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semester 2 > Biochem > Flashcards

Biochem Flashcards

1
Q

primary monosaccharides (3)

A
  • glucose
  • fructose
  • galactose
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2
Q

how are primary monosaccharides/sugar monomers (glucose, fructose and galactose) absorbed across the brush border of enterocyte

A

via carrier mediated mechanisms (which demonstrate stereo specificity, saturation kinetics and can be specifically inhibited)

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3
Q

sodium dependent glucose transporter (2)

A
  • SGLT1 (sodium-glucose linked transporter) also transports galactose, into the epithelial cell from the intestinal lumen
  • GLUT2 uniporter transports monosaccharides into the circulation/blood (facilitated)
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4
Q

is SGLT1 an e.g. of primary or secondary active transport

A

secondary

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5
Q

why is SGLT1 describes as a symport

A

because membrane bound protein binds glucose and sodium at different sites

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6
Q

what drives the SGLT1

A

-conc gradient of sodium created by the sodium/potassium ATPase, which moves sodium out of the cell in exchange for potassium, using ATP for energy

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7
Q

role of sodium co-transporters

A

-transport sodium together with another molecule, eg. SGLT1 present on the enterocyte luminal membrane (enterocyte = cell of intestinal lining)

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8
Q

how is the sodium gradient (required for glucose symport by SGLT1) maintained

A
  • by the sodium/potassium ATPase, which keeps the intracellular sodium concentration low (sodium enters blood/exits enterocyte, and potassium enters enterocyte)
  • the sodium conc gradient set up by the ATPase pump is the driving force for sodium transport into the cell from the lumen via SGLT1, which also brings in glucose (or galactose)
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9
Q

clinical signif of the SGLT1 (2)

A
  • dehydrated patients found to absorb sodium much better when glucose was also provided
  • WHO oral solution saved lives of millions of children with severe diarrhoea
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10
Q

what mediates facilitative sugar transport

A

members of the GLU transporter family

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11
Q

role of GLUT 2 uniporter

A
  • transports monosaccharides into the circulation across the basolateral enterocyte membrane
  • eg. of facilitated diffusion
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12
Q

how do members of the GLUT transporter family allow the movement of sugars across the membrane

A

via formation of an aqueous pore across the membrane

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13
Q

how frequent are the GLUT family of glycosylated transmembrane proteins predicted to span the membrane

A

12 times with both amino- and carboxyl- termini located in the cytosol

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14
Q

subclasses of GLUT transporter family

A

-on basis of sequence homology and structural similarity, three subclasses of sugar transporters have been identified

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15
Q

definition of glycogenesis

A

synthesis of glycogen from glucose

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16
Q

definition of glycogenolysis

A

breakdown of glycogen to form glucose

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17
Q

definition of gluconeogenesis

A

synthesis of glucose within the body from non-carbohydrate precursors such as amino acids, lactic acid and glycerol

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18
Q

what is glycogen

A

= main storage form of glucose in liver and muscle cells

->polymer and storage form of glucose

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19
Q

when is liver glycogen broken down and released

A

-broken down between meals and released to maintain blood glucose levels for red blood cells and brain

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20
Q

role of muscle glycogen

A
  • not available for maintenance of blood glucose levels

- provides energy via glycolysis and the TCA cycle during bursts of physical activity

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21
Q

when does blood glucose from diet peak

A

after meals

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22
Q

what determines the time and frequency of glycogenolysis

A

-fluctuates dependent upon meal times and snacking

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23
Q

when is gluconeogenesis at its peak

A

-overnight, where it is the primary source of glucose as hepatic glycogen is used up and decreases

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24
Q

structure of glycogen

A
  • polymer consisting of glucose molecules joined by alpha 1-4 glycosidic links
  • branches are introduced by alpha 1-6 glycosidic links
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25
Q

glycogenesis (step 1)

A
  • step 1 = glucose -> glucose-6-phosphate (using hexokinase) -> can either go onto glycolysis (the breakdown of glucose by enzymes, releasing energy and pyruvic acid) or forms glucose-1-phosphate (using phosphoglucomutase) -> glycogen synthesis
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26
Q

glycogen synthesis requirements

A

-requires a glycogen ‘PRIMER’ containing at least 4 glucose residues

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27
Q

what is the glycogen primer (required for glycogen synthesis) made up by/ covalently attached to

A

an enzyme called glycogenin, which uses UDP- glucose aka ‘activated glucose’

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28
Q

formation of UDP-glucose (step 2 of glycogenesis)

A
  • UTP + Glucose-1-phosphate -> UDP-Glucose + pyrophosphate (PPi)
  • reversible reaction
  • however highly active pyrophosphatase in cells hydrolyses the PPi and drives reaction in favour of UDP-glucose synthesis (PPi + H20 -> 2 Pi)
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29
Q

what enzyme catalyses the formation of UDP-glucose

A

UDP-glucose pyrophosphorylase

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30
Q

step 3 of glycogenesis

A
  • glycogen is synthesised from UDP-glucose

- > catalysed by glycogen synthase

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31
Q

what is the rate limiting enzyme of glycogenesis

A

= glycogen synthase (catalyses synthesis of glycogen from UDP-glucose)

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32
Q

role of glycogen synthase (step 3 glycogenesis)

A
  • adds ONE glucose molecule to glycogen at a time forming alpha 1-4 glycosidic bonds
  • it can only EXTEND chains of branches (cannot introduce branches or start new molecules as this requires a primer made by glycogenin)
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33
Q

what is the branching enzyme during glycogenesis (step 3)

A

= transglycosylase, which introduces alpha 1-6 glycosidic branches into glycogen (branches occur approximately every 8-10 glucose residues)

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34
Q

how often do alpha 1-6 glycosidic branches occur in glycogen

A

every 8-10 glucose residues

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35
Q

hormonal control of glycogenesis

A

-control is exerted on glycogen synthase activity (synthesises glycogen from UDP-glucose)

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36
Q

hormonal response to hyperglycaemia stimulus (include source and effect of hormone)

A

(hyperglycaemia = excess of glucose)

  • hormone = insulin
  • source = pancreatic beta cells
  • effect = activation of glycogen synthase (which synthesises glycogen from UDP-glucose)
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37
Q

hormonal response to hypoglycaemia stimulus (include source and effect of hormone)

A

(hypoglycaemia = deficiency of glucose in bloodstream)

  • hormone = glucagon
  • source = pancreatic alpha cells
  • effect = inactivation of glycogen synthase (which synthesises glycogen from UDP-glucose)
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38
Q

structure of cholesterol (5)

A
  • almost entirely carbon and hydrogen (27 carbon atoms)
  • one hydroxyl group which is often esterified to a wide range of fatty acids
  • almost completely saturated (only one double bond)
  • ring structure is almost planar therefore lies flat
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39
Q

role of cholesterol in mammalian cell membranes

A

regulator of membrane fluidity

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40
Q

3 important classes of biologically active compounds that cholesterol is a precursor of (3)

A
  • bile acids
  • steroid hormones
  • vitamin D
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41
Q

importance of cholesterol metabolism

A

cholesterol =

  • > aetiology/cause of cardiovascular disease
  • > major component of gall stones
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42
Q

amount of cholesterol in typical western diet

A
  • approx 500mg daily

- meat, eggs, dairy products

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43
Q

how much cholesterol don humans synthesise per day

A
  • approx 1g

- depends on dietary intake

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44
Q

solubility of cholesterol

A

low solubility in water (cholesterol esters are less soluble than the 30% of circulating cholesterol that is in free form)

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45
Q

how much of circulating cholesterol is in the free form

A

-only 30% (the majority is esterified through the cholesterol hydroxyl (-OH) group and are called cholesterol esters (CE) and are less soluble in water

46
Q

where are cholesterol esters stored

A

in lipid droplets in the ER

47
Q

transport/storage of cholesterol

A

cholesterol is incorporated into lipoproteins where it is present as free cholesterol and cholesterol esters which are located in the core of the molecule

48
Q

extracellular uptake of cholesterol when intracellular levels drop (5)

A
  • lipoproteins constitute a pool of extracellular cholesterol
  • LDL binds to a cell surface receptor which is internalised and digested by the lysosomes (e.g. of endocytosis)
  • > free cholesterol is released and esterified
  • > the receptor is recycled to the membrane
  • free cholesterol is a negative feedback regulator of its own synthesis
49
Q

what mediates regulation of cholesterol synthesis

A

-family of transcription factors (DNA- binding) called ‘sterol regulatory element-binding proteins’ (SREBS)

50
Q

function of SREB’s (2)

A
  • regulate the transcription of the genes encoding the enzymes involved in cholesterol synthesis (HMG CoA reductase and HMG CoA synthase)
  • regulate a gene encoding a cell surface receptor (apoprotein receptor)
51
Q

enzymes involved in cholesterol synthesis

A
  • HMG CoA reductase

- HMG CoA synthase

52
Q

effect of hepatic sterol depletion (3)

A
  • increases SREBs, therefore:
  • > increases cholesterol synthesis
  • > increases expression of the cell surface apoprotein receptor (which can bind lipoprotein particles)
53
Q

molecular weight of cholesterol

A

= 386Da

54
Q

describe endocytosis and give e.g..

A
  • receptor mediated
  • specific and saturable
  • movement into the cell
  • eg. binding of LDL - delivering cholesterol to a cell expressing the receptor
55
Q

describe exocytosis and give e.g.

A
  • secretory
  • movement out of the cell
  • eg. when chylomicrons carrying TAGs, cholesterol etc. leave the enterocytes and enter the lacteals
56
Q

role of lipoproteins

A
  • transport vehicles for lipids in the lymph and blood

- transport fat soluble vitamins too e.g. vitamin A and vitamin E

57
Q

structure of lipoprotein molecule (2)

A
  • core of hydrophobic lipids (cholesterol esters and triglycerides)
  • surrounded by a shell (made up of polar lipids aka phospholipids, apoproteins and free cholesterol)
58
Q

role of apoproteins within shell of lipoprotein (2)

A
  • structural and metabolic as they interact with cellular receptors
  • also regulate activity of enzymes involved in lipid transport and distribution
59
Q

how are lipoproteins distinguished (2)

A
  • size
  • density as each contain diff amounts of lipids and proteins (the more lipid, the lower density and the more protein, the higher density)
60
Q

what does VLDL stand for

A

very low density lipoprotein

61
Q

what does IDL stand for

A

intermediate density lipoprotein

62
Q

what does LDL stand for

A

low density lipoprotein

63
Q

what does HDL stand for

A

high density lipoprotein

64
Q

major lipid for LDL

A

cholesterol

65
Q

role of LDL

A

delivers cholesterol from the liver to cells for:

  • > cell membranes
  • > hormone production
66
Q

LDL receptor

A

= membrane bound protein which binds LDL (by binding to its apoprotein), causing it to be taken up by the cell and dismantled

67
Q

role of LDL apoprotein

A

binds to a specific LDL receptor

68
Q

major lipid of HDL

A

phospholipid

69
Q

what synthesises HDL (2)

A
  • liver

- intestine

70
Q

role of HDL (2)

A
  • circulates in blood to collect EXCESS cholesterol from cells
  • important for reverse cholesterol transport
71
Q

lipid-protein ratio of HDL

A

lowest out of all lipoproteins

72
Q

steps involved in reverse cholesterol transport (HDL role) (4)

A
  • HDL salvages excess cholesterol from cells
  • cholesterol is esterified with fatty acids
  • it is then transported back to the liver
  • and excreted as bile salts via biliary system or faeces
73
Q

what organ is capable of metabolising and excreting cholesterol

A

ONLY the liver

74
Q

what human cells can synthesise cholesterol (biosynthesis)

A

virtually all human cells

75
Q

location of cholesterol biosynthesis within cells

A

-all reactions occur in the cytoplasm but some of the enzymes are attached to the ER membrane

76
Q

site of cholesterol synthesis

A
  • main site =liver

- lesser contributions = intestine, adrenal cortex, gonads

77
Q

requirements for the synthesis of 1 molecule of cholesterol (3)

A
  • source of C atoms (18 molecules of Acetyl-CoA)
  • a source of reducing power (16 moles of NADPH)
  • significant amounts of energy (36 moles of ATP)
78
Q

what is mevalonic acid (mevalonate)

A

-3 molecules of acetyl-CoA are converted into the 6 carbon mevalonic acid

79
Q

enzymes which catalyse the conversion of 3 acetyl-CoA molecules to the 6 carbon mevalonic acid (3)

A
  • acetoacetyl-CoA thiolase
  • HMG-CoA synthase
  • HMG-CoA reductase
  • > the transcription of the genes encoding the last 2 are regulated by SREBs
80
Q

enzyme involved in catalysing the rate limiting step of cholesterol synthesis

A

HMG-CoA reductase

81
Q

structural name of HMG-CoA

A

=3-hydroxy-3-methylglutaryl-CoA

82
Q

rate limiting step of cholesterol synthesis

A
  • formation of mevalonic acid (which is irreversible)

- catalysed by HMG-CoA reductase

83
Q

location of HMGR (HMG-CoA reductase)

A

embedded within the ER

84
Q

how is HMGR (HMG CoA-reductase) controlled (4)

A
  • feedback inhibition
  • rate of its degradation
  • phosphorylation (it is active when it is NOT phosphorylated)
  • gene expression (synthesis is stimulated by fasting and inhibiting dietary cholesterol, as hepatic sterols deplete)
85
Q

effect of hormones on HMGR (4)

A
  • insulin and T3 (tri-iodothyronine) increase its activity

- glucagon and cortisol inhibit activity

86
Q

regulation of cholesterol synthesis (as a result of high intracellular free cholesterol) (4)

A
  • reduction in expression and activity of HMG-CoA reductase (limits synthesis) using drugs (statins)
  • decreased regulation of LDL receptors (limits uptake)
  • increase in efflux
  • increase in rate of conversion to bile salts
87
Q

effect of dietary restrictions on reduction of free cholesterol

A

dietary restrictions can only achieve a 15% reduction in free cholesterol

88
Q

function of statins (drugs)

A
  • inhibit cholesterol synthesis
  • lowered intracellular cholesterol leads to increase in LDL expression
  • promotes removal of LDL from blood
89
Q

rate limiting enzyme in cholesterol biosynthesis

A

HMG-CoA reductase

90
Q

what drugs inhibit HMG-CoA reductase activity

A

statins

91
Q

main metabolic product from cholesterol

A

bile salts

92
Q

how do bile salts differ from each other

A

differ in the no. and position of their hydroxyl groups (-OH)

93
Q

what synthesises and secretes bile salts

A

the liver

94
Q

formation of bile salts (2)

A
  • prior to secretion, cholic acid and chenodeoxycholic acid are conjugated through the carboxyl group (-COOH) to glycine or taurine forming the four primary bile acids
  • in physiological conditions they are ionised to form bile salts
95
Q

where are bile salts stored

A

gall bladder

96
Q

function of bile salts once released into the duodenum

A

act as detergents for emulsifying ingested fats

97
Q

products from cholesterol

A
  • bile salts
  • vitamin D
  • steroid hormones
98
Q

function of vitamin D

A

-play a role in the regulation of calcium and phosphors metabolism

99
Q

how is vitamin D a product of cholesterol

A
  • vitamin D3 is synthesised in the skin by UV radiation of 7-dehydrocholesterol
  • the active form of vitamin D3 is called calcitriol or 1,25(OH)2D which acts as a steroid hormone
100
Q

function of active vitamin D3 (calcitriol/ 1,25(OH)2D)

A

acts as a steroid hormone

101
Q

what are steroid hormones derived from

A

cholesterol

102
Q

3 groups of steroid hormones (3)

A
  • corticosteroids (21 carbon atoms)
  • androgens (19 carbon atoms)
  • estrogens (18 carbon atoms)
103
Q

location of steroid hormone synthesis (conversion of cholesterol into steroid hormones) (3)

A
  • adrenal cortex (corticosteroids)
  • testis (androgens)
  • ovary (oestrogen’s)
  • > all 3 organs are capable of secreting small amounts of steroids from other groups
104
Q

mechanism of action of steroid hormones (4, long card)

A
  • all act by binding to specific receptors (nuclear or cytoplasmic)
  • adjacent to the hormone binding domain in the receptor is a highly conserved DNA-binding domain, characterised by two zinc fingers which fit into the major groove of the DNA
  • binding of the steroid facilitates translocation of the activated receptor
  • the complex can then bind to a specific steroid response element (DNA) in a gene promoter region controlling gene expression
105
Q

other members of the superfamily of steroid hormone receptors (3)

A

include:

  • receptors for T3 (triiodothyronine)
  • active forms of vitamin A and D
106
Q

genetic variation of steroid receptors (2)

A

may be associated with hormone resistance and diverse clinical presentations

107
Q

regulation of gene transcription by glucocorticoids (corticosteroid) (5)

A
  • steroid binds to receptor in cytoplasm
  • receptor dimerises
  • exposes a nuclear localisation signal (NLS), complex enters the nucleus
  • binds to DNA at a specific response element (SRE, GRE=glucocorticoid response element) aka hormone response element (HRE)
  • activate promoter and switch transcription on (or off)
108
Q

precursor molecule of bile acids

A

cholesterol

109
Q

precursor molecule of steroid hormones

A

cholesterol

110
Q

precursor molecule of vitamin D

A

cholesterol

111
Q

transformation of cholesterol into bile salts and steroid hormones involve what type of reactions and are catalysed by what

A

involves hydroxylation reactions catalysed by cytochrome P450 monooxygenase

112
Q

how do steroid hormones bring about their biological effects

A

by binding to steroid-specific hormone receptors which can affect gene transcription (increase, or decrease)

semester 2 (9 decks)

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