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S2 Flashcards

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1
Q

Which tissues have an absolute requirement for glucose?

A

red blood cells, neutrophils, kidney medulla cells, and cells in the lens of the eye

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2
Q

What range should plasma glucose be in?

A

Normal blood glucose concentration = 4.0-6.0 mmol/L.

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3
Q

What enables blood glucose to be kept at required levels?

A

A store of glucose= glycogen

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4
Q

What is the renal threshold?

A

Renal threshold = 10 mmol/L. This is the maximum amount of glucose that the body can handle before the kidney can no longer reabsorb glucose and appears in the urine. Renal threshold can be altered by physiological state (e.g. pregnancy) and other factors such as age.

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5
Q

How is glycogen stored?

A

In granules

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6
Q

Where are the main stores of glycogen?

A

Skeletal Muscle- 300mg of glycogen stored in muscles cannot be released into the blood and can only be used by the muscle itself
Liver-100mg of glycogen is stored in the liver and can be used to raise the blood concentration of glucose

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7
Q

Describe the structure of glycogen

A

Polymer consisting of chains of glucose molecules linked into straight chains by α1-4 glycosidic bonds.
highly branched structure formed by α1-6 glycosidic bonds every 8-10 residues
branched chains clump together to form granules inside certain cells, acting as a store of glucose.

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8
Q

What is the advantage of storing glucose in branches?

A

Branches give more points for enzymes to react and release more glucose simultaneously, safe storage without drawing lots of water into the cell

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9
Q

What is glycogenesis?

A

process of turning glucose into glycogen. four reactions, two of require ATP to occur. These reactions add glucose onto the end of one of the strands of a glycogen molecule.

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10
Q

What does glycogen synthase do?

A

form α1-4 glycosidic bonds with an existing branch

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11
Q

What does branching enzyme do?

A

forms α1-6 glycosidic bonds to begin a new branch

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12
Q

What enzymes are involved in glycogenolysis?

A

Glycogen phosphorylase breaks the α1-4 glycosidic bonds.
Debranching enzyme breaks the α1-6 glycosidic bonds.
Phosphoglucomutase converts glucose 1-phosphate to glucose 6 phosphate

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13
Q

What is liver and muscle glycogen used for?

A

Used by muscle for energy production- lacks glucose 6 phosphatase
Released by liver into blood for use by other tissues- buffer of blood glucose levels

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14
Q

What is the rate-limiting enzymes of glycogen metabolism?

A

Glycogen Synthase inhibited by glucagon and adrenaline, activated in activity by insulin
Glycogen Phosphorylase inhibited by insulin, activated when glucagon or adrenaline

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15
Q

What effect does glucagon have on muscle glycogen stores?

A 
not respond to glucagon, because glucose produced from the breakdown of muscle glycogen cannot be used to raise blood glucose
adenosine monophosphate (AMP) is the allosteric activator of Glycogen Phosphorylase. High [AMP] in the muscle, glucose is released to allow for the production and release of ATP
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16
Q

What are glycogen storage diseases?

A

a rare group of inborn errors of metabolism diseases that involve a deficiency in an enzyme involved in glycogen storage
Too much glycogen storage= damage tissues and can occur if the cells are unable to break down the glycogen.

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17
Q

When and where does gluconeogensis take place?

A

after 8 hours of fasting, when glycogen stores are being depleted and a new source of glucose is needed. It occurs mainly in the liver, but also in the kidney cortex.

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18
Q

What are the three major precursors for gluconeogensis?

A

Lactate from anaerobic glycolysis in exercising muscle and RBC
Glycerol released from adipose tissue breakdown of triglycerides
Amino acids- mainly alanine

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19
Q

Why can’t you synthesise glucose from acetyl-CoA?

A

Acetyl-CoA enters TCA and loses 2C

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20
Q

What are the key enzymes in gluconeogenesis and the control sites?

A

PEPCK (phosphoenolpyruvate carboxykinase) and Fructose 1,6-bisphosphate (which are both regulated)
Glucose-6-Phosphatase (which is not regulated).

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21
Q

The two key enzymes of gluconeogensis are regulated by hormones in response to?

A

Starvation/fasting
Prolonged exercise
Stress

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22
Q

How are lipids stored in the body?

A

Triacylglycerol for storage= hydrophobic, anhydrous form in adipose
Highly efficient energy store

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23
Q

When are lipid stores utilised?

A

Prolonged exercise, stress, starvation, during pregnancy

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24
Q

What is the diameter of a typical adipocyte?

A

~0.1mm – cells expand as more fat added

Can increase in size about fourfold on weight gain before dividing and increasing total number of fat cells

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25
What is the typical weight of fat in an average adult?
~15kg
26
Describe dietary triacylglycerol metabolism
Lipids eaten in the diet are hydrolysed in the small intestine by pancreatic lipases =transported across the brush border into the lacteals (lymphatic vessels which transport digested fat, all other substances are transported in the blood). Lipids are transported in chylomicrons as TAGs and can be stored in adipose tissue if there is plenty of glucose
27
What enzyme is responsible for mobilising fat?
release of fatty acids and glycerol is under hormonal control triggered by glucagon (released when glucose levels are low) =activates the hormone-sensitive lipases to break down the triglyceride to provide an alternative fuel source.
28
What is the role of a chylomicron?
At the walls of capillaries, chylomicrons are partially metabolised by lipoprotein lipase, supplying lipid to cells that need it. Once the lipid content of the chylomicron falls below 20%, it becomes a chylomicron remnant, and travels to the liver to finish being broken down.
29
Where does lipogenesis take place and what is its substrate?
Occurs mainly in the liver Glucose to pyruvate in cytoplasm (glycolysis) Pyruvate enters mitochondria and forms acetyl-CoA and OAA which then condense to form citrate Citrate moves to cytoplasm and cleaved back to acetyl-CoA and OAA Acetyl-CoA Carboxylase produces malonyl CoA (a 3 Carbon [3C] molecule) from Acetyl CoA (2C). Fatty Acid Synthase Complex builds fatty acids using malonyl CoA as a monomer. requires ATP and NADPH to occur
30
What are the regulators of fatty acid synthesis?
Acetyl-CoA Carboxylase= key regulatory enzyme Insulin (covalent dephosphorylation), citrate (allosteric) increase activity Glucagon/adrenaline (covalent phosphorylation), AMP (allosteric) decrease activity
31
What happens in lipolysis?
TAG broken down by hormone sensitive lipase into glycerol and free FA in blood. Glycerol travels to liver and utilised as carbon source for gluconeogenesis Free FA travels complexed with albumin to muscle and other tissues
32
What are lipids?
a structurally diverse group of molecules which are hydrophobic and contain carbon, hydrogen and oxygen.
33
Name types of lipids
Fatty acid derivatives – fatty acids, triacylglycerol and phospholipids Hydroxy-methyl-glutamic acid derivatives – ketone bodies and cholesterol Vitamins – fat-soluble vitamins A, D, E and K
34
How are lipids transported in blood?
As lipids are hydrophobic, it is not feasible to transport them freely in the blood. ~2% free fatty acids are transported attached to albumin= limited capacity (~3mmol/L) ~98% are transported in lipoproteins consisting of phospholipid, cholesterol, cholesterol esters, proteins & TAG
35
What are phospholipids?
two non-polar fatty acid chains bound to glycerol with a phosphate group (it is very similar in structure to a TAG, but with a phosphate group replacing one of the fatty acids). They form bilayers, micelles, and liposomes.
36
Where do we get cholesterol from?
Diet but mostly synthesised in the liver
37
What is cholesterol needed for?
Essential component of membranes Precursor of steroid hormones: cortisol, aldosterone, testosterone, oestrogen Precursor of bile acids
38
How is cholesterol transported around body?
As cholesterol ester
39
What is a lipoprotein?
a sphere of phospholipids used to transport lipid in the bloodstream Consists of peripheral and integral apolipoproteins, phospholipid monolayer with small amount of cholesterol and cargo. There are five types of lipoprotein
40
What does lipoprotein cargo consist of?
TAG, cholesterol ester, fat soluble vitamins ADEK
41
What are the five distinct classes of lipoproteins and their functions?
Chylomicrons transport dietary TAG from intestine to tissues VLDL- very low-density lipoproteins = liver-synthesised TAG transported from liver to tissues, can evolve into IDL IDL- intermediate density lipoprotein= a VLDL particle that has been partially depleted of TAG. Precursor of LDL LDL-low density lipoproteins= IDL particle that has been mostly depleted of TAG. High proportion of cholesterol ester HDL-high density lipoproteins remove excess of cholesterol from tissues and returns it to liver for disposal as bile salts, or cells requiring additional cholesterol
42
Which lipoproteins are main carriers of fat and which are main carriers of cholesterol esters?
Main carriers of fat: chylomicron, VLDL | Main carriers of cholesterol esters: IDL, LDL, HDL
43
How are the lipoproteins classified?
Density obtained by flotation ultracentrifugation | Particle diameter inversely proportional to density
44
When are chylomicrons present in blood?
4-6h after a meal
45
How does density relate to size in lipoproteins?
More density the higher the % protein, the smaller their size
46
What are apolipoproteins?
the peripheral and integral proteins on lipoproteins
47
What are the two roles of apolipoproteins?
Structural: packaging water insoluble lipid Functional: co-factor for enzymes, ligand for cell surface receptors
48
Apolipoprotein B is important for which lipoproteins?
VLDL, IDL, LDL
49
ApoAI is important for which lipoprotein?
HDL
50
Describe chylomicron metabolism
Lipid moves from the small intestine in chylomircons with apoB-48 added, to the lymph via lacteals in the villi Chylomircons are emptied into the blood via the thoracic duct into the left subclavian vein acquiring apoC and apoE. apoC bind lipoprotein lipase (LPL) on adipocytes and muscle= releases FA to enter cells from chylomicron Once the lipid content of the chylomicron falls below 20%, it becomes a chylomicron remnant, and travels to the liver= LDL receptor on hepatocytes bind apoE and chylomicron remnant is taken up by receptor mediated endocytosis Lysosomes release remaining contents for use in metabolism
51
What does lipoprotein lipase do and where is it found?
Hydrolysis TAG in lipoproteins Requires Apo-CII as cofactors Found attached to surface of endothelial cells in capillaries
52
Describe VLDL metabolism
VLDL made in liver for purpose of transporting TAG to other tissues apoB100 added during formation and apoC and apoE added to HDL particles in blood VLDL binds to lipoprotein lipase (LPL) on endothelial cells in muscle and adipose= depleted of TAG In muscle, released FA taken up and used for energy production In adipose, FA used for resynthesis of TAG and stored as fat
53
Describe IDL & LDL metabolism
As the VLDL is metabolised by lipoprotein lipase, its TAG content is depleted, and the particle becomes a short-lived Intermediate Density Lipoprotein (IDL). IDL particles taken up by liver or rebind to LDL to further deplete TAG content =depletion to ~10%, IDL loses apoC and apoE-the predominant molecule is cholesterol ester, = a Low-Density Lipoprotein (LDL).
54
What is the primary function of LDL?
Provide cholesterol from liver to peripheral tissues Peripheral cells express LDL receptor and take up LDL via receptor mediated endocytosis Does not have apoC or apoE so not efficiently cleared by liver
55
What is the clinical relevance of LDL?
Half lie of LDL in blood is longer than VLDL and IDL = LDL more susceptible to oxidative damage Oxidised LDL take up by macrophages = foam cells that contribute to atherosclerotic plaque formation
56
Describe HDL synthesis
Nascent HDL synthesised by live and intestine (low TAG levels) HDL particles bud off from chylomicrons and VLDL as they are digested by LPL Free apoA-I can also acquire cholesterol and phospholipid from other lipoproteins and cell membranes to form nascent-lie HDL
57
Describe HDL maturation
Nascent HDL accumulate phospholipids and cholesterol from cells lining blood vessels Hollow core progressively fills, and particle takes on more globular shape Transfer of lipids to HDL does not require enzyme activity
58
Describe reverse cholesterol transport and its importance
HDL have ability to remove cholesterol from cholesterol-laden cells and return it to liver Important process for blood vessels as it reduces likelihood of foam cell and atherosclerotic plaque formation
59
What does ABCA1 protein do?
Facilitates the transfer of cholesterol to HDL | Cholesterol then converted to cholesterol ester by LCAT
60
What does cholesterol exchange transfer protein (CETP) do?
Aids HDL exchange cholesterol ester for TaG with VLDL
61
How is the scavenger receptor (SR-B1) utilised?
Cells requiring additional cholesterol can use SR-B1 to obtain cholesterol from HDL
62
What are hyperlipoproteinaemias?
group of diseases that present with high levels of one or more class of lipoprotein caused by overproduction or under-removal. There are six types and each one has a different defective component: enzymes, receptors, apoproteins.
63
Describe the types of hyperlipoproteinaemias.
I – chylomicrons present in the plasma even when fasting due to a defective lipoprotein lipase. IIa – a defective LDL receptor leading to high levels of LDL in the blood. This condition predisposes atherosclerosis due to oxidised LDL levels being high. IIb-associated with coronary artery disease. Defect unknown III – raised IDL and chylomicron remnants due to a defective ApoE (lipoprotein) on the surface preventing the lipoproteins to be metabolised. IV- associated with coronary artery disease. Defect unknown V- raised chylomicrons and VLDL in fasting plasma. associated with coronary artery disease. Cause unknown
64
What are the clinical signs of hypercholesterolaemia?
High level of cholesterol in blood Cholesterol depositions in various areas of body Xanthelasma- yellow patches on eyelids Tendon xanthoma- nodules on tendon Corneal arcus- obvious white circle around eye, common in older people but if present in young could be a sign of hypercholesterolaemia
65
How is raised serum LDL associated with atherosclerosis?
the longer half-life of LDL, giving LDL a higher chance to become oxidised and phagocytosed by macrophages to form foam cells. =lead to the narrowing of arteries, which can cause angina, and the formation of atherosclerosis can increase the chances of thrombus formation, leading to an MI or a stroke.
66
What is the first approach treatment of hyperlipoproteinaemias?
Change diet: reduce cholesterol and saturated lipids in diet. Increase fibre intake. Change lifestyle: increase exercise, stop smoking
67
What drugs are used in treatment of hyperlipoproteinaemias?
statins =inhibiting an enzyme used in cholesterol production called HMG CoA reductase, to reduce the amount of cholesterol synthesised Bile salt sequestrants= keeps bile salts in the intestine leading the liver to increase production and thus use up excess cholesterol in the blood to make more

MEH (3 decks)

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