Genomics Flashcards

1
Q

Nutrigenomics

A

Effect of diet/nutrition on gene expression
-Change in phenotype w/o a change in genotype

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2
Q

Nutrigenetics

A

Influence of gene variations modifies dietary effects.
- Polymorphisms
- SNP’S

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3
Q

Allele

A

Genes that have variations in bases

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4
Q

Differentiate between phenotype and genotype

A

Genotype: Genetic make up (ex.aabb)
Phenotype: physical characteristics

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5
Q

Autosomal recessive genes: Hbs+Hbs
Hb + Hbs

A

These genes affect RBC shape.
Hbs+Hb = AT heterozygous. Some disc-shaped, some sickle (no symptoms)

Hbs+Hbs = TT homozygous, all RBC are sickle
- Gutamic acid replaced with Valine

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6
Q

SREBP-1c (snp)

A

Increase fat deposits
High fat + overexpression = dyslipidemia, impaired glucose, T2D
- should be on a low fat diet

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7
Q

Apolipoprotein E4 (snp)

A

regulates lipoprotein-cholesterol clearance
ApoE4 + High fat = High LDL
- Should be on a low fat diet

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8
Q

How does Mysostatin influence body comp?

A

It inhibits MPS
Hetero = more fast & muscle
Homo mh = bulky + slow

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8
Q

How does Mysostatin influence body comp?

A

It inhibits MPS
Hetero = +/mh more fast & muscle

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9
Q

Prader-Willi Syndrome (PWS)

A

Chromosomal deletion, multi genes affected
Hypothalamic dysfunction, short stature, inappropriate food seeking behaviors, failure to thrive in infancy

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10
Q

Define Epigenetics

A

heritable changes in gene function that do not involve changes to the underlying DNA sequence. Changes to the DNA molecule itself or to the proteins with which DNA interacts.
Influenced by: Environment, diet, disease, exercise,

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11
Q

Epigenetic examples

A

DNA methylation
Chromatin modification: modify histones (methylation, phosphorylation, acetylation)

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12
Q

Epigenetic code

A

Determines what genes are expressed:
DNA methylation + histone modification

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13
Q

Why will two twins never usually be the same?

A

Epigenome: link between environmental factors and phenotypical changes during the lifetime

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14
Q

What is the life course model

A

non communicable disease risk will increase due to lifelong exposures with the highest increase during adulthood

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15
Q

Barker hypothesis / Developmental origins of disease hypothesis

A

There are certain environmental factors that can increase/decrease risk of fetus - suggest improving conditions for a fetus could be effective way to reduce odds of chronic disease.
- Found those with the lowest birth rate had a higher chance of CVD

16
Q

Intra-uterine growth

A

associated with increase risk of chronic disease:
SGA/LBW > LGA for chances of chronic disease, LGA is less studied

17
Q

How did babies during the dutch famine results differ depending on exposure?

A

DNA methylation changes related to growth
Late - T2D (high glucose)
Early - CVD
Mid - Microalbuminuria / kidney damage

18
Q

Low protein maternal diet

A

associated with physical changes in the structure of proteins. (Ex. GLUT 4, leptin, adipose tissue, heat tissue)

19
Q

choline deficiencies

A

Brain structure + function
Irreversible

20
Q

Methyl-group metabolism can be affected by deficiency or supplementations of

A

Choline, methionine, V B12, folate

21
Q

Why might the thrifty phenotype model be advantageous

A

Thrifty model predicts that being born into nutrient poor environment could be advantageous compared to a nutrient rich one which can lead to Met S