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NUTR2101 > Things to go over > Flashcards

Things to go over Flashcards

1
Q

sucrase

A

digests table sugar

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2
Q

phospholipid A2

A

breaks down phospholipids

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3
Q

amylase

A

digests 1-4bonds in starch

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4
Q

alpha dextrinase

A

digests 1-6bonds in starch

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5
Q

pancreatic lipase

A

cleaves fatty acids from glycerol in duodenum

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6
Q

lactase

A

breaks down lactose

cleaves galactose from glucose

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7
Q

maltase

A

digests maltose

cleaves glycosidic bond between two glucose molecules

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8
Q

cholesterol esterase

A

cleaves cholesterol esters

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9
Q

G6P

A

converts glucose-6-phosphate to glucose in glycogenolysis in liver

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10
Q

pepsin

A

cleaves peptide bonds in stomach

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11
Q

ALT or AST

A

a type of transaminase that facilitates transamination

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12
Q

alcohol dehydrogenase

A

converts alcohol in first step of alcohol metabolism

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13
Q

trypsin

A

type of protease that cleaves peptides in duodenum

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14
Q

pancreatic amylase

A

cleaves polysaccharides in duodenum

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15
Q

Glut 4

A

allows cellular uptake of glucose upon insulin signalling

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16
Q

Acetyl coa

A

starting molecule in lipogenesis
or
molecule entering CAC after glycolysis

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17
Q

acetaldehyde

A

intermediate in alcohol metabolism - cause hangovers

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18
Q

oxaloacetate

A

starting molecule for gluconeogenesis

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19
Q

ketone body

A

formed from 2 acetyl coa

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20
Q

starch

A

ppolysaccharide stored in plants

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21
Q

trans fatty acid

A

partially hydrogenated unsat datty acid

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22
Q

ribose

A

saccharide used to form nucleotide

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23
Q

mono unsat faatty acid

A

fatty acid with one double bond

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24
Q

poly unsat fatty acid

A

fatty acid with multiple double bonds

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25
Q

cholesterol

A

sterol manufactured by liver

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26
Q

phospholipid

A

similar to tryglyceride except phospohrus replaced FA

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27
Q

SCFA

A

produced by bacterial fermentation

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28
Q

eicosanoids

A

inflammatory response molecule formed from omega 3 and 6

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29
Q

how dietary fibre assists in regulation of blood sugar levels

A
  • slows down gastric emptying

- harder for enzymes to access CHO

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30
Q

Nrf2 in bodys antioxidant defense system

A

a transcription factor promoting the expression of antioxidant enzyme genes - increases antioxidant capacity

31
Q

Vit A mechanism - light dark adaptation

A

rhodopsin (opsin and II-cis-retinal) absorbes light ->converts II-cis-retinal to all-trans-retinal-> all-trans-retinal converts back to rhodopsin

32
Q

Vit A mechanism - target cell

A

binds to ceullar retinoid binding protein -> released ->enters nucleus an dbinds to RAR and RXR ->bind to DNA- promotes gene transcription -> mRNA -> cellular response

33
Q

Vit E food source

A

sunflower seeds and oil

34
Q

main function of Vit E

A

as an antioxidant - prevents propagation of free radicals in cell memebrane and LDL through oxidation of lipid

35
Q

main function of VIt K

A

as a cofactor of carboxylase enzymes in the synthesis of blood clotting (prepro to pro)

36
Q

babys given vit K injection

A

as GIT is sterile - no bacterial production of Vit K and no eating green leafy vege

37
Q

esterification

A

triglyceride FAs and/or glycerol

38
Q

beta oxidation

A

oxidation of FAs to acetyl coA

39
Q

glycogenolysis

A

hydrolysis of glycogen to glucose

40
Q

gluconeogenesis

A

making new glucose

41
Q

glycogenesis

A

glucose to glycogen

42
Q

glycolysis

A

glucose to pyruvate

43
Q

ketogenesis

A

formation of ketone bodies

44
Q

lipogenesis

A

hydrolysis of triglycerides to fatty acids and glycerol

45
Q

ketoxidation

A

ketones to acetyl coa

46
Q

deamination

A

removal of nitrogen froup of AA

47
Q

FA used as substrate for gluconeogenesis

A

no as
Gluconeogenesis starts from oxaloacetate -> Oxaloacetate is formed from glucogenic amino acids carbon backbones( GGAACB), not FA -> Pyruvate is formed from glucose or GGAACB, not FA -> Fatty acids are oxidised to acetyl-coA (2 carbons molecules) -> Acetyl coA cannot be converted back to pyruvate (irreversible reaction) -> Acetyl coA enters the CAC to form citrate with oxaloacetate. The CAC is an open cycle /circuit, meaning that the intermediates are formed from a variety of substrates coming from other pathways, and carbons atoms are lost all along as CO2 -> Therefore the acetyl coA 2 carbons do not “exist” by the time oxaloacetate is formed.

48
Q

fibre - mechanisms of action

A
  1. Promoting bowel health by increasing faecal bulk -> increase volume circulating in intestine -> increase peristalysis -> decreases risk of diverticulae
  2. Reducing obesity and weight gain risk
    - slows gastric emptying
    - reduces appetite and increases satiation
  3. Assisting in blood glucose control
    - slows gastric emptying -> slows CHO digestion and glucose absorption -> therefore no sudden rise in BGL but gradual
  4. Reducing plasma cholesterol
    - fibre binds to dietary cholesterol and be excreted
    - also promotes excretion of bile
    therefore liver needs to make more bile and requires plasma cholesterol therefore reducing plasma cholesterol
  5. promoting gut health and overall health
    fibre is a substrate for gut bacteria fermentation -> promotes growth and variety of gut bacteria
    - > also produces SCFA which decreases risk of colon cancer and has other health benefits
49
Q

digestion, absoprtion and transport of dietary lipids

A

mouth - lingual lipase
stomach - gastric lipase
SI
- CKK - triggers bile and converts to micelles and FFAs
- pancreatic lipase - breaks triglycerides down to monoglycerides and FFA’s
- cholesterol lipase/esterase - breaks down cholesterol esters into cholesterol and FFA’s
- phospholipase A2 - breaks down phopholipids to FFA and phosphoric acid

LC transport via chylomicrons (lacteals)
MC and SC transport bound to albumin

50
Q

Cholesterol uptake

A

scavenger pathway - removes oxidised LDL form epithelium

receptor pathway - LDL uptake and broken down and utilised by cells

51
Q

MCT metabolism and LCT metabolism

A

MCT - more readily utilised for energy production, high production of ketone bodies, and produces acetyl coa quickly

LCT - re-esterification and cholesterol and protein to form chylomicrons and travel via lymph

52
Q

ADH pathway

A

Alcohol -> alcohol dehydrogenase -> mitochondria: Acetaldehyde -> Aldehyde dehydrogenase-> Acetate ->
energy or lipogenesis

53
Q

MEOs pathway

A

Alcohol -> CYP2E2 -> Acetaldehyde -> mitochondria: Aldehyde dehydrogenase-> Acetate -> energy or
lipogenesis

54
Q

catalase pathway in peroxisomes

A

Alcohol -> peroxisomal catalase -> Acetaldehyde -> mitochondria: Aldehyde dehydrogenase-> Acetate ->
energy or lipogenesis

55
Q

body balances water volume for blood volume and therefore blood pressure
starting with low blood pressure

A

decrease BP - > renin released -angiotensiogen-> angiotensin I -ace-> angiotensin II - > promotes release of aldosterone -> increases sodium reabsorption -> increases water retnetion -> decreases blood volume -> increases blood pressure

56
Q

role of water

A 
transport nutrient and oxygen
regulation of temperature 
waste removal
precursor of body fluids
solvent in biochemical and metabolic reactions
57
Q

Which water solbule vitamin adds carbon dioxide to compounds such as pyruvate during cellular energy metabolism

A

biotin

58
Q

four principles functions of iron in the body including mechanism of action

A
  • immune system
  • energy porduction - in CAC
  • transport of O2 and CO2
  • oxidation-reduction reaction
59
Q

specific role of vitamins in antioxidant system

A

A - neutralises ROS

E - removes free radical intermediates and prevents propogation reactions

60
Q

cells with short life span ar emost sensitive to deificency of folate because ?

A

THFA helps in the proliferation maintenance of new cells

61
Q

4 reasons for increased risk of Vit D deficiency

A
  • season
  • skin colour
  • location
  • liver disease
  • kidney disease
62
Q

microcytic hypochromic anemia is characteristic of which 2 nutrients

A

iron and pyroxidine

63
Q

4 examples of antioxidants enzymes and their overall role in antioxidant defense system

A

superoxide dismutase - converts superoxide in hydrogen peroxide
catalase - converts hydrogen peroxide to water and oxygen
glutathione enzyme - reductase, perioxidase
nrf2 - transcription factor promoting the expression of gene in antioxidant enzymes

64
Q

Discuss the very likely nutrient deficiencies that may occur over time, the reasons why, and the possible
symptoms in chronic alcoholism

A

a) alcoholic fatty liver, alcoholic hepatitis, and cirrhosis because the liver is the principal organ for alcohol metabolism. With heavy consumption, free radicals are produced as
by-products of alcohol metabolism, acetaldehyde and fatty acids build up.

b) thiamin deficiency - Wernicke
Korsakoff syndrome; Pyridoxine (inhibition of conversion to PLP with high acetaldehyde concentration) ->
microcytic-hypochromic anemia.
- Other water soluble vitamins may be at risk too due to increased excretion
• Fat soluble vitamins: A,D,E,K: reduced bile production in liver = less absorption ability for fat-soluble constituents; less storage ability in the liver; reduced calcitriol in liver; reduced carrier protein production in the liver ).
result in
night blindness (A);
soft bone and calcium level issues (D); reduced oxidative stress protection (E); increased risk of hemorrhaging (K)
• Minerals: at risk of increased excretion with increased urination; stomach ulcers may be frequent: increased bleeding and loss of iron; minerals are required in alcohol metabolism and in the antioxidant defense as co-factors: both of these activities are increased in chronic alcoholism (Zn, Fe, Mn, Se, Cu);
reduced absorption of calcium due to reduced calcitriol alcohol may also impair
absorption of Mg and Zn). Deficiencies will be specific to minerals: iron deficiency anemia, soft bone
/osteoporosis and muscle twitching /cramping issues ( Ca, Mg); poor antioxidant activity.

65
Q

___ determines fermentability

A

solubility

-^ s = ^ f

66
Q

How do omega 3 polyunsaturated fats increase circulating HDL

A

Promotes gene expression of APOA1 which increase HDL

67
Q

how does atherosclerosis develop? How is dietary fat involved in this process?

A

-develops due to high blood cholesterol as
if high cholesterol LDL receptor synthesis is blocked -> LDL build up in blood ->LDL taken up by macrophages becoming foam cells ->foam cells trapped in wall of blood vessel ->contribute to atherosclerotic plaque formation

68
Q

Why is the regular supply of essential amino acids so important?

A

required continuously from the diet is that they cannot be made by the body, yet are required continuously for gene expression. If they are not provided by the diet, the body breaks down its muscle mass (muscle wasting) to provide these EAA for gene expression to continue adequatly

69
Q

Key steps of protein ingestion and absorption and metabolism

A

food -gastrin produced -> singals HCL production and pepsinogen secretion – HCL denatures proteins and activates pepsinogen to pepsin (which cleaves peptides into shorter fragments) - moves into SI->secretin and CKK secretions ->stimulares pancreas to release trypsinogen, chymotrypsin and carboxypeptidase (into duodenum) - > activiated enzymes breakdown polypeptides into dipeptides and AA (for absorption)-> in enterocytes dipeptides further digested by peptidase into AA ->to AA pool

70
Q

Protein in fluid balance

A

– Blood pressure pushes fluid out of capillary bed at the arterial end into interstitial space
– Plasma albumin and globulins attracts water from the interstitial space back into the capillary for venous return
– If plasma albumin is insufficient, fluid remains in interstitial space resulting in edema

71
Q

why would high protein intake be a concern for kidney health?

A

Kidney – high protein – lots of AA – possible lots of deaminiation therefore removal of amine group from AA which is converted to ammonia which is then converted to urea which is filtered by kidney therefore overload of AA can over burdens kidney

72
Q

why would high protein intake be a concern for bone health?

A

Bone – as protein increases the acid load in body which may cause calcium to leak out of the bone to neutralize acid – not much proven research however

73
Q

How is BV calculated

A 
Nitrogen retained (g) / Nitrogen absorbed (g) x
100 (retained means that the whole amino acid is used by the body)

NUTR2101 (35 decks)

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