Things to go over Flashcards
(73 cards)
1
Q
sucrase
A
digests table sugar
2
Q
phospholipid A2
A
breaks down phospholipids
3
Q
amylase
A
digests 1-4bonds in starch
4
Q
alpha dextrinase
A
digests 1-6bonds in starch
5
Q
pancreatic lipase
A
cleaves fatty acids from glycerol in duodenum
6
Q
lactase
A
breaks down lactose
cleaves galactose from glucose
7
Q
maltase
A
digests maltose
cleaves glycosidic bond between two glucose molecules
8
Q
cholesterol esterase
A
cleaves cholesterol esters
9
Q
G6P
A
converts glucose-6-phosphate to glucose in glycogenolysis in liver
10
Q
pepsin
A
cleaves peptide bonds in stomach
11
Q
ALT or AST
A
a type of transaminase that facilitates transamination
12
Q
alcohol dehydrogenase
A
converts alcohol in first step of alcohol metabolism
13
Q
trypsin
A
type of protease that cleaves peptides in duodenum
14
Q
pancreatic amylase
A
cleaves polysaccharides in duodenum
15
Q
Glut 4
A
allows cellular uptake of glucose upon insulin signalling
16
Q
Acetyl coa
A
starting molecule in lipogenesis
or
molecule entering CAC after glycolysis
17
Q
acetaldehyde
A
intermediate in alcohol metabolism - cause hangovers
18
Q
oxaloacetate
A
starting molecule for gluconeogenesis
19
Q
ketone body
A
formed from 2 acetyl coa
20
Q
starch
A
ppolysaccharide stored in plants
21
Q
trans fatty acid
A
partially hydrogenated unsat datty acid
22
Q
ribose
A
saccharide used to form nucleotide
23
Q
mono unsat faatty acid
A
fatty acid with one double bond
24
Q
poly unsat fatty acid
A
fatty acid with multiple double bonds
25
cholesterol
sterol manufactured by liver
26
phospholipid
similar to tryglyceride except phospohrus replaced FA
27
SCFA
produced by bacterial fermentation
28
eicosanoids
inflammatory response molecule formed from omega 3 and 6
29
how dietary fibre assists in regulation of blood sugar levels
- slows down gastric emptying
| - harder for enzymes to access CHO
30
Nrf2 in bodys antioxidant defense system
a transcription factor promoting the expression of antioxidant enzyme genes - increases antioxidant capacity
31
Vit A mechanism - light dark adaptation
rhodopsin (opsin and II-cis-retinal) absorbes light ->converts II-cis-retinal to all-trans-retinal-> all-trans-retinal converts back to rhodopsin
32
Vit A mechanism - target cell
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
Vit E food source
sunflower seeds and oil
34
main function of Vit E
as an antioxidant - prevents propagation of free radicals in cell memebrane and LDL through oxidation of lipid
35
main function of VIt K
as a cofactor of carboxylase enzymes in the synthesis of blood clotting (prepro to pro)
36
babys given vit K injection
as GIT is sterile - no bacterial production of Vit K and no eating green leafy vege
37
esterification
triglyceride FAs and/or glycerol
38
beta oxidation
oxidation of FAs to acetyl coA
39
glycogenolysis
hydrolysis of glycogen to glucose
40
gluconeogenesis
making new glucose
41
glycogenesis
glucose to glycogen
42
glycolysis
glucose to pyruvate
43
ketogenesis
formation of ketone bodies
44
lipogenesis
hydrolysis of triglycerides to fatty acids and glycerol
45
ketoxidation
ketones to acetyl coa
46
deamination
removal of nitrogen froup of AA
47
FA used as substrate for gluconeogenesis
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
fibre - mechanisms of action
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
digestion, absoprtion and transport of dietary lipids
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
Cholesterol uptake
scavenger pathway - removes oxidised LDL form epithelium
| receptor pathway - LDL uptake and broken down and utilised by cells
51
MCT metabolism and LCT metabolism
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
ADH pathway
Alcohol -> alcohol dehydrogenase -> mitochondria: Acetaldehyde -> Aldehyde dehydrogenase-> Acetate ->
energy or lipogenesis
53
MEOs pathway
Alcohol -> CYP2E2 -> Acetaldehyde -> mitochondria: Aldehyde dehydrogenase-> Acetate -> energy or
lipogenesis
54
catalase pathway in peroxisomes
Alcohol -> peroxisomal catalase -> Acetaldehyde -> mitochondria: Aldehyde dehydrogenase-> Acetate ->
energy or lipogenesis
55
body balances water volume for blood volume and therefore blood pressure
starting with low blood pressure
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
role of water
```
transport nutrient and oxygen
regulation of temperature
waste removal
precursor of body fluids
solvent in biochemical and metabolic reactions
```
57
Which water solbule vitamin adds carbon dioxide to compounds such as pyruvate during cellular energy metabolism
biotin
58
four principles functions of iron in the body including mechanism of action
- immune system
- energy porduction - in CAC
- transport of O2 and CO2
- oxidation-reduction reaction
59
specific role of vitamins in antioxidant system
A - neutralises ROS
| E - removes free radical intermediates and prevents propogation reactions
60
cells with short life span ar emost sensitive to deificency of folate because ?
THFA helps in the proliferation maintenance of new cells
61
4 reasons for increased risk of Vit D deficiency
- season
- skin colour
- location
- liver disease
- kidney disease
62
microcytic hypochromic anemia is characteristic of which 2 nutrients
iron and pyroxidine
63
4 examples of antioxidants enzymes and their overall role in antioxidant defense system
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
Discuss the very likely nutrient deficiencies that may occur over time, the reasons why, and the possible
symptoms in chronic alcoholism
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
___ determines fermentability
solubility
| -^ s = ^ f
66
How do omega 3 polyunsaturated fats increase circulating HDL
Promotes gene expression of APOA1 which increase HDL
67
how does atherosclerosis develop? How is dietary fat involved in this process?
-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
Why is the regular supply of essential amino acids so important?
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
Key steps of protein ingestion and absorption and metabolism
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
Protein in fluid balance
– 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
why would high protein intake be a concern for kidney health?
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
why would high protein intake be a concern for bone health?
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
How is BV calculated
```
Nitrogen retained (g) / Nitrogen absorbed (g) x
100 (retained means that the whole amino acid is used by the body)
```
