Gene Nutrient Interactions Flashcards

1
Q

Explain Nutrigenetics

A

Nutrigenetics examines how genetic variation affects the response of an organism to a given diet, evaluating the risks and benefits of specific diets and dietary components and formulating “personalised nutrition” recommendations.

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2
Q

Explain Nutrigenomics

A

Nutrigenomics investigates how nutrients (Bioactive food compounds) affect & effect chromatic presentation and gene expression

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3
Q

Explain the nutritional genomics in Nutrigenetics:

A

Nutrient absorption
Nutrient utilisation
Food/Nutrients
Tolerance
Nutrient requirements

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4
Q

Explain the nutritional genomics in Nutrigenomics:

A

Genome evolution/selection
Genome mutation rate
in-utero genome viability
Genome programming
Gene expression

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5
Q

Nutrigenomics and nutrigenetics straddle
multiple research fields:

A

Nutrition
Bioinformatics
Molecular biology
Genomics
Genetics
Epidemiology
Epigenomics & Epigenetics
Transcriptomics
Metabolomics
Proteomics
Lipidomics
The microbiome (commensals and pathogens)

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6
Q

Explain personalised nutrition:

A

a diet addressed to an individual and based upon her/his genotype, nutritional requirements and other factors (age and gender). It is expected that personalised nutrition will prevent diet related chronic diseases

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7
Q

What are the 3 nutrition-gene interactions?

A
  1. Genetic variation
  2. Epigenetic interactions
  3. Direct interactions
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8
Q

Explain genetic variation:

A

Common genetic variations such as single-nucleotide polymorphisms (SNPs) can alter the expression or functionality of genes.

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9
Q

Explain epigenetic interactions:

A

Nutrients can alter the structure of DNA and chromatin, so that DNA replication and gene expression is chronically altered

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10
Q

Explain direct interactions:

A

Nutrients, sometimes after
interacting with a receptor, behave as transcription factors that can bind to DNA and acutely induce gene expression.

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11
Q

What is the most common form of genomic variation in human genome?

A

single nucleotide polymorphisms

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12
Q

Explain Choline metabolism:

A
  • Genetic variation
  • Human daily requirements for dietary choline are much higher for approximately 50 percent of the population. These people are mostly those with one or more genetic variants associated with choline metabolism and methylation.
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13
Q

What is associated with disease risk and greater susceptibility to organ dysfunction under conditions of dietary choline restriction?

A

Single nucleotide polymorphisms (SNPs) in choline metabolising genes

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14
Q

The MMACHC gene provides instructions for making a protein that helps convert vitamin B12 (also called cobalamin) into one of two molecules:

A
  • Adenosylcobalamin (AdoCbl)
  • Methylcobalamin (MeCbl)
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15
Q

Why is AdoCbl required?

A

for the normal function of an enzyme known as methylmalonyl CoA mutase. This enzyme helps break down certain protein building blocks (amino acids), fat building blocks (fatty acids), and cholesterol.

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16
Q

Which enzyme converts the amino acid homocysteine to another amino acid, methionine?

17
Q

Which gene is associated with vitamin B12 status?

A

rs12272669

18
Q

What are copy-number variations (CNVs)?

A

Are alterations of the DNA of a genome that results in the cell having an abnormal number of copies of one or more sections of the DNA

19
Q

Explain epigenetic interactions:

A

Nutrients (or lack thereof) can alter the chromatic presentation so that gene expression is altered, this might result in imprinting, programming or adaptation. Eg lactase, folate

20
Q

Where does stressors can impact?

A

imprinting, programming or development

21
Q

Explain genomic imprinting:

A

Phenotypic variations that depend solely on the
parental origin of the chromosomes. Humans can not survive without both maternal and paternal contributions, these are differently ‘imprinted’

22
Q

Where does imprinting occurs?

A

Before or during gamete formation

23
Q

How does imprinting occur?

A

Appears to affect chromosomal regions or domains rather than single genes.
Gene silencing is associated with DNA methylation.

24
Q

Where does methyl groups are typically added?

A

at position 5 of the pyrimidine cytosine

25
Where does methylated cytosines are found?
in series CG couplets called CpG islands
26
How are DNA methylation patterns maintained in somatic cells?
Double stranded DNA is methylated on both strands. After semi-conservative replication, only the template strand is methylated. The newly synthesised strand is not methylated. Methyl groups are added to the newly synthesised strand based on the methylation patterns of the template strand.
27
What vitamin is a methyl donor?
Folate (Vitamin B9)
28
Why folate is essential?
Lack of this vital nutritional element will lead to hypo-methylation in some areas of the DNA, causing aberrant gene expression.
29
Why Biotin (Vitamin B7) is essential?
Biotin is a water-soluble vitamin that serves as a coenzyme for five human carboxylases; acetyl-CoA carboxylases 1 & 2, pyruvate carboxylase, propionyl- CoA carboxylase and 3-methylcrotonyl-CoA carboxylase. These enzymes play an important role in the metabolism of fatty acids, glucose and amino acids.
30
Why Cobalamin (Vitamin B12) is essential?
Functions as a co-enzyme in methionine synthesis and a regulator for DNA synthesis There is evidence that host–bacterial competition for cobalamin impacts human health.
31
Why Vitamin D is essential?
Vitamin D had been shown to affect the epigenome via the modulation of transcription factor binding as well as on the level of histone markers, chromatin accessibility and 3-dimensional chromatin organization. Vitamin D has (via VDR) a direct effect on the expression of several hundred primary target genes. VDR binding leads to local opening of chromatin.
32
Explain vitamin C in gene interactions?
Vitamin C maintains genomic stability through interactions with epigenetic regulators, tumor suppressor upregulation and telomere maintenance
33
Explain key point about obesity and genomic stability:
* Obesity increases oxidative DNA damage. * Obesity reduces the end-joining repair efficiency of DSBs * Obesity alters the levels of DSB end-joining repair proteins. * Obesity increases DNA repeat-mediated genomic instability.