do you test lipid metabolism?

A

-Similar to an OGTT. Feed a high fat meal and measure plasma TAG over time

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21
Q

How does postprandial blood lipid concentration differ from postprandial glucose concentrations?

A

-Lipid metabolism is much slower so it takes about 4 housrs to peak, compared to 1 hour for glucose

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22
Q

How do triglyceride responses to a meal vary based on quantity of fat ingested, when quantity of carbs and protein is the same?

A

-Positive dose response relationship

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23
Q

What is the relationship between chylomicron and LDL uptake to muscle and adipose tissues?

A
  • Chylomicron and LDL compete for transporters

- Chylomicron is preferentially taken by adipose and muscle so high chylomicron means build up of LDL in the blood

24
Q

What is the relationship between blood lipids and CHD risk? Give evidence

A

Simons et al 1986 observational study showed that nations with higher average serum cholesterol had higher CHD mortality rate

25
Q

What is the relationship betweeen blood HDL and CHD?

A

-Simons et al 1986 observational study showed that nations with higher average HDL-cholesterol had lower CHD mortality rate

26
Q

PCSK9 mutation can lead to having very little LDL. How does this show the relationship between LDL and CHD?

A

-Those with the PCSK9 mutation have dramatically lower risk of CHD, according to Cohen et al 2006

27
Q

How have drug trials supported the causal role between plasma LDL and CHD?

A

-Lulrink et al 2019 showed that giving statins to people with high CHD risk lowers their LDL and drastically drops their CHD risk.

28
Q

What impact does physical activity have on blood lipid profile? Give evidence

A

LaPorte et al 1983 showed that physical activity is associated with increased HDL concentrations

29
Q

What do we know about the fasting and postprandial serum TAG of people with CHD?

A

-Karpe et al 1992 found that people with CHD have elevated postprandial and fasting TAG

30
Q

What is the relationship between postprandial TAG and future CVD risk?

A

Norcestgaard et al 2007 found a positive association between postprandial TAG and CVD risk, which is true for both men and women, but VERY High at the highest level for women (but women rarely at that level)

31
Q

What evidence is there to suggest that postprandial TAG impacts atherosclerosis?

A

-Zilversmit 1979 suggests that atherogenesis is a postprandial phenomenon, so regular exposure to high TAG in the blood following high fat meals

32
Q

Explain forward cholesterol transports:

A
  • VLDL is secreted by the liver to be sent to the peripheral tissues
  • VLDL converted to LDL while being transported in the circulation due to gradual TAG loss through LPL and HL
  • LDL is then taken up by peripheral tissues via LDL receptor
33
Q

Explain Reverse cholesterol transport:

A
  • HDL is sent from peripheral tissues to the liver, where the cholesterol is excreted in the bile salts
  • Some cholesterol is sent from the HDL to the VLDL/LDL via CETP
34
Q

What is CETP in cholesterol transport?

A

Cholesterol Ester Transfer Protein

35
Q

What is the relationship between flux/TG Extraction and exchange of cholesterol between HDL and LDL via CETP?

A

-Slower lipid metabolism/extraction/uptake means the HDL and LDL are in the circulation for longer, meaning more opportunity for exchange via CETP

36
Q

What is the relationship between HDL and LDL/Blood TAG?

A

Less HDL means more LDL

37
Q

What is the Atherogenic Lipoprotein Phenotype?

A
  • Low HDL concentration
  • abundant levels of Small, dense LDL
  • Raised TAG concentrations
38
Q

Why is LDL a good long term marker of fat metabolism?

A

-It doesn’t change quickly, and the level of LDL is a good indicator of your level of HDL or the rate of flux (meaning more CETP exchange)

39
Q

What can observational research tell us about the relationship between training status and postprandial lipaemia?

A

-Merrill et al 1989 shows that trained individuals have a significantly reduced blood tryglyceride accumulation after a meal, both reduced at all time points and also significantly lower peak around 4 hours

40
Q

What is the difference in postprandial TAG at various times since the last bout of exercise and what does this tell us?

A
  • Postprandial TAG response reduced at 15h post exercise, but back to normal at 60h or 6.5days (Hardman et al 1998)
  • The impact of training on postprandial lipaemia is due to acute affects, not chronic adaptation
41
Q

What difference does adiposity have on the impact that exercise has on postprandial TAG?

A

Obese individuals had higher TAG response to high fat meals than lean people but the impact that exercise had on reducing that response was far greater than in lean people.

42
Q

What are the ideal conditions for exercise tohave the most impact on postprandial lipaemia?

A
  • Maraki and Sidossis 2013 say that you should:
  • Aim to expend 480-598 kcal
  • Most benefits 8-12 hours after
  • Doesn’t matter whether it is in a single bout or several 10 minute bouts across the day.
43
Q

To what extent does the impact that exercise has on postprandial TAG have to do with creating an energy deficit?

A

-Gill and Hardman 2000 found that energy deficit reduced postprandial TAG but exercise with an equal energy deficit reduce postprandial TAG even more, implying that exercise itself has a direct mechanism for decreasing postprandial TAG

44
Q

How does Fructose intake impact plasma TAG?

A

Fructose is a potent stimulator of De Novo Lipogenesis. It can also be be the substrate of DNL, but this does not happen much.

45
Q

How does fructose increase DNL?

A

Fructose intake causes glycogen storage in the liver, high liver glycogen increases PDH activity, which increases DNL and decreases hepatic NEFA oxidation, leading to net TAG synthesis

46
Q

What does the PDH complex do in the liver?

A

-Converts pyruvate to Acetyl CoA

47
Q

What impact does exercise have on fructose-stimulated de novo lipogenesis?

A

-Egli et al 2013 showed that eating a high fructose diet increased plasma TAG/DNL only when sedentary. When trained, it did not impact plasma TAG at all.

48
Q

What impact does exercise mode or intenity have on the imapct of exercise on blood TAG?

A
  • Gabriel et al 2012 found that HIIT protocol that burned only 103 calories significantly reduced plasma TAG, where 30 minutes of brisk walking that burned 240 calories did not.
  • This could be due to the afterburn effect of HIIT?
49
Q

What impact does exercise have on Liver TAG in insulin resistant people, and why?

A
  • Reduced Liver TAG and DNL

- Because muscle glycogen storage increased

50
Q

How may exercise reduce TAG via altering fat oxidation?

A
  • Exercising minly reduces VLDL secretion from the liver (Gill et al 2001)
  • Exercising increases endogenous and exogenous fat oxidation even a whole day after exercise
51
Q

How is serum betahydroxybutyrate/ketogenesis affected by exercise?

A

-Increased following a 90 minute walk the day before, compared to rest, implying ketogenesis is higher.

52
Q

Blood flow is another mechanism by which exercise may reduce postprandial TAG. Why?

A

Improving delivery of TAG to adipose, liver or muscles.

53
Q

What are the proposed mechanisms by which exercise reduces post-prandial lipaemia?

A
  • Increasing liver fat oxidation/ketogenesis
  • Decreasing VLDL secretion from the liver
  • Decreasing DNL indirectly by improved glycogen storage
  • Potent stimulation of LPL in muscle meaning increased muscle fat oxidation rate
54
Q

Why do obese people have a suppressed rate of TAG extraction from the blood, and why is this a problem?

A

Because their fat cells are already ‘full’ so can’t take on more. The TAG needs to go somewhere though, leading to ectopic fat accumulation in the muscles, liver, pancreas and around organs

55
Q

What is the problem of ectopic fat accumulation, and where does it occur?

A

Muscle, Liver, and Pancreatic Beta Cells.

  • Reduces insulin sensitivity in muscle and liver
  • Impairs insulin secretion in beta cells
  • Thus increases risk for Type 2 Diabetes
56
Q

What is the health complication associated with having too little fat? (e.g. partial or total lipodystrophy)

A
  • Same problems as with excessive adiposity:
  • Severe insulin resistance
  • Type 2 Diabetes
  • Dyslipidemia
  • Hypertension

Physiology of Exercise and Health (5 decks)

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