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Kris 307 > 1. Biochemistry of Life (Part II) > Flashcards

1. Biochemistry of Life (Part II) Flashcards

1
Q

Give an example of how an optimal level exists for each nutrient.

A
  • Goiter appears when there is iodine deficiency as well as excess
  • The pathways that lead to goiter are different in terms of deficiency and excess
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2
Q

How do fatty acids impact signal transduction pathways?

A

If the composition of membranes is changed, the protein signalling in the membrane might be restricted

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3
Q

Give an example of how vitamin A influences gene expression.

A
  • Is internalized and influences transcription factors
  • Deficiency: blindness
  • Excess: birth defects
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4
Q

What is the true cause of obesity?

A
  • While increased macronutrient intake is one true cause, the opinions vary based on the source
  • Singling on one type of food or nutrient might cause important discoveries (ex: vitamin A), but it does not give the whole picture when it comes to obesity
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5
Q

What did the “Patterns of Sedentary Behavior and Mortality in US Middle-Aged and Older Adults” demonstrate?

A
  • 8000 adults (prospective cohort study)
  • Analyzed excessive sedentary time and how this impacts quality of life
  • Associated with a high-risk of OVERALL mortality, not just obesity
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6
Q

What causes an increase in energy input?

A
  • High fat, energy dense foods
  • Palatable, low-cost, easily available foods
  • Large portion sizes
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7
Q

What causes a decrease in energy output?

A
  • Decrease in work-related physical activity
  • Decrease in activity of daily living
  • Increase in sedentary behaviour
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8
Q

Why isn’t there a single factor that causes obesity?

A
  • Because we have different genes that alter our susceptibility
  • Because we are free to intake as many calories as we want
  • Because we are free to dictate our rate of expenditure
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9
Q

How can obesity be caused socially?

A
  • People that are overweight tend to hang out with other people who are overweight; perhaps, worsening their habits
  • Also, commensal bacteria can be passed on socially
  • When we alter the proportion of microorganisms that we live with, we tip off the beneficial balance, which may render it pathogenic
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10
Q

What study demonstrates that commensal bacteria (gut microbiota) may influence metabolic status and the state of adiposity?

A
  • Microbiota transplant from an obese twin renders the recipient mouse obese
  • Microbiota transplant from a lean twin renders a mouse lean
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11
Q

How many adipocytes are we born with? What happens to them?

A
  • We are born with few white adipocytes

- The body makes more from stem cells when energy needs to be stored

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12
Q

What are the functions of white adipocytes?

A
  • Take up excess fatty acids
  • Synthesize fats
  • Store them within the adipocytes’ cytoplasm
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13
Q

Why is a long-term lifestyle change necessary to get rid of white adipocytes?

A
  • We can burn stored energy and shrink these adipocytes

- But, they have a 2-year half-life (long-lived)

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14
Q

What is atherosclerosis?

A
  • Lipid, mostly (if not exclusively) cholesterol, deposition within the arteries
  • Decreases the opening of the arteries
  • Leads to a heart attack or stroke
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15
Q

What is one of the biggest risk factors for atherosclerosis?

A

High concentration of (LDL)-cholesterol in the blood

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16
Q

What is cholesterol produced by? What products contain cholesterol?

A
  • By the liver

- Meat and dairy products

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17
Q

Does the intake of cholesterol affect your blood cholesterol?

A
  • Well, cholesterol is usually only partially absorbable
  • It is easier to intake cholesterol with fat, as they dissolve and travel with them
  • Thus, individuals with high-fat diets absorb more cholesterol
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18
Q

Why is the cholesterol from food “extra” cholesterol?

A

Every single cell in the body has the capacity to make their own cholesterol

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19
Q

What does the “Red meat + wrong bacteria = bad news for the heart” study demonstrate?

A
  • L-carnitine, present in meat, negatively influences cholesterol metabolism and increases the risk of atherosclerosis
  • A regular diet of meat encourages the growth of bacteria that turns L-carnitine into TMAO (compound responsible for alteration in cholesterol metabolism)
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20
Q

What do variations in bitter taste receptors determine?

A
  • How an individual perceives bitter taste

- Dictates (past acquired cultural tastes), an individual’s taste

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21
Q

Describe how the bitter taste bud receptor works.

A
  • Taste receptor protein (TAS2R) interacts with a bitter taste molecule
  • Causes a conformational change in TAS2R
  • Interacts with a G-Protein (hydrolysis of cGMP)
  • Calcium flows from the inside to the outside of the cell in an ion channel
  • Signal transduction to the brain signals bitter taste
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22
Q

Explain why an individual would find a certain food more bitter than another.

A

If an individual’s TAS2R protein receptor has a higher affinity to bitter ligands, they will bind at much lower concentrations, thereby increasing their sensitivity

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23
Q

Why are we able to detect sweetness from aspartame?

A

Because the structure of the protein can interact with the structure of the sweet receptor

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24
Q

What gene encodes lactase? What is special about it?

A
  • LCT gene

- It normally shuts down after weaning

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25
Q

What allows the LCT to not be shut off in certain cases?

A
  • Polymorphism
  • Lactate continues to be produced
  • These individuals have access to the nutrients of dairy products
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26
Q

What can gene variations influence?

A
  • Can determine whether specific classes of nutrients will have a change in regulating metabolic function
  • Can provide individuals’ use of nutrients that are normally only accessible during specific periods of the life cycle
27
Q

Where do the polymorphisms that cause lactase to be produced in adults occur?

A
  • Not in the LCT gene itself

- In a neighbouring gene (MCM6 gene)

28
Q

What are SNPs? What are they associated with in lactase?

A
  • Single-nucleotide polymorphism are point mutations

- Associated with lactase persistence

29
Q

What do we use instead of the word mutation? Why?

A
  • We don’t know what normal is

- Polymorphism

30
Q

What is the result of polymorphisms in the MCM6 gene?

A

Part of a regulatory domain that controls the expression of that portion of the genome, not necessarily just the LCT gene

31
Q

Most of the genome is composed of what?

A

Regulatory elements

32
Q

What are the roles of regulatory elements in our genome in terms of nutrition?

A
  • These regions of DNA sense information about nutrients (quantity, type)
  • In order for them to maintain peak metabolic capacity
33
Q

What are hypersensitive regions? Should they be there?

A
  • Technically, there should be no hypersensitive regions of DNA once it is wound with histones, but there are
  • These regions are more sensitive to degradation by DNase
34
Q

What has an impact on hypersensitivity?

A

Methylation of DNA

35
Q

What gene is thought to be responsible for the absorption of dietary cholesterol in the intestine?

A

NPC1L1

36
Q

What can cholesterol import be inhibited by? How?

A
  • Ezetimibe

- A drug that interacts with NPC1L1

37
Q

How can receptors be specific to a certain molecule?

A
  • The structure, shape, and overall conformation of the molecule
  • Amino acid side chains dictate the structures of the proteins
38
Q

What is Calnexin?

A
  • Protein that is used as a loading control (standard protein)
  • Present in cells at around the same amount; does not vary from person to person
  • Thus, we can normalize the amount in electophoresis
39
Q

How many forms of the NPC1L1 gene do we have?

A

Humans have two forms: one from mother and one from father

40
Q

What is SREBP-1C function tightly linked to?

A

Nutrient status

41
Q

What have the SNPs in SREBP-1C variants been associated with?

A

Impaired plasma glucose control and increased risk for diabetes

42
Q

Why is SREBP-1C odd?

A
  • Responsive and regulates cholesterol metabolism (most relevant)
  • Yet, the variations are associated with impaired plasma glucose control
43
Q

What can loss of sensitivity to nutrient cues result in?

A

Inappropriate metabolic response to nutrient availability or deficiency

44
Q

What does the severity of acquired metabolic syndromes depend on?

A

Different combinations of individual “gene variants”

45
Q

What activates Akt?

A

1) Growth factors bind to RKT
2) Activates PI3K
3) Generates PIP3
4) Activates Akt through phosphorylation

46
Q

What does activated Akt promote?

A
  • Glucose uptake (GLUT4)
  • Enhances glycolysis
  • Enhances amino acid uptake
  • Enhances stability of mature SREBP via inhibition of GSK3
47
Q

What does Akt stabilize? How?

A
  • Mature SREBP

- Via inhibition of GSK3

48
Q

What are the SREBP target genes?

A
  • Fatty acid synthase
  • HMG-CoA reductase
  • HMG-CoA synthase
  • Causes cholesterol and lipid biosynthesis
49
Q

What is the cyclic amino acid?

A

Proline

50
Q

What amino acids contain sulfur groups?

A
  • Cysteine

- Methionine

51
Q

What amino acids contain hydroxyl groups?

A
  • Serine
  • Threonine
  • Tyrosine
52
Q

What are the aromatic amino aicds?

A
  • Phenylalanine
  • Tyrosine
  • Tryptophan
53
Q

What are the basic amino acids?

A
  • Histidine
  • Lysine
  • Arginine
54
Q

What are the acidic amino acids (and their amides)?

A
  • Aspartic acid
  • Glutamic acid
  • Asparagine
  • Glutamine
55
Q

What links nucleic acids together?

A

Phosphodiester bonds

56
Q

What is required for the synthesis of cholesterol?

A
  • Energy

- HMG-CoA reductase

57
Q

What are the typical functions of vitamins and minerals?

A

Co-substrates, or enzyme co-factors, which determine enzymatic activity

58
Q

Which essential amino acid is conditionally essential? In which cases?

A
  • Arginine

- Preterm infants are unable to synthesize or create arginine internally

59
Q

What TYPE of fatty acids can humans NOT synthesize?

A

Fatty acids with double bonds between carbons located at position 8 or less (counting from the methyl end)

60
Q

Iron is used as a prosthetic group by many biologically important proteins. Give examples.

A
  • Hemoglobin
  • Myoglobin
  • Cytochrome c
  • Peroxidases
  • Hydrolases
61
Q

Where is iron generally found?

A

In enzymes involved in carrying or metabolizing oxygen

62
Q

What genetic diseases cause iron toxicity?

A
  • African hemochromatosis
  • Porphyria
  • Hyperferritinemia
  • Hereditary hemochromatosis
63
Q

What is secondary hemochromatosis caused by?

A
  • Excessive alcohol consumption

- Excessive use of dietary iron supplements

64
Q

What does excessive iodine result in?

A
  • Goiter in response to decreased thyroid hormone concentration
  • Results in the inhibition of thyroid hormone production

Kris 307 (19 decks)

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