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Metabolism > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

What enzyme breaks down glycogen to glucose-1-P and what 2 enzymes create it?

A

BD: glycogen phosphorylate
Make: UDP-glucose pyrophosphorylase and glycogen synthase

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2
Q

What is glucagon’s receptor type and protein it acts via?
What enzymes does it effect?
- Stimulates; glycogen phosphorylase, PEPCK and FBP1ase
- Inhibits glycogen synthase, PFK and pyruvate kinase
(affects FBP1ase and PFK by acting on bifunctional PFK2/FBP2ase reducing F-2-6-BP)

A

G protein receptor, actions through PKA
Increasing glucose in the blood by
- Stimulating glycogen breakdown in liver

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3
Q

How does the cori cycle assist glycolysis when demand for glucose is high?
What happens to the lactate?

A
  • Lactate production produces NAD+ via lactate dehydrogenase
  • NAD+ can be used by glyceraldehyde 6-phosphate dehydrogenase to make ATP
  • Lactate undergoes gluconeogenesis in liver
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4
Q

What type of receptor does insulin bind to?

What are its actions?

A

Tyrosine kinase which causes IRS1 to create PIP3 which
- causes GLUT4 translocation
- stimulates glycogen synthase (so making glycogen), glucokinase, PFK and PK
Also stimulates protein and fatty acid synthesis

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5
Q

How does oxidation create NADH/FADH2 in the TCA cycle?

A

Dehydrogenation between succinate to get fumerate, removing hydrogens to make a C=C, gets FADH2
Dehydrogenation between malate and oxaloacetate to make an aldehyde C=O, get NADH

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6
Q

How does oxidative phosphorylation generate ATP?

Where do NADH and FADH2 enter?

A

The transfer of electrons in complex 1, Q, 3 and 4 causes H+ to cross the membrane creating a proton gradient which drives ATP synthesis
NADH at complex 1
FADH2 at complex 2
Both then pass to coenzyme Q, 3,4

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7
Q

How are superoxides generated?

How does glutathione help deal with this?

A

Build up of ubisemiquinone CoQH and that one unpaired electron is transferred to oxygen to get O2-
Glutathione thats been reduced by NADPH (from PP cycle) reduces oxidised proteins so they can regain function as well as H202 from O2- to H2O, returning to its oxidised state

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8
Q

What is the Walburg effect?
How do cancer cells generate enough glucose?
How does hypoxia induce the effect?
What does the effect mean for their survival?

A

Most cancer cells shift from generating ATP from oxphos to glycolysis, even in aerobic conditions
They up regulate GLUT1
Hypoxia instead of killing the cell causes synthesis of enzymes for glycogen metabolism as well as providing glucose-6-P for PPP by up-regulating GLUT1
More NADPH means more scavenging of ROS and more precursors for synthesis
* Note also genetic alterations to increase survival

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9
Q

Describe the goal of the 2 steps of the pentose phosphate pathway including the first two steps in the 1st phase

A

1st phase is oxidation to generate NADPH.
Done by oxidising glucose-6-P to phosphogluconate, then to riboulose-5-P
The NADPH used to reduce glutathione and for reductive biosynthesis of fats, cholesterol etc. for cell growth and proliferation
2nd phase is the interconversion of the pentose sugars for DNA and protein biosynthesis

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10
Q

What are keno bodies and why are they formed?

What can this lead to and why?

A

Acetoacetae, Acetone and B-hydroxybutyrate
Formed in starvation when acetyl-coa instead of going to TCA cycle is forced into this pathway.
They lead to release of H+ which causes metabolic acidosis, can lead to a diabetic coma and death

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11
Q

What hormones mobilise fatty acids from adipose tissue? Where do they go?

A

Glucagon and adrenaline

To muscle for B-oxidation and to liver largely for ketogenesis

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12
Q

What amino acid deficiency leads to pellagra?

What are the 4 D symptoms?

A

Tryptophan and niacin

Diarrhoea, dermatitis, dementia, death

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13
Q

Draw the structure of glucose

A

Ch2OH, O, OH down, OH down, OH up, OH down

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14
Q

Which GLUT transporter is used in liver, muscle and brain

A

Liver- GLUT2
Brain- GLUT3
Muscle- GLUT4

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15
Q

What does insulin stimulate in the liver?

A

Glycogen synthesis
Fatty acid synthesis when glycogen synthesis exhausted
Glycolysis
Doesn’t increase GLUT2 expression

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16
Q

What is popes disease?

A

A glycogen storage disease from an enzyme defect which causes glycogen to build up in lysosomes.
Causes myopathy and resp failure by age 2

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17
Q

What are the benefits of a high fibre diet?

A

Peristalsis is more efficient

Good for microbiome of gut so protective against some diseases

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18
Q

What is the pathway of fats once ingested?

A
  • Eat fats which are converted to cholymicrons
    • Cholymicrons move through lymph and blood to tissues
    • LPL hydrolyses TAG into FA and glycerol which are taken up in target tissues.
    • In muscles the FA are oxidised for energy, in adipose tissue they are re-esterified for storage as TAG.
    • The CM remnants with depleted of most TAG but still with cholesterol and APL travel back to liver where they are taken up. TAG that enter the liver via this route may be oxidised to provide energy or make ketone bodies.
    • When the diet has more FA then needed for fuel the liver converts them to TAG and packages them into VLDL. The VLDLs go to adipose tissue and are stored in lipid droplets there.
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19
Q

How much Ca2+ do we need a day and why?

When can excess Ca2+ cause?

A

1g/day because kidney loses around 1g/day

Malignant hyperthermia from excess Ca2+ being released from muscle, use too much O2 and get hyperthermic

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20
Q

How much phosphate do you need a day? What are the consequences of having too little?

A

1g/day if too little get bone fragility and muscle and neurological dysfunction (less ATP)

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21
Q

How much potassium and sodium do you need a day? What are their roles?

A

3-4g/day

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22
Q

Why don’t we see sulphur deficiencies?

What does it do?

A

Cos get it from cysteine in protein so if have enough protein then all good
It stabilises protein structure eg keratin

23
Q

What role does chloride play in the GIT?

A

Its in HCl and its an emetic

24
Q

What is magnesium used to treat?

A

Ca2+ uptake and muscle cramps

25
Q

What is hereditary hemochromatosis?

A

Defects in iron carrying/storing proteins which mean get too much iron. Can cause liver issues, arthritis, diabetes and heart disease

26
Q

What is 1 role of zinc?

A

Sperm maturation and foetus formation

27
Q

What causes Menke’s disease and Wilsons disease?

A

Menke’s- not enough copper; defective keritinsation, aorta elastin and mental formation
Wilsons- too much copper; liver toxicity and ring around iris

28
Q

What mineral defends against oxidation and assist thyroid hormone production?

A

Selenium

29
Q

What mineral enhances insulin action and a def can lead to diabetes like syndrome?

A

Chromium

30
Q

What minerals can be cofactors for enzymes

A

Molybdenum; some metalloenzymes

Manganese; in photosynthesis

31
Q

What diseases are caused by thiamin (B1) deficiency?

What chemical reaction is it involved in?

A

Beriberi; weakness and wasting
Wernicke-korsakoff; uncoordinated eyes, wide step etc.
Coenzyme in decarboxylation- metabolism

32
Q

What is the role of riboflavin (B2)?

How does deficiency effect the tongue?

A

electron carriers; FMN and FAD

tongue gets swollen and magenta

33
Q

what is the role of niacin (B3)

A

electron carrier; NAD and NADP

34
Q

What is the role of pyroxidine (B6)

A

Involved in transamination in amino acid metabolism

35
Q

What is the role of biotin?

A

carboxylation, opposite to thiamin so glucose, fat and protein synthesis opposed to metabolism

36
Q

What vitamin def leads to spina bifida?

A

folate

37
Q

what is needed for B12 absorption? what does B12 def cause?

A

intrinsic factor

pernicious anaemia

38
Q

what are some roles of vitamin C?

A

cofactor in collagen synthesis

iron absorption

39
Q

What are two types of vitamin A and their role?

How is it involved in xeropthlamia?

A

Retinal- night vision
Retinol- epithelial growth of skin and eye
Xerophthalmia with retinol def, cornea doesn’t develop properly and blind

40
Q

What are some disease vitamin D can have protection against?

A

Cancer, autoimmune (possible role in MS) and infection

41
Q

Which vitamin is an antioxidant?

A

Vitamin E

42
Q

What vitamin is anti-thrombic?

A

vitamin K

43
Q

What happens to adipocytes above and below set point?

A

Above they swell with lipids and if swell too much they divide and make more.
Below set point they shrink and after 6 months they die

44
Q

What is the role of leptin?

What are the leptin levels in obese people normally?

A

Released by adipocytes and goes to hypothalamus to say energy supplies are all g and stop eating
It also stimulates energy expenditure
Usually high leptin in obese people but low receptor sensitivity

45
Q

Out of NPY, POMC, AgRP and CART which ones does leptin block that increase appetite and which ones does leptin stimulate that decrease appetite?

A

NPY and AgRP increase appetite and POMC and CART decrease appetite

46
Q

Which signalling molecule does adiponectin active? what does it do?

A

AMPK
In muscle stimulates; glucose uptake and lactate production, and fatty acid oxidation.
In liver it decreases gluconeogenesis
So it good (glitazone used to treat diabetes by raising)

47
Q

Where is ghrenlin released and what does it do?

A

Released by the stomach before meals.

It activates NPY neurons in hypothalamus to increase appetite

48
Q

How do you calculate BMI?

What are the ranges?

A

weight in kg/height in m^2
Underweight 25
Obese >30
Morbidly obese >40

49
Q

When is the adiposity rebound?

What happens to weight in puberty in males and females?

A

Age 2-6 regain some weight lost from moving around.

Puberty boys lose fat and females gain fat

50
Q

What is protein sparing?

A

When body has enough CHO and fat for energy will use protein structurally

51
Q

What is protein-energy malnutrition and what are two types you can get? What toxin from corn fungus can make this worse?

A

An inadequate amount of macronutrients
Kwashiorkor; moderate energy but severe protein deficit
Aflatoxin can make worse by damaging DNA in liver so even less albumin
Marasmus; severe energy and protein deficit

52
Q

What do we use in starvation pre and post 3 days?

What vitamin falls and why is this bad long term?

A

In first 3 days mainly muscle protein
After that fat break down established and use glycerol for gluconeogenesis and FFA oxidation
Thiamin falls, means even post feeding can have neural damage

53
Q

What happens to your villi in intestine during starvation?

Why is this a concern in refeeding?

A

They atrophy and lose absorptive capacity

If re-feed with rich food gut bacteria thrive and get septicaemia

Metabolism (6 decks)

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