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Biosci 358 > Exam > Flashcards

Exam Flashcards

1
Q

What is an epidemiology/observational study

A
  • study of disease in a population and nutrition related disease
  • observations only
  • studies association between diet exposure and disease
  • not causal evidence
  • in the past they have been used to identify many essential nutrients
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2
Q

3 types of epidemiology trial designs

A
  • ecological
  • case control
  • cohort
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3
Q

Ecological study

A
  • compare disease rates at the population level with consumption/exposure
  • commonly based on disappearance data (supplies produced and imported for domestic consumption)
  • example = correlation between daily meat intake and incidence of colon cancer
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4
Q

Pros and cons of ecological studies

A
  • pro = compares large contrasts in dietary intake
  • cons = doesnt consider other determinants which may vary in areas, lack of practical methods to measure dietary intake
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5
Q

Case control study

A
  • Compares diet of individuals with disease vs those without disease
  • looks at past exposures
  • can overcome weaknesses of ecological studies
  • participants are matched via factors such as gender, BMI
  • measured via Odds ratio
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6
Q

Pros of case control studies

A
  • small number of participants
  • can study rare disease
  • assesses a number of exposures
  • no long term follow up required
  • inexpensive
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7
Q

Cons of case control studies

A
  • selection bias
  • interviewer bias
  • information bias
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8
Q

Cohort study

A
  • prospective (looks into future)
  • collect diet information from individuals without disease and follow them to observe if disease occurs
  • measured by relative risk
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9
Q

Cohort study pros

A
  • time sequence can be determined
  • decreased recall and interviewer bias as outcomes and exposure collected at same time
  • can measure changes in diet over time
  • can examine multiple diseases
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10
Q

Cohort study cons

A
  • large number of participants
  • expensive
  • requires follow up
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11
Q

Intervention trials

A
  • aim to limit confounding variables and bias
  • randomised, double blind and placebo are gold standard
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12
Q

Randomised controlled trial

A
  • main strength is that potentially distorting variables should be distributed at random
  • decreases bias
  • random allocation to type of diet and order of dietary intervention
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13
Q

Randomised controlled trial difficulties

A
  • time required to make change may vary - hard to decide duration
  • compliance
  • participants may alter dietary pattern or behaviour
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14
Q

Types of blinding

A
  • unblinded
  • single blind
  • double blind
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15
Q

What is a placebo

A
  • inactive dummy nutrient
  • used to compare against the nutrient of interest
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16
Q

Cross over trial

A

all participants receive treatments in a random order with a washout period between treatments

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17
Q

Parallel treatment

A
  • each participant only receives one treatment
  • increased variability
  • needs more participants
  • good for those which cannot be cross over due to effects of treatments
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18
Q

Community trial

A
  • participants live at home
  • researcher prepares some of subjects diet or provides a test product
  • participants are given instructions on test foods but they are free to continue eating their normal diet
  • still required to visit research unit on regular basis
  • can vary in length
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19
Q

Community trial pros

A
  • large amount of participants
  • longer interventions
  • real life situationsC
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20
Q

Community trial cons

A
  • diet not controlled
  • minimal supervision = poor compliance
  • higher chance of a negative result
  • cannot be interpreted as causal evidence
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21
Q

Residential trial

A
  • participants live at a residential facility with provision of foods
  • all foods provided
  • regular blood and urine samples
  • vary in lengt
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22
Q

Residential trial pros

A
  • nutrients controlled
  • compliance
  • internationally recognised evidence
  • provides causal evidence
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23
Q

Residential trial cons

A
  • small number of participants
  • shorter intervention
  • expensive
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24
Q

Parental origins of health and disease

A
  • male founder mice subjected to an obesogenic environment have altered sperm which can impact fetal development and chances of adverse health conditions
  • parents with mental disorders likely to have children with mental disorders
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25
Q

Developmental origins of health and disease

A
  • nutritional deficiency and overnutrition in mothers during pregnancy can cause changes in epigenetic architecture of child
  • changes in breast milk composition can alter epigentics
  • changes in epigenetics can increase CVD etc
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26
Q

Epigenetics

A
  • childrens experiences affect the expression of their genes
  • wellness lifestyles could modify the epigenome of human reproductive cells and affecting the health of future generations
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27
Q

The dutch famine

A
  • effects on health later in life were most pronounced among those exposed to famine in early gestation
  • lesser effects in those exposed in mid or late gestation
  • shows different nutrients needed at different stages
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28
Q

first 1000 days of human development

A
  • includes preconception and pregnancy phases - account for 70% of an individuals future life
  • intervention at earlier stages can decrease risk trajectory
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29
Q

Normal weight gain during pregnancy

A
  • underweight = 12.5-18kg
  • healthy = 11.5-16kg
  • overweight = 7-11.5kg
  • obese = 5-9kg
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30
Q

Increased nutritional needs in pregnant women

A
  • folic acid, iodine, iron, VITB6 and zinc
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31
Q

Folic acid

A
  • VitB9
  • 800ug everyday for 4 weeks preconception and 12 weeks post pregnancy
  • prevent neural tube defects
  • found in peanuts, spinach, fortified flour
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32
Q

Iodine

A
  • important in all 3 trimesters
  • body cannot make enough
  • in milk, cheese, fortified salt
  • pregnant = 220ug/day
  • breastfeeding = 290ug/day
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33
Q

Iron losses during pregnancy

A
  • fetus
  • placenta
  • RBC mass
  • obligatory basal lossses
  • delivery
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34
Q

Mothers with undernutrition, type 1etc can have what health outcomes in their offspring

A
  • increased blood pressure
  • insulin resistance
  • increased adiposity
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35
Q

Mothers with insulin resistance, type 2 etc can have what health outcomes in their offspring

A
  • decreased fertility
  • metabolic syndrome
  • CVD
  • obesity
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36
Q

Effects of mother consuming an imbalanced diet

A
  • alteration in methylation causes changes in genetic programming (epigenetics)
  • neuroinflammation
  • gut microbiome endotoxicity = SCFA made which cross blood brain barrier causing inflammation
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37
Q

Breast milk composition

A
  • 90% water
  • organisms/cells
  • nutrients
  • bioactives
  • contains less protein and calcium than cows milk
  • contains more MUFA, PUFA and lactose than cows milk
  • composition can change with mothers health and age
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38
Q

Key factors influencing breast milk composition and maternal/infant health

A
  • age
  • diet
  • activity
  • alcohol
  • gestational age
  • mode of delivery
  • environment
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39
Q

3 stages of breast milk

A
  • colostrum
  • transitional milk
  • mature milk
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40
Q

Colostrum

A
  • days 1-4
  • yellow/cream colour
  • high concentration of fat soluble vitamins, minerals, proteins and immunoglobulins
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41
Q

Transitional milk

A
  • 4-20 days
  • high concentration of fat, lactose and water soluble vitamins
  • more calories
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42
Q

Mature milk

A
  • > 20 days
  • 90% water
  • 10% carbs, proteins and fats
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43
Q

Nutrition of baby for first 2 years

A
  • 1st 6 months = breast feeding
  • at 6 months start introducing solid foods
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44
Q

Nutrition recommendations for breastfeeding mothers

A
  • 9 servings of grainy food
  • 7 servings vegetables
  • 2.5 servings milk or milk alternatives
  • 2.5 servings legumes, nuts, fish etc
  • 2 servings fruit
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45
Q

What in the human milk system effects offspring epigenetics

A
  • nutrients
  • signalling proteins
  • probiotic
  • postbiotic
  • all involved in driving miRNA formation which is important for epigenetic modifications
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46
Q

What in the human milk system effects offspring gut microbiome

A
  • nutrients
  • signaling proteins
  • lactoferrin
  • immuno-globulins
  • probiotics
  • postbiotics
  • prebiotics
  • immune cells
  • fatty acids
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47
Q

What in the human milk system effects offspring gut integrity

A
  • nutrients
  • signaling proteins
  • immuno-globulins
  • probiotics
  • postbiotics
  • immune cells
  • fatty acids
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48
Q

miRNAs and epigenetic modifications

A
  • miRNAs produced in breast milk are packaged into vesicles
  • vesicles enter blood circulation to cross blood-brain barrier causing epigenetic modifications in the offspring
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49
Q

Obesity in bottle fed vs breast fed

A

higher level of obesity in those which were bottle fed

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50
Q

Why infant formula cannot replace breast milk

A

doesnt contain all key ingredients

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51
Q

Evidence on the inclusion of components in infant formula

A
  • addition of LCFA saw increased immunity
  • addition of protein saw increased growth
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52
Q

Developmental milestones and nutrition

A
  • senses and motor = increased protein, calcium and vit D needs
  • social and emotional = increased VitB needs
  • cognitive and language = increased VitC, iron, zinc, LCFA needs
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53
Q

UNICEF framework for decreased prevalence of micronutrient deficiencies

A

improve food, health, water/sanitation and social protection systems leading to good diets for young children

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54
Q

Nutrition guidelines for 0-2yr

A
  • Breastfeed for 2+ years
  • introduce solid food at 6 months
  • no added salt or sugar
  • dont force them to eat
  • breast milk and water only
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55
Q

Early life nutrition and health trajectory

A
  • what you eat as a child dictates 70-80% of what you eat in the future
  • introduction of unhealthy foods as a child can decrease health as an adolescence
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56
Q

What is the population structure problem with having less young people

A
  • lower fertility and reproduction = less new population
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57
Q

What is successful aging

A

a multidimensional concept which involves both health and physiological aspects

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58
Q

Theories of aging

A
  • genetic control
  • telomere shortening
  • antagonistic pleitrophy
  • disposable soma
  • genetic mutation
  • caloric restriction
  • waste accumulation
  • mitochondrial theory
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59
Q

Antagonistic pleitrophy theory

A
  • aging as a side effect of selection of genes for fitness and fertility
  • genes can enhance fitness early in life but diminish it later
  • ex = ApoE4 is beneficial for cognition early in life but detrimental later
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60
Q

Disposable soma

A
  • trade off between reproductive fitness and longevity
  • high reproduction = increased aging
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61
Q

Gene mutation theory

A
  • accumulation of mutations leads to a decrease in cellular function
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62
Q

Genetic control of aging theory

A
  • switching on and off of certain genes with age
  • partial loss of INR + IGF-1R can lead to decreased growth with increased lifespan
  • decreased Fox01 can increase longevity as it decreased INR etc
  • decrease in pro-inflammatory cytokines can increase longevity
  • genes can effect mitochondrial health and numbers
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63
Q

Mitochondrial theory

A
  • mitochondrial dysfunction increases with age
  • in dysfunctional mitochondria = ROS accumulates causing mutations and oxidative damage = decreased cellular function
  • Mediterranean diet could combat mitochondrial dysfunction
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64
Q

Telomere theory

A
  • telomeres are repeating sequences at the end of chromosomes to protect from damage
  • increased age = decreased telomere length = increased damage
  • could be protected against via caloric restriction
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65
Q

Caloric restriction theory

A
  • decreased caloric intake correlated with a decreased ROS production
  • japanese population has lower caloric intake and have high successful aging
  • may decrease insulin signaling which decreases cell division and increases cell repair
  • decreased ROS = decreased DNA damage = genome stability
  • cells can manage stress better = more repair
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66
Q

Waste accumulation theory

A
  • accumulation of waste such as lipofuscin can impair autophagy
  • decreased autophagy = increased aging
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67
Q

Physiological changes with age

A
  • immune system
  • musculoskeletal system
  • CV system
  • CNS
  • digestive system
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68
Q

Nutritional disorders in older adults

A
  • malnutrition
  • micronutrient abnormalities
  • overnutrition
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69
Q

Malnutrition conditions

A
  • under-weight
  • cachexia
  • sarcopenia
  • frailty
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70
Q

Malnutrition risk factors

A
  • diarrhea
  • depression = decreased motivation to eat
  • dementia
  • dentition = inability to chew
  • dysgeusia = decreased appetite
  • dysfunction
  • drugs = decreased nutrient absorption
  • disease
  • dysphagia = inability to eat
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71
Q

inflammaging

A
  • age related declines in intestinal tissue function due to altered gut microbiota causing chronic immune stimulation
  • leads to inflammation
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72
Q

Strategies to promote healthy aging

A
  • improve nutrient intake (protein and fibre)
  • limit inflammation
  • decrease oxidative stress
  • promote gut microbiota balance
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73
Q

Modifiable factors modulating aging

A
  • nutrition
  • physical activity
  • sleep quality
  • stress
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74
Q

unmodifiable factors modulating aging

A
  • gender
  • genes
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75
Q

aging and the digestive system

A
  • Nose and mouth = decreased taste
  • Oesophagus = decrease peistalsis, trouble swallowing
  • stomach = decreased elasticity = decreased food eaten
  • liver = shrinkage, decreased ability to detoxify
  • pancreas = decreased secretion of enzymes = decreased nutrients
  • large intestine = decrease peristalsis, altered microbial fauna
  • small intestine = compromised gut-associated lymphoid tissue capacity
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76
Q

Ghrelin

A
  • increases appetite
  • decreases with age
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77
Q

PYY

A
  • suppresses appetite
  • increases with age
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78
Q

CCK

A
  • suppresses appetite
  • increases with age
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79
Q

Insulin

A
  • suppresses appetite
  • decreases with age
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80
Q

Leptin

A
  • inhibits hunger
  • increases with age
  • EVIDENCE IS CONFLICTING
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81
Q

Anorexia of aging GI motility changes

A
  • decreased stomach compliance = early satiety
  • delayed gastric emptying = post prandial satiety
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82
Q

Age related disruptions in the gut-brain axis

A
  • disrupted immune cell function leads to pro-inflammatory cytokines which cross the impaired blood brain barrier = INFLAMMATION
  • cognitive decline due to decreased hippocampal neurogenesis
  • altered microbial composition and function = decreased SCFA and mucus integrity
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83
Q

Nutrition factors which affect metabolic aging

A
  • dietary fat (increased MUFA/PUFA = GOOD)
  • dietary protein
  • caloric restriction
  • CV function
  • dietary carbs
  • western style diet
  • nutrient status
  • meeting nutritional requirements
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84
Q

Dietary protein and aging

A
  • anabolic so promotes muscle build up
  • older people have anti anabolic modulators so you must increased protein intake to overcome anabolic resistance
  • need high quality protein and balanced intake
  • saw that 2x intake can increase lean muscle mass
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85
Q

Micronutrient and aging

A
  • micronutrient sufficiency = normal aging
  • micronutrient deficiency = accelerated aging
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86
Q

VIT B12 deficiency in elderly

A
  • decreased absorption leading to deficiency
  • causes neurologic damage and anemia
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87
Q

Folic acid deficiency in elderly

A
  • due to inadequate consumption or drug/alcohol
  • causes megoblastic anemia
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88
Q

Vit C deficiency in elderly

A
  • due to inadequate consumption
  • causes impaired wound healing and swollen gums
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89
Q

Vit D deficiency in elderly

A
  • due to lack of sun exposure
  • causes osteomalacia and muscle weakness
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90
Q

Diet strategies for promoting healthy aging

A
  • okinawa
  • DASH
  • harvard healthy eating plate
  • mediterranean diet
  • nordic
  • planetary health
  • all focus on low fat and calories
  • lead to decreased inflammation, oxidative stress, mitochondrial dysfunction etc
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91
Q

BMI and body composition

A
  • commonly used to assess disease risk as its easy to measure
  • bad as it cannot distinguish between muscle and fat
  • obesity threshold is based on european populations
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92
Q

2 compartment model of body composition

A
  • total body fat and FFM
  • has to be measured indirectly
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93
Q

Underwater weighing - 2 compartment model

A
  • estimates body volume using archimedes principle
  • measures difference between weight on land and underwater weight to calculate body density and fat
  • body density corrected for residual lung volume
  • fat density = 0.9
  • FFM density = 1.1 (assumed but varies)
  • limited clinical application
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94
Q

Air displacement plethysmography/ BOD POD - 2 compartment

A
  • tight minimal clothing required
  • pressure sensors determine vol of air displaced
  • body volume = air vol empty - air vol person inside
  • body density corrected for residual lung volume
  • limited clinical application
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95
Q

3D photonic scanning - 2 compartment

A
  • 4 laser scanning pillars with integrated cameras
  • optical triangulation and suitable calibration yields 3D image
  • tight minimal clothing requirement
  • limited clinical application
  • good agreement of body volume with underwater but small volume differences produces large differences in fat = NOT GOOF
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96
Q

Skinfold anthropometry - 2 compartment

A
  • caliper measurement of subcutaneous tissue at multiple sites
  • assumes chosen site provides adequate info on entire fat
  • assumes fixed relationship between subcutaneous and non-subcutaneous fat
  • difficult for obese subjects
  • needs experienced operators
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97
Q

3 compartment model

A

composition from mass, TBW and body volume

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98
Q

DXA - 3 and 4 compartment

A
  • sends 2 low dose x-rays which are absorbed differently by bones and soft tissue
  • directly provides bone mineral and soft tissue
  • possible to partition soft tissue into fat and lean components
  • relies on values which are normally based on hydrated tissue
  • fast
  • high precision
  • regional composition analysis
  • can estimate visceral fat
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99
Q

Why is there no threshold of visceral fat mass for risk of mortality

A

odds ratios are specific for each individual

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100
Q

Dilution of tracer - total body water

A
  • usually dueterated or tritiated water
  • plasma, urine or saliva samples collected and assayed after 3hr equilibration
  • time consuming
  • can be used to calculate total body fat
  • healthy individual = 73% of TBF
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101
Q

Bioelectrical impedance analysis - TBW

A
  • used to measure body composition via applied current flows through fluid in body
  • fat is a non-conductor
  • total fluid vol = ht^2/R
  • to increased relationship factors such as weight,age and sex are included
  • gold standard for determination of total body water
  • similar to DXA results
102
Q

Bioimpedance phase angle

A
  • uses raw impedance data
  • reactance due to capacitive nature of cellular tissue
  • decreased cellular integrity and cellular tissue = decreased angle = decreased prognosis for survival
  • Considers resistivity so PA is sensitive to fluid changes
103
Q

4 compartment model

A

Fat calculated off body volume, water, body mass and weight

104
Q

Skeletal muscle index values for sarcopenia

A
  • <38.5 for women
  • <52.4 for men
  • varies between people of the same BMI
105
Q

Measuring skeletal muscle mass

A
  • MRI/CT
  • DXA = need to adjust FFM threshold for those with reduced muscle mass
  • Bioimpedance analysis = need to adjust FFM threshold for those with reduced muscle mass
  • ultrasound
106
Q

MRI/CT advantages - SMM

A
  • provides regional analysis
  • can seperate intramuscular and visceral fat from subcutaneous
107
Q

MRI/CT disadvantages - SMM

A
  • expensive
  • not widely available
  • CT has high radiation dose
108
Q

Ultrasound advantages - SMM measure

A
  • non invasive
  • no ionising radiation
  • can track muscle changes over time
  • low cost
  • clinically available
109
Q

Ultrasound disadvantage - SMM

A
  • need an optimal and accurate way to conduct ultrasound measurement in clinical population s (obesity etc)
  • limited data
110
Q

What is a nutrient

A

a substance or ingredient that promotes growth, provides energy and maintains life

111
Q

Gustatory system

A
  • main sensory system responsible for the perception of flavour
  • interacts with olfactory and trigemal
  • signals nutritional value
  • signals body to digest and process nutrients
  • contributes to the activation of satiety and reward systems in the brain
112
Q

Lingual papillae on tongue

A
  • circumvalate
  • foliate
  • fungiform
  • filliform
113
Q

Circumvalate papilla

A
  • largest
  • 10-14 in humans
  • 100s taste buds
  • sit along the edge of the suleus terminalis at the posterior end
114
Q

Foliate papillae

A
  • dozens of taste buds
  • found on the sides of the tongue
115
Q

Fungiform papillae

A
  • mushroom shaped
  • towards the anterior 2/3
  • 0-15 taste buds
116
Q

Filliform papillae

A
  • most common
  • no taste buds
  • contain keratin
  • run in strips parallel to median
  • associated with texture and sensation of touch
117
Q

Type 1 taste cell characteristics

A
  • low salt
  • glial like
  • spindle shaped support cells with long microvilli
  • no synapse
  • most common
118
Q

Type 2 taste cell characteristics

A
  • sweet, bitter or umami
  • vesicular synapse
  • secrete ATP and Ach
119
Q

Type 3 taste cell characteristics

A
  • sour taste
  • synapse
  • secrete serotonin, GABA and noradrenalin
120
Q

Type 4 basal taste cell characteristics

A
  • found at base of taste bud
  • undifferentiated
121
Q

Central transduction of taste

A
  • taste bud depolarised and activates afferent nerves
  • afferent nerves then activate cranial nerves
  • nerves synapse in the NTS which relays taste info to thalamus
  • thalamus to gustatory cortex in brain
122
Q

Cranial nerves

A
  • facial nerve (VII)
  • Glossopharyngeal (IX)
  • Vagus (X)
123
Q

Hot and cold receptors in trigeminal nerve

A
  • TRPV1 = hot
  • TRPM8 = cool
124
Q

Type 1 taste cell signalling

A
  • Na from salt activates ENaC
  • Na enters cell causing depolarisation
  • depolarisation causes calcium channels to open
  • calcium causes neurotransmitter release
125
Q

Type 3 taste cell signalling

A
  • H+ enters cell through Otop1 causing depolarisation
  • depolarisation causes sodium channels to open = depolarisation
  • calcium channels open = neurotransmitter release into a synapse of the afferent nerve
126
Q

Type 2 taste cell receptors

A
  • Tas1R = sweet or umami
  • Tas2R = bitter
127
Q

TAS1R

A
  • obligatory dimers
  • sweet = T1R2/T1R3
  • umami = T1R3/T131
  • Ligands bind to the extracellular venus fly trap domain or transmembrane pocket
  • couple and activate gustducin
  • may also signal via Gas
  • Ko models show obligatory dimer
128
Q

TAS2R

A
  • monomeric
  • diverse ligands
  • ligands bind in a TM domain pocket - possible other parts of receptor may be involved in snatching ligands
  • couple and activate gustducin
129
Q

Gustducin

A
  • G protein
  • Heterotrimer
  • a subunit = a-gustducin
  • GBy = Gy13 + GB3
130
Q

TAS1R and TAS2R signalling

A
  • receptor couples and activates gustducin
  • a-gustducin activates PDE which causes cAMP to be broken down into AMP
  • By subunit activate PLC
  • PLC breaks down PIP2 into DAG and IP3
  • IP3 binds IP3 receptor on ER causing calcium channel to open = increased Ca in cytoplasm
  • Ca sensitive TRPM4/5 transmembrane channels open = Na into cytoplasm = depolarisation
  • depolarisation opens Na channels = increased Na
  • action potential
  • actional potential causes ATP to be released outside via CALHM1/3
  • ATP activates P2X2 or P2X3 on afferent cranial nerve causing signal to go to gustatory cortex
131
Q

Kokumi (richness) signalling

A
  • Calcium sensing receptor
  • Gaq/11 coupled obligate dimer receptor
  • may enhance Tas1/2 via PLC activation
  • Gai/o activation could also synergise with a-gustducin via decreased cAMP
  • causing increased neurotransmitter release
132
Q

6 main components of the digestive system

A
  • ingestion
  • movement
  • physical breakdown = mainly in mouth and stomach
  • chemical breakdown = mostly in small intestine
  • absorption - mostly in small intestine
  • defecaton
133
Q

GI tract

A

muscular tube running from mouth to anus - containing regions with specialised functions in the digestive process

134
Q

2 main parts of digestive system

A
  • GI tract
  • accessory organs = pancreas, gallbladder
135
Q

Gallbladder digestion

A

release bile salts which emulsify and break down fat

136
Q

Pancreas in digestion

A

exocrine pancreatic cells secrete enzymes

137
Q

Gut microbiome - GI tract

A
  • GI tract is colonised by bacteria
  • densest bacterial population in the large intestine
  • bacteria metabolise fiber and other compounds such as bile acids
  • bacteria synthesise SCFA and vitamins
138
Q

How digestion alters tastants present

A
  • chewing and mixing frees nutrients/tastants from food particles
  • enzymes release tastants from larger molecules
  • microbiome produces new tastants
  • absorption removes tastants from GI tract
139
Q

Enteroendocrine cell characteristics

A
  • nutrient sensing cells in the GI tract
  • share common activation and signalling mechanisms with type II taste cells
  • express gustducin, PLC B and TRPM5
  • release GI peptides such as GLP-1
  • act locally or remotely
  • found in gastric and intestine
  • express a variety of taste receptors
140
Q

Types of enteroendocrine cells and location

A
  • X/A cells = stomach
  • I and K cells = duodenum and first third of intestine
  • L cells = small and large intestine
141
Q

What do X/A cells secrete

A

Ghrelin = increase appetite acutely and then decreases it

142
Q

What do I cells secrete

A

CCK = inhibits food intake and delays gastric emptying

143
Q

What do K cells secrete

A

secrete GIP

144
Q

What do L cells secrete

A

GLP-1 and PYY = delays gastric emptying and increases insulin sensitivity

145
Q

Bitter taste receptors (TAS2R) and enteroendocrine

A
  • In X/A, I and L cells
  • induce ghrelin, CCK and GLP-1
146
Q

Sweet or umami and enteroendocrine

A
  • TAS1R3 (sweet or umami) in L, P and K cells
  • Sweet (TAS1R3/TAS1R2) induces PYY, GLP-1 and GIP
  • Umami (TAS1R3/TAS1R1) induces ghrelin and GLP-1 release
147
Q

FA receptors and enteroendocrine

A
  • FFAR4 expresssed in X/A, K, I and L cells = release of GIP, GLP-1 and CCK
  • FFAR1 has widespread expression
  • SCFA receptors (FFAR2 and FFAR3) expressed in L cells = release of GLP-1 and PYY
148
Q

Pancreatic enteroendocrine cells

A
  • Beta, alpha and delta cells in pancreatic islets
  • insulin and amylin release is stimulated by nutrient influx
  • amylin is currently a major target for obesity
  • reportedly express gustducin and nutrient receptors
149
Q

Surgical interventions for obesity

A
  • bariatric or metabolic surgery
  • Roux en-Y bypass and laporoscopic band
  • reduced food intake
  • only recommended in patients with a BMI >40
  • effective long term weight loss
150
Q

Difference between endogenous (peptides) and exogenous (drugs) molecules

A

endogenous only activate receptors at specific times/locations while exogenous activate any accessible receptors

151
Q

GLP-1 effects and how they are mediated

A
  • via vagal afferents in the gut/portal vein in order to arrest food intake
  • triggers satiety signal and inhibit gastric emptying via the brainstem
  • enhances insulin release
152
Q

GLP-1 half time

A

1-2 minutes in circulation

153
Q

GLP-1 mimetics

A
  • have stabilising modifications to increase circulation half life
  • modifications = AA sequence, lipids (too big to filter out) and antibody
  • stimulate insulin release
  • primarily involves GaS but also Gaq
  • administered via injection
  • liraglutide, semaglutide and trizepatide
154
Q

Semaglutide

A
  • GLP-1 mimetic
  • saw 11% weight loss in clinical trials
  • weight was gained back rapidly after withdrawal
  • 1mg weekly
  • 30% of weight loss was lean body weight (muscle)
155
Q

Trizepatide

A
  • GLP-1 and GIP mimetic
  • 18% weight loss at phase III clinical trials
156
Q

Ghrelin and obesity

A
  • hunger hormone
  • peaks immediately prior to a meal and acts in the hypothalamus to induce food intake
  • no current drugs targeting
  • blockade reduces food intake but no changes in body weight
  • decreases insulin release so would block GLP-1 action
157
Q

Amylin and obesity

A
  • initially identified from pancreatic amyloid deposits in diabetes patients
  • co-secreted with insulin by enteroendocrine islet B-cells
  • half life = 20-30 minutes
  • release induced by glucose and amino acids (arginine) = enhanced when both
158
Q

Amylin effects

A
  • mediated via brainstem causing mean ending satiation
  • inhibits gastric emptying
  • decreases blood glucose
  • inhibits glucagon release
159
Q

Pramlintide

A
  • Amylin mimetic
  • modified AA sequence to reduce amyloidogenesis
  • 3 injections per day after meals
  • 5% reduction in body weight in clinical trials
  • discontinued as expensive and other molecules were more effective
160
Q

Amycretin

A
  • oral dual amylin and GLP-1 mimetic
  • in trial
  • trial had 13% weight loss but this isnt peer reviewed
161
Q

Functional food

A

provides some extra physiological benefits apart from its basic nutritional functions and also may decrease the risk of chronic disease

162
Q

Nutraceutical

A
  • a product isolated or purified from foods generally sold in medicinal form
  • demonstrated to have a physiological benefit or provide protection against chronic disease
163
Q

Inorganic minerals

A

a chemical element required as an essential nutrient by organisms to perform functions necessary for life

164
Q

Vitamins

A
  • a group of organic compounds which are essential for normal growth and nutrition
  • required in small quantities in the diet because they cannot b e synthesised by the body
165
Q

Probiotics

A
  • live microorganisms that can confer health benefits to the host
  • found in fermented foods
  • most are species of lactobacillus
166
Q

Probiotic potential health benefits

A
  • treatment of diarrhoea
  • symptoms of IBS
  • UTI
  • decreased duration of intestinal infections
  • manage lactose intolerance
167
Q

Prebiotics

A
  • non-digestible substances
  • insoluble or soluble dietary fibre
168
Q

Herbs

A

plants with savory or aromatic properties used for flavoring and garnishing foods along with having some medicinal properties

169
Q

Phytochemicals

A
  • chemicals produced by plants via primary or secondary metabolism
  • carotenoids and poly phenols
  • ex = catechins and anthocyanins
170
Q

Considerations when deciding a functional food or a nutraceutical

A
  • dosage (can you eat enough of it)
  • taste
  • storage (can you get it to people fresh)
171
Q

Nutraceutical considerations

A
  • poor regulatory control in some countries
  • lack of scientific evidence
  • may not contain amount or ingredients that it claims it does (Ginseng example)
  • safety
  • does it work
172
Q

Safety issues with St Johns Wort

A
  • inhibit liver enzyme CYP1A1
  • involved in drug metabolism
  • leads to a higher concentration of drug in the blood
  • also induces CYP3A4 which can decrease indinavir concentration in the blood leading to drug resistance and treatment failure
173
Q

Ephedra safety issues

A
  • contains active ephedrine
  • mimics adrenaline
  • activates alpha and beta adrenergic receptors
  • caused heart attacks, strokes and seizures in some leading to 155 deaths
174
Q

Bioactivity

A
  • capacity to induce a physiological response
  • assessed in vitro, ex vivo and in vivo
175
Q

Bioaccessibility

A
  • quantity of a compound released from food matrix into GI
  • assessed in vitro
176
Q

Bioavailability

A
  • amount that ends up in the blood unmodified
  • assessed in vivo
177
Q

Problem with bioavailability in nutritional sciences

A

lacks the well-defined standards associated with the pharmaceutical industry

178
Q

Quercetin

A
  • phytochemical
  • highly bioactive in in vitro assays
  • low water solubility limits its bioaccessibility
  • has very low levels of bioavailability = 0% in humans
  • study found that there was an increase in quercetin metabolites as body was trying to convert it into a low bioactive compound
179
Q

Digestion considerations when designing a compound

A
  • the region you want it to target (mouth, stomach, intestine etc)
  • pH
  • enzymes
  • stability
180
Q

Stimulated in vitro digestion assessing bioaccessibility

A
  • had conditions which mimicked the different areas of the digestive system
  • found that the addition of a excipient can allow for altered dispersion increasing bioactivity
181
Q

Ex-vivo/in-situ experiment adavantages

A
  • assesses absorption and bioavailability
  • can be used to look at tissue specific absorption
  • rapid and reliable results
  • used for optimisation of formulation
182
Q

Ex-vivo/In-situ experiment disadvantages

A
  • often requires complex surgical procedures and instrumentation
  • results are similar but no the same as in intact animals
183
Q

Methods to get evidence for bioactivity

A
  • chemical determination
  • chemical/enzymatic/bioassays
  • animal trials
  • clinical trials
184
Q

Chemical determination

A
  • infer biological activity from the content of the product
  • look for bioactive compounds (THC)
185
Q

Assay limitations

A
  • difficult to assay toxicity
  • only assess bioactivity
  • if not done carefully it may have zero relevance to in person effects
186
Q

Animal trial advantages

A
  • excellent for assessing toxicity
  • complicated measurements can be done
187
Q

Animal trial disadvantages

A
  • not suitable for all outcomes
  • animal bioavailability is often different from people
  • issues around animal cruelty
188
Q

Human clinical trial advantages

A
  • best level of evidence
  • excellent for determining bioactivity
  • participants can give subjective feedback
  • used for regulatory approval
189
Q

Human trial disadvantages

A
  • limited options for tissue sampling
  • often not done in target group
  • complaints
  • lots of trial regulations
190
Q

Oxidative stress

A

excessive oxidative load put on the body by disruption of the balance between oxidant and antioxidant function

191
Q

free radical

A

an unpaired e- alone in orbit, can cause oxidative damage damage to lipids, proteins and DNA

192
Q

Hydroxyl

A
  • OH
  • Most biologically relevant due to splitting of O-H in H2O
  • once formed damage is unavoidable
  • highly reactive
  • dealt with by repair systems - DNA repair enzymes
193
Q

Superoxide

A
  • O2-
  • molecules such as adrenalin react with O2 to make superoxide
  • deliberate generation by defences against bacteria and viruses
194
Q

Nitric oxide/dioxide

A
  • NO has physiological functions such as regulation of BP and intracellular signalling
  • excess NO is toxic causing tissue injury
  • NO2 is formed when NO reacts with O2-
195
Q

Oxidative stress and obesity

A
  • measured urinary creatinine to assess oxidative damage
  • smoking, diabetes and BMI were highly associated with systemic oxidative stress
196
Q

Antioxidant

A

compound or molecule that can inhibit the oxidation of other molecules or compounds, can suppress oxidative stress

197
Q

2 ways antioxidants can act

A
  • chemical
  • indirect
198
Q

Direct chemical antioxidant action

A

antioxidant molecules act to delocalise free radicals decreasing reactivity and preventing cellular damage

199
Q

Vitamin E/a-tocopherol

A
  • the most important free radical scavenger within membranes and lipoproteins
  • inhibits lipid peroxidation via scavenging peroxyl radical
200
Q

Vitamin C

A
  • inhibits the carcinogenicity of dietary nitrosamines
  • recycles a-tocopherol
201
Q

Known important antioxidants

A

Vitamin C and E

202
Q

How might Vit C act as a prooxidant

A

in the presence of Fe it can react via the fenton reaction to produce free radicals

203
Q

Enzymatic antioxidants

A
  • involved in processing many different oxidants within the body
  • may be consumed in the diet but unlikely to be absorbed as it is large
  • Superoxidase dismutase (SOD)
  • catalase and glutathione peroxidase
  • glutathione reductase and glutathione
204
Q

Superoxidase dismutase

A
  • processes super oxide into O2 and H2O2
  • KO mice develop health problems
205
Q

Catalase and Glutathione peroxidase

A

process H2O2 into H2O to prevent reaction with Fe2+

206
Q

Glutathione reductase and glutathione

A
  • act together to suppress oxidative stress
  • GSH donates an e- to free radicals and becomes oxidised to GSSG
  • GSSG back to GSH via glutathione reductase using NADPH
207
Q

Epidemiological evidence of antioxidants preventing disease

A

people who consume a diet rich in fruit and veges have a decreased risk of cancer, CVD and all cause mortality

208
Q

Intervention study looking at B-carotene and lung cancer

A
  • smoking increases markers of ox stress along with decreasing Vit C and B-carotene
  • short term supplementation decreases oxidative stress
  • long term supplementation saw an increase by 28% of lung cancer while placebo with fruit and vege protected
209
Q

Intervention study looking at Vit E,C and B-carotene supplementation with CVD risk

A
  • high risk individuals were safe
  • blood vit conc increased but no decrease in mortality or incidence
210
Q

Hormesis

A

low dose of ox stress provides an adaptive benefit while high dose leads to tissue damage

211
Q

Antioxidant responsive element

A
  • increase in pro-oxidant phytchemicals caused NRF2 dissociation from KEAP1
  • NRF2 goes into nucleus where it promotes production of antioxidant enzymes
  • both antioxidant and pro-oxidants are needed for NRF2 dissociation
212
Q

CO-Q10

A
  • 3 forms
  • found in mitochondria where most free radicals are
  • lipid soluble which limits bioavailability
  • decreased by statins
213
Q

MitoQ10

A
  • added mitocondrial targeting tag tripohenyl alkyl phosphonium cations to allow entrance into mitochondria
  • work via reduction via complex 2
  • decreased exercise induced mitochondrial DNA damage after 21 days
214
Q

Probiotics and decreasing obesity

A
  • suggested to increase GLP-1, PYY and CCK which suppresses appetite and food intake
  • meta-analysis shows an insignificant weight loss
215
Q

Dietary fibre/prebiotic and decreasing obesity

A
  • increases gastric transient time
  • inhibits ghrelin secretion
  • increases GLP-1 and CCK
  • Majority of studies showed and increase in satiety
  • acute supplementation saw a decrease in EI
  • Chronic supplementation showed modest weight loss
216
Q

Capsaicinoids and decreasing obesity mechanisms

A
  • best supplement
  • ## Activate thermogenesis by inducing mitochondria uncoupling proteins in brown adipose fat, inhibit adipogenesis and increase production of fat regulating hormones
217
Q

Capsaicinoids and decreasing obesity clinical trials

A
  • 40 men and women supplement with 6mg per day showed changes in abdominal fat and increased fat oxidation but no changes in EE
  • 20 healthy participants supplemented with 4-5mg per day showed and increase in BAT = increased fat oxidation
  • meta-analysis showed good evidence for thermogenic effects, increased EE and increased lipid oxidation (RQ = 0.7)
218
Q

Green tea and decreasing obesity mechanism

A
  • main compound is catechins
  • increase GLP-1
  • improves insulin resistance
  • inhibits pancreatic lipase
  • increases thermogenesis
  • increases satiety
  • enhances fat oxidation
  • inhibits intestinal glucose absorption and glucose uptake
  • HOWEVER MAJOR PROBLEM IS THAT BIOAVAILABILITY DIFFERS BETWEEN PEOPLE
219
Q

Green tea and decreasing obesity clinical trials

A
  • 500mL catechin beverage for 12 week in obese participants did not show and considerable difference in weight or EI
  • another trial showed a high dose of green tea could lead to a significant reduction in weight, BMI, WC and lipid profiles
  • meta-analysis showed significant difference from baseline but not always placebo
220
Q

Curcumin and decreasing obesity

A
  • suggested anti-obesity mechansims via anti-hyperlipidemic and increasing thermogenesis
  • clinical trials showed no significant weight loss with regular supplementation but treatment with enhanced bioavailability curcumin showed decrease in BF but no significant change in weight
221
Q

Resveratrol and decreasing obesity

A
  • found in red grapes, berries and pomegranates
  • proposed to increase GLP-1 and inhibit adipogenesis
  • clinical trial showed that treatment had no effect on GLP-1 levels in obese men
222
Q

The bitter brake

A
  • bitter compounds in the stomach stimulates appetite
  • bitter compounds in the small intestine and colon suppresses appetite
223
Q

Experiment investigating whether the human gut has bitter taste receptors

A
  • took samples from gastroscopy and colonoscopy
  • found receptors all throughout the gut
  • elevated in the gastric fundus and terminal ileum
224
Q

Enteroendocrine cell assay to stimulate the bitter brake in the lab

A
  • tested over 1000 different compounds
  • measured changes in intracellular Ca2+ as this is a marker for receptor activation
  • found Amarasate (Hop) was the best
225
Q

Amarasate (Hop)

A
  • activates the bitter brake response
  • a higher concentration lead to an enhanced increase in CCK release
  • quantification showed it contained 6 bioactives
  • toxicity assay to validate whether CCK release was from molecule or cell death validated it was from molecule
  • required an excipient to enhance gut dispersion
226
Q

Amarasate ad libitum clinical trial

A
  • Randomised, double blind, placebo and cross over
  • 3 treatment groups = gastric, duodenum and placebo
  • fixed breakfast but ad libitum lunch and snack
  • Ghrelin stimulated by both treatments (likely due to back flow)
  • increase in CCK, GLP-1 and PYY in both treatments
  • Duodenum treatment had longer lasting effects
  • insulin decreased in both treatments
  • saw 28% decrease in EI
227
Q

Amarasate 24hr water fast clinical trial

A
  • randomised, double blind, placebo and cross over
  • treatments = high dose, low dose and placebo
  • decreased hunger over time
  • 14% decrease in EI
  • increased fullness over time in females
  • decreased cravings in females
228
Q

ATP-PC system

A
  • ATP and PC present in very small amounts in muscle cells
  • can supply energy very quickly
  • no O2 needed
  • no lactic acid produced
229
Q

Anaerobic glycolysis

A
  • uses glycogen
  • no O2 needed to resynthesise ATP
  • energy is produced quickly
  • lactic acid produced
230
Q

Aerobic system

A
  • uses glycogen/glucose and fat to replenish ATP
  • energy production takes longer but can last for a longer duration
  • no lactic acid produced
  • marathon etc
231
Q

VO2 max

A
  • the max volume of O2 the body can deliver to the working muscles per minute
  • an index of the bodys efficiency at producing work
  • higher max is key for a better aerobic performance
232
Q

What factors affect VO2 max

A
  • muscle morphology
  • join mechanisms
  • elastic elements
233
Q

Lactate threshold

A
  • the intensity of exercise at which lactate being to accumulate in the blood at a faster rate than it can be removed
  • failure of contracting muscles to meet ATP demands = rate of pyruvate delivery > rate of pyruvate oxidation = increased lactic acid production
  • mainly determined by oxidative capacity of skeletal muscle
234
Q

Physiological factors dictating anaerobic athletic performance

A
  • muscle mass
  • muscle fibre type = Type 2 fast twitch is better
  • muscle fibre cross sectional area = thicker is better
  • muscle architecture and strength
  • availability of PC and glycogen
  • efficacy of the breakdown of glucose and glycogen into lactic acid
  • accumulation of reaction products = decreased pH leading to decreased enzyme activity
235
Q

Ways to improve aerobic performance

A
  • increase VO2 max
  • increase efficiency
  • improve lactic acid threshold
236
Q

Ways to improve anaerobic performance

A
  • increase muscles
  • increase short term energy stores
  • stop muscles fatiguing
237
Q

Ecdysones and studies in rats

A
  • natural anabolic agent
  • in rats it increases fibre sizes of C2C12 myotubes better than anabolic androgenic steroids
  • decreases corticosterone and IGF-1 in rats = increased cell repair and decrease inflammation
238
Q

Ecdysone mechanism in rats

A
  • C2C12 cells were incubate with estradiol, ecdy or a estrogen receptor B-specific agonist
  • either with or without an estrogen B-receptor blocker
  • saw myotube growth was blocked when B-signalling was blocked
  • results indicate Ecdy work via this receptor
  • Stimulate satellite cell activation, proliferation in injured skeletal muscle and modulates inflammatory responses
239
Q

Ecdysones clinical trial

A
  • 46 healthy weight trained males
  • 200mg/day or 800mg/day
  • placebo
  • 10 week resistance training program
  • 2kg gain in muscle mass
  • increased bench press weight
  • maintenance of IGF-1 levels
240
Q

Creatine mechanism

A
  • increases PCr levels in the muscles
  • PCr is used by creatine kinase to generate ATP
  • increases the capacity to make ATP thus increases performance
241
Q

Creatine clinical trials

A
  • increased creatine stores in muscles
  • increased anaerobic performance seen via increased max squat and bench press weight
  • increased muscle mass = increased FFM but fat is unchanged, increase in cross sectional areas of muscle fibres
  • no effect on endurance exercise
242
Q

Disadvantages of creatine supplementation

A
  • short term side effects such as gut issues and nausea
  • water retention
  • possibly kidney issues (not proven)
  • possible hormone issues (increase DHT = increased balding)
  • mostly short term energy
  • lack of long term studies
243
Q

HMB

A
  • anti catabolic agent
  • metabolite of leucine
  • used in the medical field to protect from muscle loss during age related sarcopenia
  • prevents protein breakdown but there is no well defined mechanism
244
Q

Possible mechanisms for HMB

A
  • inhibits proteasome = decreased proteolysis
  • inhibits autophagy
  • increased Ca release from SR
  • increases proliferation of satellite cells = increased tissue repair
  • increases mitchondrial biogenesis
  • increases cholesterol synthesis = increased tissue repair
  • increased GH and IGF-1 = increased protein synthesis
  • stimulates mTOR path = increased protein synthesis
245
Q

Glutamine

A
  • anti catabolic
  • most abundant AA in human muscle
  • conc decreases following prolonged exercise
  • increases muscle recovery and decreases soreness
246
Q

Glutamine target/mechanism

A

inhibits muscle breakdown signalling protein degradation associated genes = MURF-1 and MAF-bx

247
Q

Beetroot

A
  • high level of evidence associated with improving athletic performance with adequate dosing
  • evidence for efficacy during high intensity exercise
  • clinical trials = improved cycling economy
  • contains nitrate
248
Q

Beetroot mechanism of action

A
  • mouth microorganisms reduce NO3 to NO2
  • stomach acids reduce NO2 to NO
  • NO increases mitochondrial biogenesis, mitochondrial respiration and muscle contraction/relaxation
249
Q

Soidum bicarbonate

A

improves HIIT performance

250
Q

B-alanine

A
  • improves HIIT performance
  • increases muscle carnosine levels which can act as a buffer to reduce acidity in active muscles
251
Q

NZ blackcurrent mechanisms to improve athletic performance

A
  • increase motivation via inhibiting MAO-B which prevents dopamine breakdown
  • inhibition of post-exercise inflammation
  • improvements in blood flow (induces eNOS which increase NO levels)
  • improved cardiac output
252
Q

NZ blackcurrent characteristics

A

contain high levels of anthocyanins due to NZ UV levels from the ozone hole
- has different anthocyanins then some other berries = delphinidin-rutinoside and cyandin-rutinoside

Biosci 358 (3 decks)

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