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Nutr 307 > Extra reading > Flashcards

Extra reading Flashcards

1
Q

Is vitamin D strictly a Vitamin

A

No, it’s also a prohormone

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2
Q

Which form of Vit D does our skin make?

A

d3

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3
Q

What is the better predictor of CHD risk?

A

the ratio of total cholesterol to HDL

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4
Q

Benefits of omega-3

A
  • prevention of fatal arrhythmias
  • risk reduction of coronary
    heart disease
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5
Q

Trans-fatty acids __ LDL and __ HDL; __ the proportion of small, dense, and atherogenic LDL particles; __ lipoprotein(a) and __ inflammatory markers that have been related to CHD risk

A

Trans-fatty acids increase LDL and decrease HDL; raise the proportion of small, dense, and atherogenic LDL particles; raise lipoprotein(a) and increase inflammatory markers that have been related to CHD risk

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6
Q

What does a high lipoprotein (a) level mean?

A

A high level of lipoprotein (a) may mean you are at risk for heart disease

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7
Q

What is lipoprotein (a)

A

Lipoprotein (a) or Lp(a) is one type of lipoprotein that carries cholesterol in the blood. It consists of a low-density lipoprotein (LDL) molecule with another protein (Apolipoprotein (a)) attached to it

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8
Q

Benefits of reduction of salt intake

A

Decreased blood pressure

Decreased incidence of stroke

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9
Q

Benefits of folate intake

A

Reduced risk of neural tube defects

prevention of cardiovascular disease, especially stroke

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10
Q

Which demographic groups have a higher prevalence of iron deficiency?

A

non-Hispanic black and

Mexican-American women

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11
Q

What are the risk of consuming excess vit A?

A

risk of hip fracture

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12
Q

What is an epigenome?

A

An epigenome consists of a record of the chemical changes to the DNA and histone proteins of an organism;

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13
Q

What are SNPs

A

they are defined as nucleotide base pair differences in the primary sequence of DNA and can be single base pair insertions, deletions, or substitutions of one base
pair for another

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14
Q

What are the most common polymorphism

A

Nucleotide substitutions are the most common polymorphism

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15
Q

What are the 2 classifications of Nucleotide substitutions

within protein coding regions of a gene?

A

nonsynonymous substitutions

synonymous substitutions

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16
Q

What are nonsynonymous substitutions?

A

nonsynonymous substitutions, result in an amino acid replacement substitution within a protein

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17
Q

What are synonymous substitutions?

A

synonymous (silent) substitutions do not change
amino acid sequence resulting from degeneracy in the
genetic code

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18
Q

How can synonymous (silent) substitutions have functional consequences?

A

by altering mRNA splicing and protein translation efficiency.
SNPs in introns, promoters, and intergenic regions may
also be involved in regulating gene expression.

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19
Q

What are the effects of SNPs?

A

SNPs contribute to susceptibility for common diseases and developmental anomalies, and polymorphic alleles have been identified that increase the risk of common disorders including neural tube defects, cardiovascular disease, cancers, hypertension, and obesity

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20
Q

What are haplotypes.

A

Inherited blocks of genetic variation

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21
Q

What are the mutations related to lipid metabolism?

A
  • Apo-E variations account for variance in cholesterol concentrations in human populations. Furthermore, the E4 allele is associated with hypercholesterolemia and an increased risk of late-onset Alzheimer disease
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22
Q

What is Nutritional genomics?

A

Nutritional genomics, also known as nutrigenomics, is a science studying the relationship between human genome, nutrition and health.

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23
Q

WHat is HIF

A

Hypoxia-inducible factor (HIF) is a dimeric protein complex that plays an integral role in the body’s response to low oxygen concentrations
It is induced by iron deficiency

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24
Q

What is a transcriptome

A

All transcribed mRNAs within a cell or tissue at a particular time

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25
Q

What is a SNP

A

Single nucleotide polymorphism- Single base substitution in coding sequence of a gene; frequently determines phenotypic differences in a population

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26
Q

What is a response element?

A

Portion of a gene sequence that must be present for that gene to respond to a stimulus; response elements are binding sites for transcription factors

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27
Q

What is qPCR?

A

Quantitative PCR in which the relative abundance of a sequence (mRNA derived
cDNA) is compared to a normalizing sequence

Polymerase chain reaction (PCR) is a relatively simple and widely used molecular biology technique to amplify and detect DNA and RNA sequences.

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28
Q

What is protein array?

A

Antibodies or other proteins immobilized to a matrix allowing abundance of specific proteins to be qualitatively detected or
interacting proteins to be identified

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29
Q

miRNA vs siRNA

A

siRNA inhibits the expression of one specific target mRNA

miRNA regulates the expression of multiple mRNAs.

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30
Q

siRNA inhibits the expression of one specific target mRNA

miRNA regulates the expression of multiple mRNAs.

A

It can be activating or deactivating

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31
Q

Describe the procces and the consequences of DNA methylation

A

This process leads to a conversion of cytosine to thymidine through a methylation reaction. When the CpG sequences of gene promoters are methylated, the affinity of the TF for the target gene is altered. As a result of this DNA methylation, the transcription rate for the gene can be substantially altered

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32
Q

Describe the procedure that is used to estimate the abundance of a specific protein?

A

blotting procedure
The proteins are separated by
size by polyacrylamide gel electrophoresis (PAGE), and then the protein of interest is detected immunologically
with a specific antibody.

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33
Q

What is western blotting?

A

Western blotting or immunoblotting is a technique technique that combines the resolution of proteins by gel electrophoresis to the specificity of immunochemical detection

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34
Q

What does transgenic mean?

A

relating to or denoting an organism that contains genetic material into which DNA from an unrelated organism has been artificially introduced.

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35
Q

What happened in mice with GLUT4 overexpression?

A

Overexpression resulted in higher glucose transport rates, lower glucose tolerance curves, and greater body fat.

36
Q

Are elevated HDL levels good or bad?

A

Good

elevated HDL levels are associated with reduced coronary risk in humans

37
Q

Which lipoproteins are associated with Apo-B48?

A

chylomicrons and intestinally derived VLDL.

38
Q

Which lipoproteins are associated with Apo-B100?

A

Which lipoproteins are associated with Apo-B100?

39
Q

Where is Apo-E made?

A

liver

40
Q

Which lipoproteins are associated with Apo-E

A

all of them

41
Q

How is chylomicron assembly within the intestinal enterocyte regulated?

A

Chylomicron assembly within the intestinal enterocyte is tightly regulated by the production of apolipoprotein-B (Apo-B) and the activity of microsomal TG transfer protein (MTP), which transfers lipids onto nascent Apo-B particles

42
Q

What are FABPs?

A

The fatty-acid-binding proteins (FABPs) are a family of transport proteins for fatty acids and other lipophilic substances. These proteins are thought to facilitate the transfer of fatty acids between extra- and intracellular membranes

43
Q

What happens in terms of lipid metabolism when hepatic lipase is absent?

A

When hepatic lipase is absent, accumulation of large LDL particles and TG-rich lipoproteins (TRLs) occur

44
Q

In which part of blood are lipoproteins found?

A

plasma

45
Q

What are 2 ways of removing HDL form circulation?

A

1) HDL2 can transfer CE molecules to either Apo-B–containing lipoproteins or directly to cells
2) entire particles of HDL2 can be taken up by LDL receptors and possibly by a separate Apo-E receptor on hepatocytes.

46
Q

How can CH be moved form HDL?

A

Movement of CH from HDL2
occurs through CE transfer protein (CETP) that mediates
the transfer of CE from HDL2 to VLDL and chylomicrons in exchange for TG, after which Apo-B containing particles transport CE to liver.

47
Q

Link between trans fats and CETP and LDL?

A

trans fat consumption may increase CETP activity, thus explaining the higher circulatory LDL levels

48
Q

How are LCFAs transported across mitochondrial membrane?

A

Using carnitine (made from lysine and methionine) shuttle

49
Q

How does HDL2 and HDL3 vary?

A

HDL2 is larger and more effective in cholesterol removal than HDL3

50
Q

Would a fasted person have chylomicrons in his plasma?

A

no

51
Q

What does serum total cholesterol measure reflect?

A

of the amount of cholesterol contained within circulating very-low-density lipoproteins (VLDLs), LDLs, HDLs, and chylomicrons

52
Q

Through what does LDL bind to LDL receptor?

A

apoB100

53
Q

What is PCSK9?

A

It is a protease that that
regulates the degradation of the LDL receptor and thus plays a major role in the control of cholesterol influx into cells

54
Q

heterozygous gain of function mutation in PCSK9
what is the Gene defect?
Clinical findings?

A

autosomal dominant hypercholesterolemia (ADH)

Clinical findings- Similar to FeFH

55
Q

Name MONOGENIC DISORDERS CAUSING ELEVATED LOW-DENSITY LIPOPROTEIN CHOLESTEROL LEVELS

A

Heterozygous familial hypercholesterolemia (HeFH)
Homozygous familial hypercholesterolemia (HoFH)
PCSK9 mutations
Familial defective Apo-B
Autosomal recessive hypercholesterolemia (ARH)

56
Q

Autosomal recessive hypercholesterolemia (ARH)

Gene defect?

A

Mutations in adaptor protein that is essential, in the liver, for clathrin-mediated endocytosis of LDL

57
Q

What is the result of loss of function mutation in PCSK9

A
  • increased LDL receptor expression
  • reduced LDL serum levels
  • reduced risk of CVD
58
Q

Inherited forms of hypercholesterolemia resulting from mutations in the __, __, or _ gene have an __ __ pattern of inheritance.

A

Inherited forms of hypercholesterolemia resulting from mutations in the LDLR, APOB, or PCSK9 gene have an autosomal dominant pattern of inheritance.

59
Q

What is APOB gene codes for and what does mutations in this gene lead to?

A

APOB gene encodes for LDL receptor binding domains (ApoB protein)
Mutations in this gene reduce the binding affinity of LDL particles to the LDL receptor

60
Q

What are the 2 disorders that cause high HDL-C levels?

A

1) CETP (cholesterol ester transfer protein) deficiency

2) Hepatic lipase deficiency

61
Q

What is SR-B1?

A

It is a scavenger receptor that is an HDL receptor

62
Q

What are some of the functions of hepatic lipase?

A

remodel VLDL remnants to LDL

particles by hydrolyzing TGs.

63
Q

What is the treatment for individuals who have monogenic disorders that result in very low plasma HDL-C concentrations

A

reasonable treatment strategy is to reduce plasma LDL-C by using diet and pharmacotherapy, as appropriate

64
Q

What is tangier disease?

A

nearly total absence of HDL particles in the plasma
Caused by a defect in a gene preventing formation of HDL. This gene encodes a cell membrane protein that governs cholesterol efflux and is a key component of the RCT pathway

65
Q

What are the physical characteristics of tangier disease?

A

Corneal opacities; yellow-orange tonsils; hepatosplenomegaly;
cardiovascular disease risk probably increased

66
Q

What is hypoalphalipoproteinemia?

A

low plasma HDL-C concentrations

67
Q

What are the 2 diseases associated with LCAT deficiency? WHat is the gene defect?

A

Familial LCAT deficiency- complete absence of LCAT activity
Gene defect- Homozygous defect in LCAT gene leading
to absent or markedly reduced LCAT enzyme

Fish eye disease (partial LCAT
deficiency)- partial deficiency
of LCAT activity
Gene defect- Homozygous defect in LCAT leading to normal measurable LCAT levels but ineffective ability to esterify free cholesterol in HDL

68
Q

Name conditions which are characterised by low HDL-C

A

Tangier disease
Familial LCAT deficiency
Fish eye disease
Apo-A-I deficiency

69
Q

What is Familial Hypertriglyceridemia?

A

it based on the definition of fasting plasma TG exceeding the 95th percentile of the population distribution

70
Q

Name conditions with low plasma levels of cholesterol or TGs

A

Abetalipoproteinemia (ABL)- low CH and TGs- Fat malabsorption
Familial hypobetalipoproteinemia
(FHBL)
Familial combined hypolipidemia

71
Q

Describe PCSK9 Deficiency

A

loss of function mutations in PCSK9 result in increased levels of the LDL receptor and enhanced clearance of LDL particles. Heterozygotes for loss of function mutations in PCSK9 have markedly depressed levels of LDL-C and of Apo-B, and they also have a markedly reduced
lifetime risk of CAD

72
Q

WHat ia the main location of cholesterol synthesis?

A

liver

73
Q

How does substituting fats with PUFAs affect CH levels/synthesis?

A

It results in a decrease in the ratio of hepatic intracellular free to esterified CH that, in turn,
up-regulates both LDL receptor number and cholesterogenesis.

74
Q

What is the cite of most PUFA metabolism

A

liver

transforms dietary C18 EFAs into 20–22C PUFA

75
Q

What is the first step of producing eicosanoids?

A

Phospholipids are acted upon by Phospholipase A2 to make 20:4n-6 (which is a precurosr for eicosanoids)

76
Q

Is n-6 family of FAs important for humnas

A

Yes! It is essential

77
Q

WHat is CHD caused by

A

by atherosclerosis, a process in which the coronary arteries as well as other arteries become occluded

78
Q

what is MI?

A

A heart attack or myocardial infarction (MI) occurs when one or more of the three major coronary arteries becomes
blocked

79
Q

What is a stroke?

A

A stroke occurs when one or more of the arteries supplying the brain becomes occluded

80
Q

What is CVD?

A

Coronary heart disease (CHD) and stroke together

81
Q

What risk do statins reduce?

A

CHD and stroke risk

82
Q

How do Fibrates function?

A

Fibrates are among the most widely used lipid-modifying agents, and they are the most effective available triglyceride-lowering agents

83
Q

What is the effect of niacin?

A

Niacin is the most effective agent currently available for raising HDL-C and its use has been associated with CHD risk reduction

84
Q

How does ezetimibe work?

A

• Ezetimibe is a second-line agent for LDL-C lowering blocks intestinal cholesterol absorption by inhibiting intestinal cholesterol uptake via NPC1C1

85
Q

Describe Apo E and ApoC

A

• ApoE and ApoC are exchangeable apolipoproteins meaning they can jump to any lipoprotein (CM, VLDL, LDL, IDL, HDL)

86
Q

What is the difference between exchangeable and structural lipoproteinsÉ

A

The difference between exchangeable and structural lipoproteins is that for structural lipoproteins such as ApoA or ApoB they are necessary for the structure so if you take remove them, the entire lipoprotein will fall apart where as ApoE can jump from different species

Nutr 307 (8 decks)

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