human metabolism: carbs, fats proteins (biochem) Flashcards
which is the only fuel that can be respired anaerobically?
carbohydrates
which 2 parts of body rely especially on carbohydrates?
brain
erythrocytes
monosaccharides examples x2
which foods are they found in?
glucose and fructose
(both found in fruit & honey)
disaccharides examples x2
what are their monosaccharide components?
which foods are they found in?
lactose (milk sugar)
glucose, galactose
milk
sucrose (table sugar)
glucose, fructose
cane sugar, prepared foods
trisaccharide (1)
what is its monosaccharide component?
which food is it found it?
trehalose
glucose
mushrooms
polysaccharides examples (3)
i) monosaccharide components
ii) foods they are found in
amylose
i) glucose (linear)
ii) plant starch
amylopectin
i) glucose (branched)
ii) plant starch
glycogen
i) glucose (branched)
ii) meat
what is the first stage of both aerobic and anaerobic respiration?
glycolysis
in which part of the cell does glycolysis occur?
what are the start and end products?
cytosol
glucose –> 2x pyruvate
under anaerobic conditions what happens to pyruvate?
which enzyme does this?
what other substance is involved in anaerobic respiration of pyruvate and what is it turned into?
reduced to lactate
lactate dehydrogenase
NADH –> NAD+
where does aerobic metabolism take place?
mitochondria
what is the cycle for aerobic respiration called?
tricarboxylic acid cycle (Krebs cycle)
what initially happens to pyruvate during aerobic respiration?
which enzyme catalyses this reaction?
what other substance is involved and what is it converted to/from?
pyruvate –> acteyl CoA + CO2
PDH (pyruvate dehydrogenase)
NAD+–> NADH
what happens to acetyle CoA in tricarboxylic acid acid?
acetyl CoA (C2) + oxaloacetate (C4)–> citrate (C6) –> cis-acetonate (C6) –> isocitrate (C6)
what happens to isocitrate in tricarboxylic acid cycle?
isocitrate (C6) –> a-ketoglutarate (C5) + CO2
NAD+–> NADH facilitates this reaction
what happens to a-ketogluterate (C5) in tricarboxylic acid cycle?
–> succinyl CoA (C4) + CO2
facilitated by NAD+ –> NADH
how does succinyl CoA become oxeloacetete in tricarboxylic acid cycle?
succinyl CoA –> succinate
facilitated by GDP –> GTP
succinate –> fumerate
facilitated by FAD–> FADH2
fumerate –> malate
malate –> oxaloacetate
facilitated by NAD+ –> NADH
products of each TCA cycle:
reduced co-factors: 3x NADH, 1x FADH2
high energy compound: 1x GTP
decarboxylation products: 2x CO2
how many moles of ATP are produces by:
i) aerobic respiration
ii) anaerobic respiration
i) 30-32
ii) 2
examples of partially anaerobic tissues: (4)
- renal medulla
- retinal cells
- red blood cells
- white (type 2) muscle fibres
white muscle fibres
- which fuel can they use?
- what do they store?
- what is storage product broken down to?
- only glucose
- glycogen
glycogen is broken down to glucose -1-phosphate then intermediate glucose-6-phosphate
how much glucose does the brain consume per day in:
i) fed state
ii) starved state
How quickly are glycogen stores used up in starvation?
i) 100g/day
ii) 25g/day
within 1st 24 hrs
how is glucose obtained during starvation?
breakdown of muscles
protein –> amino acid –> oxoacid
amino acid–> oxoacid
allows pyruvate –> alanine
alanine –> pyruvate in liver
which then allows for glucose production in the liver
what is the site of ketogenesis?
the liver
which transport molecule allows glucose to be taken up into brain?
GLUT 3
how is fat stored in the body?
triaglycerol (TAG/ triglyceride)
this forms lipid droplets in cytosol of adipocyte
major roles of fats in the body (5)
+ the form of fat involved in each
- energy storage
- triglycerol - membrane formation
- phospholipids - hormone synthesis
- eicosanoids (prostaglandins, thromboxanes, leucotrienes formed from essential fatty acids) - intracellular signalling
- membrane phospholipids broken down to second messengers when hormone binds to its receptor - regulation of gene transcription
- fatty acids (+ fat-soluble vitamins)
TAG (triaglycerol structure)
threecarbon glycerol backbone that is esterified to three
fatty acid side chains and the free fatty acid molecule constitutes the accessible energy source for cells and
tissues.
which enzymes catalyses liberation of of fatty acid from TAG?
hormone-sensitive lipase (HSL)
what affects HSL (hormonesensitive lipase) levels?
stimulated by:
- glucagon
- adrenaline
- noradrenaline
inhibited by:
- insulin
(HSL is elevated in diabetics due to poor insulin sensitiv/ porduction)
how are fats transported in blood?
in protein complexes (as are hydrophobic and insoluble)
Elevated levels of which one of LDL/ HDL can be sign of high fat diet?
LDL
chylomicron
i. main fat constituent
ii. function
i. dietary TAG
ii. transports TAG from intestine to other tissues for oxidation or storage (fed state)
VLDL (very low density lipoprotein)
i. main fat constituent
ii. function
i. endogenous TAG, cholesterol
ii. Transports TAG produced in the liver to other tissues where it can be oxidised (fasting state)
LDL
i. main fat constituent
ii. function
i. cholesterol and cholesteryl ester
ii. transports cholesterol from liver to other tissues
HDL
i. main fat constituent
ii. function
i. cholesteryl ester
ii. Scavenges cholesterol from many tissues and takes it to the liver for excretion
fatty acid-albumin
i. main fat constituent
ii. function
i. fatty acid
ii. Transports fatty acids from adipose tissue to other tissues where they can be oxidised (fasting state)
which 2 aerobic tissues consume and oxidise fatty acids at high rates?
heart tissue
red fibres of skeletal muscle
name of pathway which oxidises fatty acids?
which part of cell does it occur in?
what are its products
diagram:
beta oxidation pathway
mitochondria
1x acetyl CoA
1x FADH2
1x NADH
what is drawn to the liver to fuel gluconeogenesis during starvation?
oxaloacetate
imbalance in of oxeloacete and acetyl CoA in liver during starvation
[liver takes up high levels of fatty acid so beta oxidation rates remain high resulting in an imbalance between CoA and oxeloacetate levles]
what does liver do with excess acetyl CoA?
ketogenesis
how much of brain’s energy supply do ketones account for during starvation?
what level of ketones is sustained in body?
which is main ketone used for energy supply?
75%
8mmol/l
acetoacetane (acetone is what is excreted in urine)
what elements are amino acids made from?
carbon
hydrogen
oxygen
nitrogen
in amino acid breakdown what is disposed of separately from carbon skeleton?
why?
the amino group
to maintain nitrogen balance and prevent accumulation of toxic nitrogenous compounds such as ammonium ion (NH4+)
what’s the first stage in amino acid metabolism?
removal of the amino group
what happens in transamination?
which enzyme is involved?
amino group is transferred to a different carbon skeleton
a-ketogluerate –> glutamate
amino transferase
(remember is reversible in case NH4+ levels are low)
what happens in de-amination?
enzyme involved
amino group is released as NH4+
glutamate +H2o–> a-ketoglutarate + NH4+
facilated by NAD+ –> NADH
glutamate dehydrogenase
(remember is reversible in case NH4+ levels are low)
NB. the pathway of amino acid degradation includes many aminotransferase enzymes with specificity for individual amino acids but only one enzyme (glutamate dehydrogenase) with deaminating activity
urea cycle
- which organ does it occur in?
- which part of the cell?
- what is its purpose?
- liver
- mitochondria and cytosol
- detoxify ammonium to produce urea (non-toxic vehicle for transport of nitrogen out of body)
upper limit of normal NH4+ in blood?
at what levels do sx of toxicity delevlop?
20 micromoles/ L (except for hepatic portal vein where concentrations are like 10x higher)
200 micromoles/L +
urea cycle equation:
NH4+ + bicarbonate + asparte (amino acid) —> urea + fumerate (TCA intermediate)
facilitated by 3ATP –> 2ADP + AMP
amino acids that are converted to which substance are ketogenic?
acetyl CoA
which are the 2 main amino acids released by the brain during starvation?
what % of broken down amino acids do they account for?
alanine
glutamine
60-70%
conversion of glucogenic amino acids to glucose
phenylketonuria (PKU)
i. what is it?
ii. incidence in UK
iii. how many different polymorphisms account for this phenotype
i. absence/ greatly diminished activity of enzyme phenylalinase hydroxylase
ii. 1 in 10,000
iii. 300
PKU what happens
i. acculumation of pheylalanine
interferes with uptake of other amino acids by competition with the saturable amino acid transporter
results in severe impact on developing brain
screening test for PKU?
when is it done?
cut-off level for dx?
Guthrie test
6-14 days post natally
240 micromoles/L
PKU mgt
exclude phenylalaline from diet but include tyrosine and other amino acids
must be followed strictly until 11 years
must be resumed in pregnancy
which amino acid is phenylalanine closely linked to?
what appearance can this result in?
tyrosine
occulocutaneous albinism
insulin sensitivity:
i. in early pregnancy vs normal
ii. in 3rd trimester vs normal
i. increased
ii. reduced by 50-70%
TAG/ fatty acids in:
i. maternal tissues
ii. foetal tissues
i. deposition (early pregnancy)
oxidation and ketogenesis (later in pregnancy)
ii. little oxidate capacity, stored in late gestation
glucose in:
i. maternal tissues
ii. foetal tissues
i. reduced insulin sensitivity so reduced uptake
ii. oxidised at high rates, staored as glycogen in late gestation
amino acids:
i. in foetal tissues
consumed for proteins synthesis
ketone bodies:
i. maternal tissues
ii. foetal tissues
i. higher circulating levels (indicate high ration of use)
ii. little if any oxidate capacity
foetal metabolism
no gluconeogenesis initially as no glycogen stores in liver
fatty acid oxidation in liver ^^ post natally (but lipogenic capacity remains low until weaning)
what else does neonate need dietry fat for (2)
- CNS development (3rd trimester to 3 months post natal)
especially DHA, a derrivatiev of a-linoleic acid (an omega 3 fatty acid) - thermogenesis
- fatty acids are metabolised by brown adipose tissue for thermogenesis (infant does not have right muscles to shiver)
