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Nutrition Metabolism > Nutrigenomics > Flashcards

Nutrigenomics Flashcards

1
Q

t/f: RDA has a safety factor built in

A

true!

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2
Q

RDA is set _______ SD above the mean, meaning that it will meet needs of _____% of the population

A

1.2 Sd above mean population requirement–> meets 98%

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3
Q

what is the problem with a person eating at the RDA?

A

maybe eating too much?! could be quite a bit more than what they need to eat

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4
Q

main problem with RDA

A

not individualized! misses 2% of pop’n and not precise

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5
Q

3 factors that generally affect nutrient requirements

A
  1. physical characteristics(sex, life cycle stage, body size)
  2. lifestyle: PA, smoker?, urban v. rural, etc.
  3. genetics: gene–> nutrient metabolism
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6
Q

currently main dietetics “diagnostic tools” are what 2 things?

A

blood profiles and anthropometrics

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7
Q

________ allele determines lipid metabolism

A

apoE2

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8
Q

apoE2 allele is very responsive to what two lifestyle changes?

A

soluble fiber intake and physical activity

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9
Q

in the future, what other “diagnostic tool” is probably going to be used in dietetics?

A

genetic profile

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10
Q

3 genetics implications for dietetics

A
  1. tailor nutrient requirements according to genetic profile
  2. tailor diet therapy
  3. functional foods for certain genotypes
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11
Q

22 pairs of autosomes are numbered by _________ size

A

descending

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12
Q

the center of the chromosome is called what? what are the ends called?

A

centromere

telomeres

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13
Q

karyotype

A

and appearance of chromosomes in one cell

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14
Q

t/f: all human cells have 46 chromosomes

A

false! cancer cells often have more or less

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15
Q

the shorter portion of the chromosome off the centromere is labeled as ______, while the longer portion is designated as _______

A

p=shorter

q=longer

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16
Q

each “arm” of a chromosome is further divided into smaller sections designated by #s. the larger the #, the closer of further to the telomere?

A

closer!

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17
Q

in a cell, where is there extra nuclear DNA?

A

small part of genome in the mitochondria

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18
Q

genetics is the study of _________, which are what?

A

mutations-changes in genomic DNA

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19
Q

two types of mutations

A
  1. small scale: mutations in DNA sequence

2. large scale: changes in chromosomal structure, like deletion of a large portion of a chromosome

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20
Q

synonym for small-scale DNA mutation

A

DNA sequence variants

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21
Q

if a DNA variant is found on less than 1% of population, then it is called _____________, while if its on greater than 1% it is called ____________

A

mutation for less than 1%

polymorphism=greater than 1%

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22
Q

SNP

A

single nucleotide polymorphism (single base pair changed)

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23
Q

VNTR

A

variable number tandem repeats(copies of sequences is abnormal)

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24
Q

what is the “reference” sequence called?

A

wild-type

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25
Q

INDEL

A

insertion/deletion polymorphism(missing part of reference sequence)

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26
Q

SNPs are found often in how many versions?

A

two–> minor and major

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27
Q

minor allele frequency range

A

> 1%-50%

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28
Q

t/f: SNPs are frequent in the human genome

A

true! very frequently… at least 1 per every few hundred basepairs

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29
Q

in contrast to SNPs, VNTRs are highly _____________, meaning what?

A

polymorphic –> many known alleles(not just 2 like with SNPs)

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30
Q

a number of diseases have been implicated to be from VNTRs of how many base pairs?

A

3 basepair repeats

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31
Q

VNTRs are goof for _____________ studies, while SNPs are good for _____________ studies

A

VNTR=family-based linkage studies

SNPs=population based association studies(genome-wide associations)

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32
Q

3 major sources of variants (SIT)

A
  1. spontaneously: mistakes in replications
  2. induced: by chemicals or radiation that cause strand breaks
  3. transposable elements: ancient viruses that could “jump” in the genome
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33
Q

a spontaneous chem rxn can convert adenine to ___________. What are two things that can happen after this?

A

inosine–> repair mechanism back to adenine

unrepaired—> pairs with cytosine (AT base pair becomes IC base pair)

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34
Q

during DNA replication, an IC base pair will result in what two pairs? ultimate consequence?

A

I with C and C with G–> AT base pair became a CG base pair in offspring

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35
Q

ENU is a chemical that can react with guanine and adds a __________ to make ___________, which pairs with what?

A

methyl group–> ethyl guanine which pairs with thymine

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36
Q

what is the difference b/t a coding SNP and non-coding SNP?

A

coding: changes AA sequence of protein

non-coding: alters amt of protein formed

37
Q

haplotype

A

set of SNPs(6-8) that tend to be inherited together

38
Q

how many haplotypes are thought to occur throughout the population?

A

3-5

39
Q

what is the catalog of common SNPs in humans?

A

HapMap!

40
Q

epigenetics

A

changing phenotypes without changing genotype(affecting whether gene will be transcribed or not)

41
Q

3 components of chromatin

A
  1. DNA
  2. histone proteins
  3. non-histone proteins
42
Q

components of a nucleosome

A

146 base pairs (2 superhelical turns)+ core of 8 histones

43
Q

____________ of the tail amino ends of histones is thought to play a key role in expression of genes because histones do what?

A

acetylation of histones b/c histones regulate shape and conformation of DNA

44
Q

2 enzymes involved in histone acetylation

A

HAT(histone acetyl transferase)

HDAC(histone deactylase)

45
Q

acetylation by HAT causes what to happen to DNA?

A

causes to uncoil from histones and is accessible for transcription

46
Q

function of HDAC

A

deactylases the histones, causing DNA to coil and become unaccessible for transcription

47
Q

1 method to modify DNA

A

methylation

48
Q

3 methods to modify histones

A
  1. methylation
  2. acetylation
  3. biotinylation
49
Q

some examples of changes in phenotype

A

longevity, resistance to disease, behavior, physical appearance, stress response!

50
Q

methylation of what portion of the DNA affects transcription of exon?

A

the promotor region of the gene(Not exons themselves)

51
Q

t/f: HAT and HDAC can be affected by diet

A

true!

52
Q

cur cumin can reduce activity of _________, and reduce transcription of pro___________ genes

A

HAC–> fewer pro inflammatory chromatin

53
Q

what other diet factor has been shown to reduce HAC activity?

A

calorie restriction

54
Q

nutrigenomics v. nutrigenetics

A

nutrigenetics: how genes affect metabolism of nutrients(ex. gene makes absorption of certain nutrients lower)
nutrigenomics: how food + nutrients can affect phenotype(expression of genes)

55
Q

Vitamin ______________ binds to RARC on gene is an example of nutrigenomics

A

A retinol(but not epigenetic!)

56
Q

genomics

A

studying the gene sequences and variations in genetic material

57
Q

transcriptonomics

A

studying how much mRNA of each type there are

58
Q

proteinonomics

A

how much of each type of protein is expressed in each cell

59
Q

metabolonomics

A

study of how much of reaction intermediates there are, which can affect how body handles nutrients and health

60
Q

in order to do genetic testing, we can sample what two things?

A

WBC(but a pain); cheek swab inside… both can extract DNA

61
Q

PCR stands for what?

A

polymerase chain rxn

62
Q

what is a PCR used for?

A

amplifying # of copies of specific region of DNA in order to produce enough DNA to be adequately tested

63
Q

t/f: there can be a DNA variant between paired chromosomes

A

true!

64
Q

how many alleles (except last set for me) does a person have?

A

two for each gene

65
Q

difference b/t DNA sequencing and genotyping

A

DNA sequencing: looking for new DNA variants

genotyping: identifying what variant a person has based on already known variants

66
Q

most routine DNA sequencing has what two steps?

A
  1. PCR: amplify # of copies of gene

2. Sanger sequencing

67
Q

what is the beginning of a sequence labeled as? end?

A

5’–> 3’

68
Q

what is the relationship b/t the 2 DNA strands called/

A

reverse complementarity

69
Q

you need to add 2 _______________s at the beginning of the PCR procedure to define what regions to amplify

A

2 PCR primers around each exon desired to amplify

70
Q

1st step of PCR is _____________, attained by applying ___________, which breaks ___________

A

denaturation—> apply heat which breaks H bonds b/t DNA base pairs

71
Q

2nd step of PCR is _____________ at a lower temp, allowing H bonds to form between __________s and DNA

A

annealing b/t primers and DNA strands(one for each)

72
Q

3rd step of PCR is ____________ that adds nucleotides to the _____ end of the strand

A

elongation by DNA polymerase to 3’ end

73
Q

the # of DNA molecules ___________ in each round of PCR

A

doubles

74
Q

elongation during Sanger sequencing by a primer + polymerase will be terminated when a ________ is added. why?

A

ddNTP–> dideoxy so cannot attach another phosphate

75
Q

products of electrophoresis will be separated by ____________ because why? how does this help genome sequencing?

A

separated by size b/c smaller strands will move through electrified capillary tube faster–> laser will read fluoresecently colored peaks, giving the sequence of nitrogenous bases

76
Q

what if there are two color peaks in the same position in an electropherogram?

A

means ind. is heterozygous for that gene…

77
Q

exome

A

all protein coding genes in a genome(about 1% of total genome)

78
Q

what does “alignment” mean in DNA testing?

A

during whole exome testing, exome is compared to reference sequences from human genome project… if differences, may indicate DNA variants

79
Q

most DNA variants known to be responsible for disease are found in ___________ sequences

A

coding

80
Q

t/f: we can determine if a non-coding sequence will have a functional effect

A

false(at least right now)

81
Q

if known DNA variants already exist and are defined, is PCR needed?

A

nope! just genotyping of that particular region

82
Q

what is the biggest benefit of genotyping?

A

much much cheaper than whole-genome or whole-exome sequencing

83
Q

GWAS stands for what?

A

genome wide associated studies that look for genetic variation across the entire genome(huge amount of SNPs)

84
Q

what are two concerns about genetic testing?

A
  1. privacy: info used v. person like employer/health care company
  2. health care delivery: who pays? who should get tested? which discipline should take charge/counsel patients? (genetic counselors? nutritionists?) will we create “worried well”?
85
Q

gene with high __________ implies that person with that gene will likely get disease

A

penetrance

86
Q

most autosomal dominant genes cause ________% penetrance for disease

A

100

87
Q

___________ and _______________ of gene variant determines who should be tested

A

prevalence and effective prevention/txt

88
Q

consumer centered model of genetic testing + problems

A

consumer contacted private testing labs(no involvement of clinician)
**problem: don’t understand penetrants, no follow-up

89
Q

what are the other models for genetic testing?

A

health care practitioner model(clinician involved) esp with serious genetic issues
public health model

Nutrition Metabolism (4 decks)

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