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Biosci 358 > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Macronutrients

A
  • Carbs
  • Fats
  • Protein
  • Alcohol
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2
Q

Carbs and fat oxidation

A

Fully oxidised

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3
Q

Protein oxidation

A

not fully metabolised

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4
Q

EI = EE

A

weight stable

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5
Q

EI > EE

A

weight gain

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6
Q

EE > EI

A

weight loss

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7
Q

Food diary advantages

A
  • shows within and between individual variation
  • more information on less frequently eaten foods
  • portions can be assessed or weighed to increase accuracy
  • doesn’t depend on memory
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8
Q

Food diary disadvantages

A
  • respondents must be literate and cooperative
  • response bias
  • some may alter usual eating habits
  • respondent burden
  • under-reporting
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9
Q

24hr recall advantages

A
  • administration time can be short
  • does not require literacy
  • allows probing for incomplete information
  • no respondent burden
  • doesnt influence usual diet
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10
Q

24hr recall disadvantages

A
  • relies on memory and recall
  • portion size difficult to remember
  • 1 day only so not representative of the usual intake
  • interviewer variability
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11
Q

Food frequency questionnaire advantages

A
  • creates an overall picture of diet
  • not affected by season
  • useful for screening
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12
Q

Food frequency questionnaire disadvantages

A
  • relies on memory
  • requires ability to judge portion sizes
  • no meal pattern data
  • food lists often include common foods only
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13
Q

Diet history interview advantages

A

provides clarification of issues

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14
Q

diet history interview disadvantages

A
  • relies on memory
  • requires interview training
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15
Q

Doubly labelled water

A
  • used to measure energy expenditure
  • stable isotopes = deuterium and oxygen-18
  • isotopes measured in urine and difference between them used to calculate CO2 production
  • assumes subjects are in an energy balance
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16
Q

Protein intake biomarker

A

nitrogen in urine

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17
Q

Fat intake biomarker

A

erythrocyte phospholipid analysis

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18
Q

Carb intake biomarker

A

none

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19
Q

Micronutrients which are under tight control so dont have a biomarker

A
  • calcium
  • retinol
  • Vit E
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20
Q

Split of EE

A
  • 12% exercise
  • 28% non-exercise physical activity
  • 10% thermic effect of food
  • 50% resting metabolic rate
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21
Q

BMR

A

energy required for the work of vital functions such as maintaining ionic equilibrium, cell and protein turnover, cardiovascular function

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22
Q

What is the most important factor influencing BMR

A

fat free mass

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23
Q

Fat free mass

A
  • influenced by weight, height, gender and age
  • contains tissues and organs with high metabolic activities
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24
Q

BMR variability

A

can vary between individuals with same characteristics due to genetic factors

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25
Q

Methods to measure/estimate BMR

A
  • equation
  • O2 and CO2 production measured via mask, hood or whole body chamber
  • direct calorimetry
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26
Q

Disadvantages of ventilated hoods

A
  • takes a long time
  • patient has to remain still
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27
Q

Room calorimeter disadvantages

A
  • expensive
  • less sensitive due to its large volume
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28
Q

Relationship between body weight and BMR

A

if one increases so does the other

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29
Q

Indirect calorimetry

A
  • measures O2 consumption and CO2 production
  • EE and RQ
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30
Q

RQ =

A

VCO2/VO2

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31
Q

macronutrient with immediate oxidation but no storage

A

alcohol

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32
Q

macronutrient with rapid oxidation and a small storage

A

protein and carbs

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33
Q

macronutrient with slow oxidation and large storage

A

fat

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34
Q

Conditions which are correlated with obesity

A
  • hypertension
  • atherosclerosis
  • CHD
  • Type 2 diabetes
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35
Q

Direct costs of obesity worldwide

A
  • health services
  • lab tests
  • radiology
  • drug therapy
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36
Q

Indirect costs of obesity worldwide

A
  • increased sick leave = decreased efficiency
  • increased insurance premiums for employers
  • wages
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37
Q

What does BMI measure

A

index of adiposity

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38
Q

do people with obesity have a lower metabolic rate

A

no studies have shown they have a higher EE due to higher BMR, so a low metabolic rate is unlikely the cause of obesity

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39
Q

Virus associated with obesity

A
  • Ad-36 is the only human adenovirus correlated with obesity in humans
  • US study found that 30% people with obesity had serum AD-36 antibodies whereas 11% of non-obese had them
  • Odds ratio = 2x with antibodies
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40
Q

Ob gene in mice

A

mice which are monogenic for ob causes an absence in leptin

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41
Q

Ob gene in humans

A
  • humans can be heterozygous for ob gene homologue
  • causes an excess of leptin which increased body fat
  • however only 14 people found with this so unlikely a major cause of obesity
  • leptin therapy has seen a decrease in weight for these people
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42
Q

Genetic associations with obesity

A
  • ob gene
  • > 100 SNPs such as FT0
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43
Q

FT0 gene

A
  • found on chromosome 16
  • most clinically significant SNP
  • 16% of population is homozygous
  • causes poor appetite control
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44
Q

Mitochondrial deficiences and dysfunctions correlation with obesity

A
  • enhancer not causal
  • people with an accumulation of fat cells causes inflammation, insulin resistance and oxidative stress causing mitochondrial defects
  • decrease in SIRT1-7, PPARy and PGC-1a causes altered B-oxidation, decrease biogenesis and increase ROS
  • MOT-C
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45
Q

MOTS-C

A
  • mitochondrial peptide which can diffuse in blood
  • plays a role in insulin sensitivity
  • ## when MOT-C decrease then increased insulin resistance
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46
Q

Current fat intake recommendations

A

30-35%

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47
Q

High fat diet correlation with obesity

A

correlated with obesity due to a high fat diet causing a higher EI and lower satiety of fat than carbs etc

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48
Q

Blocking oxidation of fatty acids

A
  • CPT1 transfers long chain fatty acids from cytoplasm to mitochondria for oxidation
  • CPT1 can be blocked via MP leading to blocking fat oxidation
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49
Q

Medium chain triglycerides vs long-chain triglycerides

A
  • MCT = rapid oxidation, higher satiety and decreased EI
  • LCT = slow oxidation, lower satiety and increased EI
  • However human studies didnt see a difference in EI between MCT, LCT and SCT
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50
Q

What is De novo lipogenesis and how can you measure it

A
  • conversion of carbs to fat
  • can be measured via whole body calorimetry or isotopes
  • RQ > 1 indicates carb has been used to make fat
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51
Q

De novo lipogenesis isotope results

A
  • difference between lean and obese participants
  • obese = lower DNL than lean when on a low fat and high carb diet
  • DNL also depends on the type of carb - fructose has higher DNL than glucose
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52
Q

What is central to the control of energy balance

A
  • appetite control
  • regulation of EI
  • physiological mechanisms
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53
Q

Health guidelines for a healthy weight

A
  • enjoy a variety of nutritious foods which are low in energy
  • drink more water
  • eat smaller portions
  • be as active as possible
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54
Q

Is a low fat strategy successful for long term weight loss

A
  • could work long term
  • studies saw a significant reduction in body weight
  • low fat can mean low EI, high fibre and more nutritious foods
  • but can mean a higher sugar diet
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55
Q

Does a high added sugar diet promote weight gain

A
  • only if it increases EI
  • no evidence that sugars are a major problem but more the overconsumption of energy
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56
Q

Why are beverages a problem for weight loss

A
  • hard to regulate intake
  • most drinks are high in sugar
  • studies saw children which had a higher sugar sweetened beverage intake had an increased BMI
57
Q

Can protein aid long term weight loss

A
  • a diogenes trial studied families with at least one parent with obesity
  • diets were either HP LGI, LP LGI, HP HGI, LP HGI
  • saw that HP LGI was the only group to maintain weight loss
  • HP diets always had a greater reduction in weight than LP on the same GI
58
Q

Is high energy density the problem for obesity

A
  • a study with men on low ED, med ED or high ED diets saw that when ED increased so did EI
  • when ED was kept constant than EI didnt change
  • key to obesity = higher EI
59
Q

Portion sizes and obesity

A

larger portion sizes = increased EI = increased weight gain

60
Q

Best diet for obesity

A

no best diet just one you can maintain

61
Q

what public health recommendations for obesity should be

A

decreased ED and portion sizes

62
Q

Mediterranean diet decreases obesity?

A
  • thought to increase mitochondrial function
  • decreases ROS, increased AMP/ATP and Increased NAD
  • causes an increase in PGC-1a which increases mitochondrial biogenesis
63
Q

What is metabolic syndrome

A

adverse metabolic health characterised by a cluster of easily measured risk factors caused by weight gain and obesity

64
Q

Types of fat

A
  • Subcutaneous = above abdominal muscles
  • Visceral = under abdominal muscles, around organs
  • Ectopic = leakage of lipids into organs such as pancreas and liver
65
Q

What can ectopic fat cause

A
  • lipotoxicity
  • deterioration in organ function
66
Q

Type 1 diabetes

A
  • Insulin deficient
  • early onset
67
Q

Type 2 diabetes

A
  • insulin resistance
  • insulin cannot promote disposal from venous circulating in fasting and fed state
  • late onset
  • majority of diabetic cases
  • primary risk factor = obesity
68
Q

What is diabetes correlated with

A
  • age
  • gender (men at higher risk)
  • BMI (high BMI = high adipose tissue - not always true because of TOFI)
  • ethnicity (TOFI)
69
Q

TOFI study

A
  • thin on outside, fat in the inside
  • compared european and asian women with the same normal BMI
  • asian women carried a greater amount of abdominal and visceral fat = increased risk of diabetes
70
Q

Oral glucose tolerance test

A
  • used to identify impaired fasting glucose and impaired glucose tolerance = prediabetes
  • 75g glucose drink consumed and blood samples are collected over 2 hours
71
Q

Fasting and oral glucose tolerance test results for impaired fasting glucose

A
  • Fasting = >100mg/dl
  • 2hr = <200mg/dl
72
Q

Fasting and oral glucose tolerance test results for impaired glucose tolerance

A
  • fasting = <100mg/dl
  • 2h = 140-199mg/dl and remains high
73
Q

Fasting and oral glucose tolerance test results for combo of impaired fasting glucose and impaired glucose tolerance

A
  • fasting = >100mg/dl
  • 2h = 140-199mg/dl and remains high
74
Q

Fasting and oral glucose tolerance test results for normal samples

A
  • fasting = <100mg/dl
  • 2h = <140mg/dl
75
Q

How is metabolic syndrome classified

A

having atleast 3/5 biomarkers

76
Q

Risk biomarkers for metabolic syndrome

A
  • high waist circumference
  • high circulating triglycerides = >150mg/dl
  • low HDL = <40mg/dl (males) and <50mgl/dl (females)
  • Raised blood pressure = >130/>85
  • Raised fasting blood glucose = >100mg/dL
77
Q

Central obesity

A
  • high visceral fat and ectopic fat instead of high subcutaneous fat
  • can be estimated via waist circumference
  • can be assessed via MRI or CT
78
Q

HELENA trial

A
  • Intervention trial to prevent diabetes in groups of obese people
  • Group 1 = 25% of required caloric intake for 2 days and a healthy balanced diet for 5 days
  • Group 2 = 80% of required caloric intake over the week
  • Control group = healthy balanced diet
  • Those in group 1 and 2 both had a 5-10% weight loss and maintained it
  • weight loss led to decrease in visceral and ectopic fat
79
Q

What can a 5-10% weight loss improve

A
  • decreased HBA1C = decreased risk of diabetes
  • decreased cholesterol
  • increased HDL
  • decreased triglycerides
  • increase insulin sensitivity
80
Q

Finnish diabetes prevention study

A
  • intervention group told to decrease fat intake, increase fibre intake, increase physical activity and lose weight
  • 58% decreased risk of diabetes
81
Q

US diabetes prevention study

A
  • intervention group = maintain a 7% weight loss, eat a healthy low calorie and low fat diet, exercise at least 150min per week
  • one group was treated with metformin
  • saw a decrease in fasting plasma glucose and glycosylated haemoglobin = decreased risk of diabetes by 58%
  • intervention group performed better than metformin group
82
Q

Chinese Da Qing diabetes prevention study

A
  • intervention = reduce weight, low fat diet, healthy diet, increase exercise
  • decreased risk of diabetes by 31-46%
83
Q

Current diet recommendations to prevent metabolic syndrome

A
  • low in SFA and trans fat
  • high in fibre
  • high in fruit and veg
  • mediterranean diet
84
Q

High protein diet and prevention of metabolic syndrome

A

lack of evidence to evaluate metabolic response to high protein diets but there is currently an eu trial underway

85
Q

Direct trial for diabetes

A
  • intervention = low energy diet over 3-5 months and then slowly reintroduce foods, withdrawn off medication
  • Goal = lose 15kg
  • 50% of participants achieved normal glycaemia
86
Q

Functions of dietary fat

A
  • fuel
  • cell signalling
  • carrier of fat soluble vitamins
  • immune function and inflammatory response
  • membrane phospholipids
  • metabolic regulation
87
Q

Properties of fat

A
  • organic molecule made up of C,H,O
  • hydrophobic
  • require emulsification with bile to be degradaed
88
Q

3 types of dietary fats

A
  • triglycerides
  • phospholipids
  • sterol
89
Q

Triglycerides

A
  • glycerol backbone + 3FA
  • major fat source
  • neutral
  • storage molecule
90
Q

Phospholipid

A
  • membrane
  • amphiphilic
  • glycerol + 2FA + phosphate + choline
91
Q

Sterol

A
  • no FA on carbon ring structure
  • active molecules
  • usually from animal fats
92
Q

How are fatty acids classified

A
  • Length of carbon chain
  • Degree of unsaturation
  • Orientation of double bond (cis or trans)
  • Location of double bond (omega 6 or 3)
93
Q

Classification of FA via carbon chain length

A
  • SCFA = <6
  • MCFA = 6-10
  • LCFA = 12+
94
Q

How are trans fats formed

A
  • hydrogenation
  • H2 is added across double bond
  • converts oil to solid
95
Q

Fat digestion

A
  • Mouth = salivary lipase breaks down TAG
  • stomach = gastric lipase breaks fats into small droplets
  • gall bladder = releases bile into the small intestine for emulsification
  • small intestine = pancreatic lipase released into SI to break TAG into monoglycerides and FA
  • SCFA and MCFA = passive diffusion into bloodstream
  • LCFA = chylomicrons into bloodstream
96
Q

What do lipoproteins carry

A

cholesterol and triglycerides

97
Q

4 major lipoproteins

A
  • chylomicrons
  • VLDL
  • LDL
  • HDL
98
Q

Chylomicrons (what are they, properties and mechanism)

A
  • transient lipoproteins secreted by enterocytes
  • incorporation of LCFAs allows transport firstly through lymphatics and renders them soluble so they can be transported into the blood
  • once chylomicrons enter the bloodstream they are metabolised into FFA and remnants
  • remnants are used to create LDL and VLDL
99
Q

Arteriosclerosis

A
  • development of plaque between the intima and media of the arterial wall
  • oxidised LDL in arterial wall recruits macrophages = plaques begin to form
  • plaques are composed of cholesterol and immune cells
  • blood vessels narrow = heart attack
  • eventually the plaque will rupture
100
Q

Postprandial lipemia

A
  • a rise in TAG post meal
  • a greater rise in TAG is correlated with increased heart attack and all causes of mortality
  • type of dietary fat effects postprandial
  • SCFA and MCFA will have lower TAG chylomicrons due to rapid absorption
101
Q

How can post prandial lipemia be modified

A
  • changing lipase specificity = lipases act on sn-1 and sn-3 so you can alter what FA are found here
  • emulsification = rise in TAG reduced with emulsification due to small size
  • Protein addition = can decrease TAG
102
Q

LDL-C and its evidence for being liked with CVD

A
  • major atherogenic lipoprotein
  • works via aggregation to the vessel walls and oxidation
  • genetic forms of elevated LDL have an increased CVD risk
  • statins which lower LDL can decreased CVD risk
  • for every 0.026mmol/L increase of LDL then CVD is increased by 1-2%
103
Q

HDL-C and its evidence for lowering CVD risk

A
  • protective lipoprotein
  • involved in reverse cholesterol transport
  • circulates cholesterol from the tissues back to the liver where its incorporated into bile for excretion
  • may also retard oxidation and prevent LDL aggregation
  • those with low HDL have a higher CVD risk
  • lack of evidence as those with genetically and pharmacologically high HDL didnt have a reduced CVD risk
104
Q

MRFIT study - impact of lifestyle factors on CHD risk

A
  • studied a large group of men at risk of CHD and stroke
  • one group had extra care (decrease BP and smoking help) and received dietary advice
  • other group received usual care
  • they saw a decrease in CHD deaths with lifestyle changes
  • saw that 46% CHD deaths were accounted for by >4.65mmol/L cholesterol
105
Q

Major cholesterol raising agents in the diet

A

saturated fatty acids = lauric acid, myristic acid, palmitic acid

106
Q

How saturated fatty acids raise LDL and total cholesterol

A
  • stimulate the secretion of lipoproteins containing VLDL and LDL
  • suppress LDL receptors to delay removal of lipoproteins and excess cholesterol into LDL
107
Q

Stearic acid

A
  • saturated fatty acid
  • doesnt have same effect as other SFA due to its lack of absorption
  • rapidly converted to oleic acid via desaturation
  • oleic acid doesnt raise cholesterol
108
Q

Apo B-100

A
  • allows LDL to attach to specific receptors on the cell surface
  • allows for receptors to transport LDL where they are broken down to release cholesterol
109
Q

Possible mechanism of action by SFAs to increase CVD risk

A
  • SFA stimulate LDL receptors
  • LDL receptors release VLDL and LDL
  • SFA suppress receptors from removing lipoproteins from the plasma
  • excess cholesterol is packed into each LDL
  • increased LDL = increased chance of aggregation and oxidation
110
Q

How do Cis MUFAs and omega 6 PUFAs lower LDL

A
  • decrease secretion of lipoproteins containing apoB-100
  • activity of LDL-C receptors is increased
  • decreased VLDL and LDL
  • increased clearance of cholesterol
  • decreased cholesterol content of LDL
  • not all individuals respond in the same way (ApoE4)
111
Q

ApoE4

A
  • carriers have increased CVD risk
  • carriers have highest level of cholesterol compared to other ApoE genotypes as they dont respond well to cholesterol
112
Q

Nurses health study - replacing SFA in the diet

A
  • large group of female nurses
  • questionnaires completed on medical history and lifestyle
  • 14 years
  • those with high SFA and TFA had a higher risk of CHD
  • those with high UNHYDROGENATED MUFA and PUFA had a lower risk of CHD
113
Q

Replacement of SFA by omega 6 PUFAs??

A
  • initially thought to help CHD
  • reanalysis of data saw that increased omega 6 was correlated with increased deaths from CVD and CHD
  • recommendation cannot be made
114
Q

SFA from dairy products

A
  • might be protective for heart disease
  • no associations with increased risk of death, CHD and CVD
  • more clinical trials are needed to understand the causality
115
Q

Long chain omega 3 PUFA from fish

A
  • EPA
  • DPA
  • DHA
116
Q

What do epidemiological studies do

A

determines associations via observational studies

117
Q

What do intervention studies do

A

assess causality via measuring effects

118
Q

Greenland inuits - omega 3 benefits

A
  • similar fat intake as Danes and USA but had much lower CHD mortality
  • high intake of omega 3 PUFA
  • low intake of SFA
  • Danes had higher omega 6 and lower omega 3
119
Q

Epidemiological evidence for the benefits of omega 3 for CHD risk

A
  • US physicians health study = male physicians, FFQ used, saw that those which consumed atleast 1 fish meal per week reduced risk by 52%
  • nurses health study = healthy female nurses, diet and health questionnaires used, those with a higher fish intake had a significantly lower CHD risk compared to hoe which rarely ate fish
120
Q

GISSI intervention study - omega 3 and CHD

A
  • participants were supplemented with omega 3 and/or vitamin E
  • consumption of fish oil for 3.5 years resulted in 20% decrease in all cause mortality and a 45% decrease in sudden death
  • vitamin E had no additional effect
121
Q

Omega 3 mechanisms in preventing CHD

A
  • anti-arrhythmic = stabilises electrical activity of heart via preventing Ca2+ overload during periods of stress
  • anti-thrombotic = EPA may inhibit synthesis of PG which cause platelet aggregation
  • Hypotriglyceridemic = inhibition of VLDL and TG synthesis in liver = decreased TG levels
  • Retard growth of atherosclerotic plaque = decreased macrophage adhesion to vessel wall
122
Q

Adverse effects of fish oil capsules

A
  • fishy aftertaste
  • GI upset
  • increased susceptibility of LDL to oxidation
123
Q

Results of Study looking at omega 3 for primary and secondary prevention of CVD

A
  • increased EPA/DHA/ALA had little effect
  • omega 3 capsules did not decrease heart disease
  • ALA may be slightly protective
  • inconclusive
124
Q

Linoleic acid metabolism

A
  • metabolised into AA
  • AA triggers pro-inflammatory via COX 2
  • pro inflammatory = PG2, LTB4 and TXA
125
Q

Alpha linoleic acid (omega 3) metabolism

A
  • metabolised into EPA and DHA
  • EPA can be metabolised into anti-inflammatory proteins via COX-2
  • anti-inflammatory = PG3, TXA 3, LTB5
  • DHA metabolised into anti-inflammatory resolvins
126
Q

What is synthesis of EPA, DHA and AA dependent on

A

the availability of ALA and LA as their metabolic pathways use the same enzymes

127
Q

Effect of O3/O6 on platelet membrane activity

A
  • PUFAs are a important component of platelet phospholipid membranes
  • increased fish intake = increased O3 = increased EPA/DHA in membrane = decreased AA = increased anti-inflammatory = normal blood clotting activity
128
Q

Effect of O3 on rheumatoid arthritis

A
  • RA is correlated with increased proinflammatory cytokines
  • intervention study found that those supplemented with fish oil and those with fish oil/olive oil had a significant improvement in pain and inflammation
129
Q

O3 effect on depression

A
  • decreased O3 correlated with mood disorders
  • intervention study found that those supplements with DHA and EPA had a significant decrease in depression rating over 4 weeks
130
Q

O3 effect on cognition

A

intervention study found that those supplements with DHA and EPA had a significant improvement in memory and their ability to store/recall information for longer

131
Q

O3 and pregnancy

A

no adverse or beneficial effects with fish oil supplements

132
Q

O3 and immune function

A
  • observational studies saw that those which took fish oil during pregnancy had deceased allergies and asthma in their infants
  • post-natal supplementation had no effect
  • intervention study saw that fish oils could have immunomodulatory properties which are allergy protective for infants
133
Q

O3 FA signalling

A
  • inhibits AA
  • inhibits activation of pro-inflammatory TF = NFkB
  • activation of anti-inflammatory TF = PPARy
134
Q

O3 and metabolic health

A
  • insulin sensitising
  • can reduce dietary induced insulin resistance
  • may prevent type 2 diabetes
  • observation study = saw obese men which consumed high O3 had increased insulin sensitivity
  • intervention study = O3 stabilised IFG or IGT
  • rat models saw reversed insulin resistance
135
Q

Krill oil and insulin sensitivity

A
  • decreased sensitivity with krill oil consumption
  • doesnt have same effect as fish oil likely due to differing composition and high phospholipids
136
Q

PUFA recommendations for patients without CHD

A

eat a variety of fatty fish at least twice a week

137
Q

PUFA recommendations for those that need to lower triglycerides

A

2-4g of EPA and DHA per day

137
Q

PUFA recommendations for patients with CHD

A

consume 1g EPA and DHA per day

138
Q
A

Biosci 358 (3 decks)

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