Biochemistry (Gareth's Section) Flashcards
(94 cards)
1
Q
- Describe the ‘Glycemic Index’ and how it’s obtained.
A
Describes the postprandial glucose response: The area under the ‘test’ food glucose curve divided by the area under a ‘reference’ food glucose curve (normally 50 g glc).
Expressed as a %, it’s essentially the RATIO of test:reference.
2
Q
- Glycogen structure: If all the glycogen molecules in a liver cell had up to four tiers of branches, what would be the most effective way of increasing glycogen stores in that cell?
a) Adding more branches
b) Increasing the length of individual branches
c) Having more glycogenin
d) Making more glycogen synthase enzymes
e) none of the above
A
c) Having more glycogenin
3
Q
- Bile Salts: What statement about bile salts is INCORRECT?
A made in the liver, stored in the gall bladder
B represent the end point of cholesterol metabolism
C most pass into lower bowel after secretion into gut
D have both charged & hydrophobic portions
E none of the above
A
C most pass into lower bowel after secretion into gut
4
Q
- Lipase inhibitors: Lipase inhibitors are potentially useful for weight loss. Which statement about them is INCORRECT?
A they inhibit the release of fatty acids from adipose tissue
B they discourage people from eating fat
C they reduce the digestion of dietary fat
D they reduce energy intake
E all of the above
A
A they inhibit the release of fatty acids from adipose tissue
5
Q
- Lipoprotein Lipase (LPL): What statement about chylomicrons is INCORRECT?
A they are made in the intestinal epithelial cells
B they enter the bloodstream at lymph nodes
C they encounter peripheral tissues before the liver
D they have the highest density of all the lipoproteins
E all of the above
A
D they have the highest density of all the lipoproteins
6
Q
- Which is NOT a non-essential amino acid?
a) asparatine
b) arginine
c) leucine
d) glutamine
e) serine
f) they are all non-essential
A
c) leucine - it is essential
Non-essentials (11): alanine, arginine, asparagine, aspartate, cysteine, glutamate, glutamine, glycine, proline, serine, and tyrosine.
(AlArAsAsCyGlGlGlPrSeTy)
Essentials (9): Histidine, Isoleucine, Leucine, Lysine, Methionine, Phenylalanine, Threonine, Tryptophan, Valine.
7
Q
- Fat substitutes: What would be an effect of consuming chips that had been fried in OLESTRA?
A fat soluble vitamins would be stripped from the body B impossible: the chips would not fry properly
C no OLESTRA would be absorbed from the gut
D blood chylomicrons would contain OLESTRA
E none of the above
A
C no OLESTRA would be absorbed from the gut
8
Q
- Glycemic Index: First the subject consumes 50 g of pure G & their BG response is recorded. A day later, the same measurements are made after they consume 50 g apple. How do you then calculate the GI of apple?
a) express area apple as % area glucose
b) express peak glucose as % peak apple
c) express peak apple as % peak glucose
d) measurement not done properly
e) none of the above
A
d) measurement not done properly
Test food needs to be given in an amount that will give 50 g digestible carbohydrate (not just 50 g weight of the test food…)
9
Q
- Lipogenesis, like other anabolic pathways, needs ATP. However, it also needs something else. What is that thing and where does it come from?
A acetyl CoA from the Krebs Cycle B NADPH from the Pentose Phosphate Pathway C reductant from glycolysis D NADH from the Krebs Cycle E none of the above
A
B NADPH from the Pentose Phosphate Pathway
10
Q
- Essential amino acids: Which statement is CORRECT?
A. Egg proteins contains all the essential amino acids except methionine
B. A high quality protein is one that contains 18 out of the 20 amino acids
C. A high quality protein contains less than <5% non-essential amino acids
D. A food that contained twice the amount of lysine as egg protein would be low quality
E. Certain types vegetable tend to be deficient in at least one essential amino acid
A
E. Certain types vegetable tend to be deficient in at least one essential amino acid
11
Q
- Glycemic Index: What statement is FALSE?
a) adding fructose to foods lowers their GI
b) soft drinks have a lower GI than rice
c) some foods have a GI of >100
d) low GI foods give you slow burning energy
e) none of the above
A
d) low GI foods give you slow burning energy
12
Q
- Lipid Transport: What best represents the disposal of cholesterol?
a) reverse cholesterol transport
b) chylomicron remnants
c) VLDL remnants (IDL)
d) a & c
e) none of the above
A
a) reverse cholesterol transport
13
Q
- Glycogen structure: What is glycogenin?
a) A form of glucose
b) A protein
c) A phospholipid membrane anchor
d) A form of glycogen synthase
e) none of the above
A
b) A protein
14
Q
- Lipid transport: Where does CETP act?
a) reverse cholesterol transport
b) VLDL
c) VLDL remnants (IDL)
d) LDL
e) c & d
A
a) reverse cholesterol transport
Cholesterol Ester Transfer Protein (CETP) is a problem for the action of HDL (high-density lipoprotein), as it impedes its cholesterol-collecting action. It can intercept HDLs on their way back to the liver and remove CE, putting them back into things like VLDLs & chylomicrons.
15
Q
- Cholesterol Metabolism: Consuming certain ‘resins’ binds bile salts & stops their re-absorption from the gut. This affects blood cholesterol levels. What is a MISCONCEPTION?
A. The resins will reduce blood LDL B. The liver will make more bile salts C. Tissues will express more LDL receptors D. Fat will no longer be digested E. All of the above
A
D. Fat will no longer be digested
16
Q
- Glucose Uptake: Glucose doesn’t simply diffuse into cells. It needs transporters (GLUTs). Which is FALSE?
a) GLUT-1 are present on all cells
b) GLUT-1 catalyse a continual trickle of glucose uptake
c) Insulin increases number of GLUT-4 in cell membrane
d) Glucose CAN’T move back out into the blood
e) none of the above
A
d) Glucose CAN’T move back out into the blood
17
Q
- G disposal in liver: What is the key difference bw ‘push’ & ‘pull’ models of glycogen synthesis (GS)?
a) Insulin stimulates ATP levels to ‘push’ GS
b) Insulin creates more glycogenin to ‘pull’ GS
c) G stimulates glycogen synthases to ‘push’ GS
d) Insulin stimulates G uptake to ‘pull’ GS
e) none of the above
A
c) G stimulates glycogen synthases to ‘push’ GS
‘Push’ mechanism in the LIVER. Glycogenesis responds to BG w/o the need of insulin. (insulin however will stimulate glycogenesis further.)
‘Pull’ mechanism in MUSCLES. Insulin stimulates GS to convert G into glycogen.
18
Q
- First few hours of starvation: What process is MOST RESPONSIBLE for keeping blood glucose steady during the first five hours of starvation?
A. The secretion of insulin
B. The mobilisation of liver glycogen
C. The release of glucose from muscles
D. The inhibition of muscle glucose oxidation by fatty acids
E. A reduction in the rate of glucose oxidation by the brain
A
B. The mobilisation of liver glycogen
19
Q
- Esterification: The final step of fat synthesis is esterification. What does this mean?
A The reaction of fatty acids with glucose
B The release of the fatty acyl CoA from FAS
C The attachment of fatty acids to a glycerol backbone
D The formation of glycerol 3-phosphate from glucose
E none of the above
A
C The attachment of fatty acids to a glycerol backbone
20
Q
- Which of the following does NOT describe something about the way in which FAS converts malonyl CoA into fatty acyl CoA ?
A ATP is consumed
B NADPH is consumed
C during synthesis, the fatty acid is anchored to FAS
D FAS is a single protein with many enzyme activites
E none of the above
A
A ATP is consumed
Each round of 2C addition requires 2 molecules of NADPH, but NO ATP.
It also requires the release of the CO2 that went on during the production of malonyl-CoA
21
Q
- Glucogenic & Ketogenic amino acids: What statement is INCORRECT?
A. Carbon skeletons that are anaplerotic to the Krebs Cycle CAN ALL contribute to gluconeogensis
B. Ketogenic skeletons can NOT be made into glucose C. Every carbon skeleton is ultimately converted into pyruvate
D. Ketogenic skeletons are NOT anaplerotic to the Krebs Cycle
E. Ketogenic skeletons can be made into fatty acids
A
C. Every carbon skeleton is ultimately converted into pyruvate
22
Q
- Following consumption of 50 g of glucose, what blood glucose level would indicate that a person was GLUCOSE INTOLERANT?
a) >10 mM after 30 min
b) >8 mM after 120 min
c) <4 mM at time zero
d) 5 mM at time zero
e) none of the above
A
b) >8 mM after 120 min
23
Q
- When does the PPP make reductant?
A As G6P is made into 5-carbon sugar phosphates
B As 5-carbon sugar phosphates are rearranged
C As PPP products enters glycolysis
D Only when glycogen synthase is inhibited
E none of the above
A
A As G6P is made into 5-carbon sugar phosphates
24
Q
- Glycolysis: How is muscle phosphofructokinase (PFK) stimulated after a meal?
a) By an increase in insulin
b) By a rise in cell glucose concentration
c) By an increase in the demand for ATP
d) in response to higher glycogen levels
e) none of the above
A
c) By an increase in the demand for ATP
PFK is regulated allosterically; stimulated by low energy charge; the balance of ATP, ADP & AMP. An increase in cellular ADP/AMP and a decrease in ATP creates an ‘energy demand’ for ATP.
Thus, insulin ‘indirectly’ stimulates PFK & glucose oxidation, but its direct effect first creates the low energy charge.
25
29. What is lipogenesis?
```
A formation of fat cells
B storage of dietary lipid
C formation of fatty acids from acetyl CoA
D disposal of glucose by adipose tissue
E all of the above
```
C formation of fatty acids from acetyl CoA
26
63. What best represents the distribution of endogenously made cholesterol to body tissues?
a) Chylomicrons
b) VLDL
c) LDL
d) b & c
e) none of the above
d) b & c (VLDL & LDL)
27
20. Glycogenesis: What statement about glycogen synthase (GS) is FALSE?
a) GS is switched off when it is phosphorylated
b) GS uses UDP-glucose as a substrate
c) GS adds glucoses to an existing glycogen chain
d) GS uses ATP to drive glycogen synthesis
e) all of the above
d) GS uses ATP to drive glycogen synthesis
I think: Using UTP releases PP (pyrophosphate?); PP hydrolysis pulls the reaction to completion - the driving factor.
GS doesn't use ATP to drive glycogen synthesis, but it does contribute in making UDP back into UTP:
UDP + ATP -> UTP + ADP
(??? unless PP uses ATP rather than GS?)
28
91. Early starvation: Imagine the situation 24 hours into starvation. Which statement is TRUE?
A. At this stage, the brain is using about 5 g glucose per hour
B. The glucagon levels will go back down to zero over the next few hours
C. The Cori-cycle represents de novo synthesis of glucose
D. The contribution of protein to the maintenance of blood glucose is negligible at this stage
E. The contribution of glycerol to the maintenance of blood glucose is negligible at this stage
A. At this stage, the brain is using about 5 g glucose per hour
*Proteins have a negligible contribution of AMINO ACIDS, but they do contribute to the conversion of pyruvate to lactate for the Cori-cycle (I think).
29
90. PDH in starvation: Which feature of pyruvate dehydrogenase (PDH) is FALSE?
A. PDH is stimulated by dephosphorylation
B. PDH is activated by PDH phosphatase
C. PDH is inhibited when fatty acids are being oxidised
D. PDH is switched off by cAMP-dependent protein kinases
E. PDH kinase is activated by acetyl CoA
D. PDH is switched off by cAMP-dependent protein kinases
30
57. Lipoproteins: Two hours after a fatty meal, blood plasma turns milky. Why?
A the presence of chyme in the plasma
B more free fatty acids in the plasma
C lots of bile salts are co-absorbed in fat uptake
D increased levels of very large lipoproteins
E don’t know
D increased levels of very large lipoproteins
i.e. chylomicrons
31
68. What is the most important role of cholesterol ?
A. Making female & male sex hormones
B. Burnt for energy
C. Making bile salts to aid fat digestion
D. Ensuring structural integrity of membranes
E. All of the above
D. Ensuring structural integrity of membranes
32
3. Which does NOT describe the problem of postprandial hyperglycemia?
a) protein glycosylation
b) lipid glycosylation
c) root cause may be impaired ability of tissues to respond to insulin
d) glucose intolerance is outlined by high blood glucose levels after each meal and persisting for several hours
e) euglycemic levels are not maintained
b) lipid glycosylation
(I don't think this occurs but only 90% sure)
Insulin resistance and hyperglycemia underpin Type II diabetes.
Euglycemic is what we call the maintained 5 mM blood glucose concentration
33
72. Amino acid digestion & tissue uptake/release: Which statement is TRUE?
A. After digestion in the gut, amino acids directly enter the lymphatic system
B. The enzymes involved in amino acid degradation are classic rate limiting steps (slow, irreversible, highly controlled)
C. Excess amino acids are stored in special membrane vesicles in the liver
D. In the liver, the first step of amino acid processing is to release the amine group as ammonia
E. The amino acid composition of the blood entering the liver is very different to the amino acid composition of the blood leaving the liver
E. The amino acid composition of the blood entering the liver is very different to the amino acid composition of the blood leaving the liver
34
21. Glycogenesis: How does insulin stimulate the rate of glycogen synthase (GS)?
a) It activates the enzymes that make UDP-glucose
b) It increases the rate of glycolysis
c) It stimulates protein phosphatases
d) It drives glucose uptake which then stimulates GS
e) all of the above
f) none of the above
c) It stimulates protein phosphatases
GS is regulated by reversible phosphorylation. As it is active when dephosphorylated (and inactive when phosphorylated), Insulin stimulates dephosphorylation catalysed by phosphatases, specifically protein phosphatase I, PPI.
35
93. Catabolic meltdown: Very high rates of lipolysis and proteolysis are associated with metabolic inefficiency. What is NOT a reason for this?
A. Ketone bodies can decarboxylate and be lost from the breath, sweat or via the urine
B. Energy is used in converting amine groups into urea for excretion
C. Energy is used in converting amino acid carbon-backbones into glucose
D. Ketone bodies are much less efficient than glucose as a fuel
E. Energy is used in converting glycerol into glucose
D. Ketone bodies are much less efficient than glucose as a fuel
(not a strong option but the best answer, as A,B,C,E are true)
36
1. Which of the following is CORRECT?
a) We get the majority of our dietary carbohydrate from amylose
b) Amylose & amylopectin are starch derivatives that are branched and easy to digest
c) Amylopectin is a linear polymer of glucose, that forms helices and can be difficult to digest, causing flatulence
d) none of the above
d) none of the above
We get the majority of our dietary carbohydrate from starch in general, this includes both amylose AND amylopectin (not just amylose). They are both polymer chains of glucose.
Amylose: linear, forms helices, difficult to digest, flatulence.
Amylopectin: branched, easy to digest.
They are both completely different types of molecules in shape but still consist of glucose monomers end to end.
37
6. How is glycogenesis similar in liver & muscle?
- Energy is required (ATP)
- Branch points
- There is a limit to the size the glycogen molecule can get to bc the branches start to bump into each other
38
18. Glucose Uptake: In muscle, the enzyme that traps glucose, hexokinase, is inhibited by a build up of glucose 6-phosphate. What is the consequence of this?
a) If G6P isn't used, GLUTs stop working
b) if G6P is used quickly, GLUT's go faster
c) Glucose uptake is influenced by glucose disposal
d) High rates of glucose uptake drive more glucose use
e) none of the above
c) Glucose uptake is influenced by glucose disposal.
HK is easily saturated with G; Km ~0.1 mM for G. (Recall, Km is a constant for the 'substrate concentration at half the maximum velocity of the enzyme').
39
9. Which is amylose (and not amylopectin)?
a) polymer has branch points
b) not just glucose
c) rapidly digested
d) causes flatulence
e) all of the above
d) causes flatulence
40
47. Lipogenesis Regulation: Insulin directly stimulates many of the steps involved in the formation of fat from glucose. What is NOT one of those steps?
A Glucose uptake from the bloodstream
B Formation of acetyl CoA in the mitocondria
C Formation of malonyl CoA
D Activity of the Pentose Phosphate Pathway
E All of the above are influenced by Insulin
D Activity of the Pentose Phosphate Pathway
41
89. Glucose fatty acid cycle: How do fatty acids help prevent the oxidation of glucose in insulin-sensitive cells?
A. High levels of fatty acids stop the secretion of insulin from pancreatic beta cells
B. Fatty acids compete with glucose for GLUT-1 transporters
C. Fatty acids compete with glucose for GLUT-4 transporters
D. Fatty acids cause the endocytosis of GLUT-4 transporters so that there are less of them on the plasma membrane
E. The oxidation of fatty acids inhibits the pyruvate dehydrogenase complex
E. The oxidation of fatty acids inhibits the pyruvate dehydrogenase complex
Whenever FAs are oxidised, there are high levels of acetyl-CoA present. This positively influences PDH kinase to phosphorylate PDH, inactivating the enzyme. This inhibits PDH from oxidising glucose; pyruvate to acetyl-CoA, which is a 'point of no return' (irreversible reaction - it is a decarboxylation step, and acetate groups cannot be converted back into carbohydrate).
42
40. Fatty Acyl Synthase (FAS): What is the main purpose of FAS?
A it adds molecules of activated acetyl CoA together
B it makes malonyl CoA
C it oxidises acetyl CoA
D it prevents carbon dioxide from being fixed
E none of the above
A it adds molecules of activated acetyl CoA together
43
77. Essential Amino Acids: What is the consequence of a diet lacking in lysine but with plenty of all the other essential amino acids?
A. All the proteins are made normally, with isoleucine just substituting for leucine
B. All the proteins are made normally, with any essential amino acid randomly substituting for leucine
C. Other branched chain amino acids are converted into leucine
D. Most proteins cannot be made
E. Protein degradation stops
D. Most proteins cannot be made
44
60. Lipid transport: The flow of dietary cholesterol to body tissues is mostly by:
a) LDL
b) VLDL remnants
c) Reverse cholesterol transport
d) Chylomicron remnants
a) LDL.
VLDL is assembled in the liver from fat & cholesterol esters, and exported to the blood. LPL in peripheral tissues works on VLDL in the same way as chylomicrons, depleting its fat and leaving a remaining particle relatively cholesterol-rich: LDL.
Tissues take up LDL through LDL receptors, an endocytotic process like chylomicron remnants. This is how cholesterol is delivered to the tissues.
45
11. Euglycemia: What happens when blood glucose is ~4-5 mM?
a) no damaging glycosylation of proteins
b) brain cannot take up glucose
c) tissues become insulin resistant
d) none of the above
d) none of the above
NB re (a): glycosylation of proteins always occurs at a low background level
46
81. Liver amine processing: Under what circumstances does the liver make the LEAST amount of urea?
A. After two days of starvation
B. After three weeks of starvation
C. On a relatively low protein diet but in dietary nitrogen and energy balance
D. In positive nitrogen balance and a few hours after consumption of a high protein diet
E. After four days of eating a no protein diet
C. On a relatively low protein diet but in dietary nitrogen and energy balance
47
19. Glucose Uptake: In muscle cells, what is NOT a possible fate of G6P?
a) Conversion to glycogen
b) Entry into glycolysis
c) Conversion to glucose
d) Accumulation in the cell
e) none of the above
c) Conversion to glucose
48
75. Essential amino acids: Which statement is INCORRECT?
A. Some amino acids are essential during childhood but not in twenty-year olds
B. Essential amino acids can be made in the liver but no other tissues
C. Alanine, glutamate and aspartate NEVER have to be in the diet
D. ALL the branched chain amino acids are essential
E. Vegetarians can get all the essential amino acids they need from the diet
B. Essential amino acids can be made in the liver but no other tissues.
Essential amino acids CANNOT be synthesised by us!!
49
94. Late starvation: Imagine the situation 3 days into starvation. Which statement is FALSE?
A. The use of ketone bodies has reduced the brain requirement for glucose to about 30 g per day
B. Ketone bodies can be used for gluconeogenesis
C. Liver glycogen will be making a tiny (<5%) contribution to blood glucose homeostasis at this time
D. The beta-cells of the pancreas will be secreting very little insulin
E. Muscle can use fatty acids at this time, not just ketone bodies
B. Ketone bodies can be used for gluconeogenesis
50
24. Glucose disposal in liver: What best summarises the differences bw the G handling systems of liver & the other tissues? In the liver:
a) Insulin very strongly stimulates G uptake
b) Insulin stimulates the G trapping reaction
c) G6P gets high enough to stimulates GS
d) PFK can be stimulated by insulin
e) none of the above
c) G6P gets high enough to stimulates GS
51
79. Flow of amino acids from muscle: What statement regarding muscle amino acid handling is CORRECT?
A. During starvation there is negligible protein synthesis in muscle
B. Muscle preferentially takes up branched chain amino acids from arterial blood
C. The veins draining from muscle are proportionally high in branched chain amino acids
D. All the alanine molecules released from muscle have come directly from proteolysis of muscle protein
E. After feeding there is negligible proteolysis in muscle
B. Muscle preferentially takes up branched chain amino acids from arterial blood
52
2. Why is glucose required to be kept in a strict range?
a) ~5 mM concentration keeps the brain functional
b) a prolonged period of blood glucose > 8 mM can do damage to the tissues
c) if you can't dispose of glucose within a few hours, you're deemed to be glucose intolerant which means you're perpetually in hyperglycemia = protein glycosylation
d) all of the above
e) a & b
d) all of the above (a, b & c)
53
38. Acetyl CoA Carboxylase (ACC): What is the primary purpose of ACC?
```
A it burns acetyl CoA to make ATP
B it makes reductant
C it activates acetyl CoA
D it fixes atmospheric carbon dioxide
E none of the above
```
D it fixes atmospheric carbon dioxide
ACC activates a-CoA & 'primes' it for LG, it does this however by FIXING C02 (in the form of bicarbonate).
54
69. Which statement regarding the pathways and control of amino acid metabolism is NOT correct?
A. Each carbon skeleton requires a different pathway of degradation
B. Each carbon skeleton requires a different pathway for synthesis
C. The synthesis of each protein is differentially regulated
D. The degradation rate of each protein is different
E. Some carbon skeletons cannot be metabolised by the human body
E. Some carbon skeletons cannot be metabolised by the human body
(?????)
55
33. Which fact about PDH and lipogenesis is INCORRECT?
A PDH is stimulated when insulin binds to fat cells
B PDH provides the substrate for lipogenesis
C PDH is active when it is phosphorylated
D Insulin stimulates PDH phosphatase
E none of the above
C PDH is active when it is phosphorylated
56
84. Euglycemia: Our homeostatic systems are designed to keep blood glucose at about 5 mM & NOT at <4 mM or >6 mM. What is NOT a reason for this?
A. At 5 mM there is no damaging glycosylation of proteins
B. Brain glucose transporters don’t take up glucose fast enough at 2 mM
C. 10 mM is not necessary since the brain will only trap glucose at the same rate at which it uses it
D. The longer glucose and protein are in contact, the more that proteins are glycosylated
E. In the fed state, it is necessary to keep [glucose] over 3 mM as the brain cannot get enough energy from other blood fuels (ie, faXy acids or amino acids)
A. At 5 mM there is no damaging glycosylation of proteins
57
23. Glucose disposal in muscle: GS, PFK, insulin & GLUTs are all involved in the disposal of BG by muscle:
a) Insulin drives ATP production which stimulates GS
b) Increased GS lowers ATP which increases glycolysis
c) Insulin drives GLUT-4 which forces glycolysis
d) Increased PFK lowers glucose which activates GLUTs
e) none of the above are true
b) Increased GS lowers ATP which increases glycolysis
Increased GS increases rates of glycogenesis; anabolic process requiring ATP for activation of glucose.
Drop in cellular [ATP] and increase in [ADP/AMP] i.e. drop in 'energy charge' stimulates PFK & glucose oxidation, and hence glycolysis.
Essentially this is the coupling between glycogenesis & glycolysis; the signals to store fuels also cause fuels to be burnt.
58
56. Lipoproteins: What is the importance of the reaction of cholesterol to cholesterol ester?
A it is the only way of gettig rid of cholesterol from the body
B it is the first step in cholesterol oxidation
C it makes the cholesterol easier to transport in lipoproteins
D it only happens in foam cells
E all of the above
C it makes the cholesterol easier to transport in lipoproteins
59
13. Glycemic Index: When the glycemic index of food is determined (a GI test), what does the postprandial glucose response to that food tell us?
a) amount of glucose in the food
b) rate of digestion of the food
c) degree to which the food raises blood glucose levels
d) the insulin sensitivity of the subject
e) none of the above
c) degree to which the food raises blood glucose levels
60
5. How does glycogenesis differ in the liver vs. in the muscle?
Liver: 'push' mechanism; glycogenesis responds to bl. glc. W/O the need of ins. (although ins. WILL stim. glycogenesis further)
Muscle: [G6P] never high enough to stim. GS. 'Push' method doesn't occur; more of a 'pull' as ins. stim's GS to convert glc into glycogen; ins. is req'd!!
61
51. Bile Salts: What is NOT a consequence of a blockage in the bile duct?
A decreased ability to digest fat
B increase in the appearance of fat in the large intestine
C decrease in pancreatic lipase secretion
D flatulence
E none of the above (they are all consequences)
C decrease in pancreatic lipase secretion
62
44. The early steps of the PPP make 5-carbon sugar phosphates. What happens to these?
```
A Rearranged for entry into glycolysis
B Used to make the bases of nucleotides
C Used to get rid of nasty free radicals
D Used to esterify newly fatty acid made in lipogenesis
E all of the above
```
A Rearranged for entry into glycolysis
63
37. ATP-Citrate Lyase (ACL): What might happen if we inhibited ACL?
A acetyl CoA would still get into the cytoplasm
B citrate would still get into the cytoplasm
C the Krebs Cycle would be stimulated
D PDH would increase to compensate
E don’t know
B citrate would still get into the cytoplasm
ACL cleaves CYTOPLASMIC citrate into oxaloacetate and acetyl-CoA, facilitated by ATP -> ADP + phosphate (i.e. energy).
Inhibiting ACL would only prevent this action, as it doesn't act on the mitochondrial acetyl-CoA, which would still transport from the mitochondria into the cytoplasm via oxaloacetate as citrate.
64
25. Glucose disposal in liver: What is NOT a genuine difference bw glucokinase & hexokinase?
a) Hexokinase is inhibited by a build up of G6P
b) Hexokinase works at Vmax when G is 5 mM
c) Glucokinase can catalyse the hydrolysis of G6P
d) Glucokinase never works at Vmax in real life
e) none are differences bw the enzymes
c) Glucokinase can catalyse the hydrolysis of G6P
GK rapidly converts G -> G6P.
(I don't think it catalyses further hydrolysis of G6P)
65
39. Quite a few things stimulate ACC. What is NOT one of them?
A dephosphorylation of the enzyme
B molecules of the enzyme joining with each other
C a build up of the lipogenic product
D the binding of insulin to receptors on the cell surface
C a build up of the lipogenic product
66
12. Persistent Hyperglycemia: What happens when blood glucose is >8 mM for several days?
a) increase in extent of glycosylation of proteins
b) brain takes up glucose super fast
c) insulin stops being secreted
d) all of the above
e) none of the above
a) increase in extent of glycosylation of proteins
67
73. Amino acid processing: Which of the following reactions is NOT an example of an aminotransferase (a transaminase)?
A. Pyruvate acquires an amine group and becomes alanine
B. Alanine loses an amine group and becomes pyruvate
C. Oxaloacetate reacts with alanine to give pyruvate and aspartate
D. glutamine loses an amine group to become glutamate
E. An alpha-keto acid takes an amine group from an amino acid
D. glutamine loses an amine group to become glutamate
In the glutamine synthesis pathway, glutamine loses an amine group via glutaminase to give glutamate. This is not an aminotransferase reaction. The glutamate generated along with the amine release enter the urea cycle as carbamoyl phosphate.
68
32. The two tissues that can make glucose into fat are liver and adipose tissue. What is NOT a difference between fat synthesis these tissues?
A Liver can send the glucose to glycogen too
B Liver will export the fat it makes
C Adipose tissue does not have glycogen synthase
D Insulin does not stimulate lipogenesis in adipose tissue
D Insulin does not stimulate lipogenesis in adipose tissue
This occurs in both the liver and white adipose tissue (WAT).
69
50. Fat digestion - bile salts: How do bile salts assist in the uptake of fat into intestinal epithelial cells?
A bile salts join to the fat and carry them across
B bile salts form a shell around the fat and carry them across
C bile salts attack the glycerol part, releasing fatty acids D bile salts help increase accessibility for lipases
E all of the above
D bile salts help increase accessibility for lipases
70
49. Amphiphilic Molecules: How do molecules like this help fat metabolism?
A they can form lipid bilayers
B they can form monolayer shells around lipid
C formation of these uses up fat
D formation of these neutralises fat hydrophobicity
E none of the above
B they can form monolayer shells around lipid
71
46. Esterification: Esterification requires a source of glycerol 3-phosphate. How is this made?
```
A From glucose going down glycolysis
B From glycerol released by fat hydrolysis
C From excess malonyl CoA
D From excess acetyl CoA
E don’t know
```
A From glucose going down glycolysis
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74. Amino acid processing: Which statement is CORRECT?
A. Glutamate dehydrogenase transfers amine groups to a 2-oxoacid
B. Glutamate dehydrogenase releases ammonia
C. Glutamate dehydrogenase makes glutamine
D. Glutamine is made by combining two glutamate molecules
E. The formation of glutamine from glutamate is irreversible
B. Glutamate dehydrogenase releases ammonia
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55. Lipoproteins: What statement about a chylomicron lipoprotein is INCORRECT?
A the outer shell is a phospholipid bilayer
B the protein 'blob' on the outer surface is an apolipoprotein
C the inside is hydrophobic
D the type of lipoprotein is mainly defined by the protein 'blob'
E none of the above
A the outer shell is a phospholipid bilayer
The shell of a chylomicron lipoprotein is made of phospholipid MONOLAYER.
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48. Fat is hydrophobic. This makes digestion, absorption & transport challenging. What is NOT an adaption to this?
A formation of an emulsion in the gut
B transport around the blood in lipoproteins
C use of lipases which are hydrophobic on the outside
D storage in phospholipid encased vacuoles
E none of the above
C use of lipases which are hydrophobic on the outside
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59. Where do we find LPL?
A secreted by the pancreas into the gut
B secreted by the liver & circulating freely in the bloodstream
C expressed on the outside of cells that want fat
D embedded into lipoproteins that deliver fat
E don’t know
C expressed on the outside of cells that want fat
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61. Lipid transport: What best represents the flow of dietary FAT to body tissues?
a) Chylomicrons
b) VLDL
c) Chylomicron remnants
d) all of the above
e) none of the above
a) Chylomicrons
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85. Glucose Stores: Which statement about whole body glucose stores is FALSE?
A. Our bloodstream contains a teaspoon of glucose (5 g)
B. 200-400 g of our body is glucose in the form of glycogen (liver and muscle combined)
C. Our store of glucose as fatty acids is negligible
D. In total, the glycerol in our fat stores can give us about 30 g glucose
E. We can make about 1 g glucose from every 3 g of protein
D. In total, the glycerol in our fat stores can give us about 30 g glucose
It can give us 30 g glucose PER DAY, rather than in total (a value which depends on a person's total body fat reserves).
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36. Acetyl CoA can’t cross membranes. It is made in the mitochondria & used in lipogenesis in the cytoplasm. How does it get into the cytoplasm?
A it rides on the back of oxaloaceate
B it just diffuses into the cytoplasm
C it becomes acetate, then crosses the membrane
D it becomes citrate and then enters the Krebs Cycle
E none of the above
A it rides on the back of oxaloaceate
Although D is almost correct...
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```
70. Nitrogen Flux: Approximately what percentage of our WHOLE body protein is destroyed and re-created every day?
A. <0.5%
B. 0.5-1 %
C. 2-4%
D. 5-10%
E. >10%
```
C. 2-4%
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7. Which of the following regarding the trapping enzymes of glucose is incorrect?
a) Glucokinase (GK) only works for glucose and is active in the liver beta cells
b) Hexokinase (HK) works on any 6C sugar and is active in muscle & adipose
c) If G6P isn't used immediately, its build up inhibits GK
d) All of the above are correct
c) If G6P isn't used immediately, its build up inhibits HEXOKINASE in the muscle/adipose tissues.
GLUCOKINASE in the liver is NOT inhibited by G6P, even with increasing build-up.
Further:
GK; high Km for glc (~10mM), responsive to changes in [bl. glc].
HK; Km for glc ~0.1mM, easily saturated w glucose.
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80. Flow of amino acids from muscle: What statement BEST describes the relationship between liver & muscle with respect to amino acid metabolism?
A. Most amino groups are transported from muscle to liver on alanine and glutamine
B. During starvation, liver sends muscle amino groups to make new amino acids
C. After feeding, muscle takes up alanine and glutamine produced by the liver
D. The mixture of amino acids arriving at the liver from the muscle strongly reflects the amino acid composition of the muscle protein
E. Muscle does NOT oxidise amino acids that came from liver
A. Most amino groups are transported from muscle to liver on alanine and glutamine
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78. Flow of amino acids from gut: After digestion of protein in the gut, what statement about the composition & fate of the amino acids is CORRECT?
A. Most go into the lymphatic system and enter the bloodstream at the lymph nodes
B. The branched chain amino acids go into the lymphatic system, all the others go to the liver
C. The liver extracts the branched chain amino acids and lets the others into the general circulation
D. The liver stores any excess amino acids not immediately needed by the body in vesicles of the Golgi apparatus
E. The amino composition of the amino acids in the hepatic portal vein is very similar to the amino acid composition of the protein in the last meal
E. The amino composition of the amino acids in the hepatic portal vein is very similar to the amino acid composition of the protein in the last meal
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83. PKU: What statement is INCORRECT?
A. Subjects with PKU must avoid phenylalanine
B. Subjects with PKU should avoid aspartame
C. A build up of phenylalanine causes neuronal defects
D. PKU is the most common genetic disorder affecting amino acid metabolism
E. PKU is screened for at birth in Australia
A. Subjects with PKU must avoid phenylalanine
They must avoid ALANINE as they cannot metabolise it. Build up leads to mental retardation. It is still an essential amino acid however and is thus required, but it in excess it is toxic.
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66. Cholesterol Metabolism: What is the most likely to reduce blood cholesterol levels?
A. Reducing consumption of meat
B. Taking statins
C. Reducing consumption of saturated vegetable fat
D. Reducing consumption of eggs and dairy foods
B. Taking statins - this is an inhibitor of the key enzyme HMG-CoA Reductase. Our cells are very able in making their own cholesterol, converting acetyl-CoA in a multi-step process, using HMG-CoA Reductase, to cholesterol. Taking statins would likely have a greater impact in reducing blood cholesterol levels, as dietary intake is very small in comparison to our body stores; reducing consumption by lowering meat/dairy intake may prove minimal.
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34. Acetyl CoA can’t cross membranes. It is normally burnt in the Krebs Cycle. But it is also the substrate for lipogenesis. So what statement is TRUE?
A during lipogenesis, the Krebs Cycle must be inhibited
B we need to get acetyl CoA into the cytoplasm
C lipogenesis occurs in the mitocondria
D lipogenesis uses acetyl CoA made by cytoplasmic PDH
E don’t know
B we need to get acetyl CoA into the cytoplasm
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87. Muscle glycogen in starvation: The muscle is said to be ‘selfish’ with its glycogen. Which statement related to this idea is TRUE?
A. Muscle only responds to glucagon in later starvation B. Muscle does not have the phosphorylase enzymes with which to break down glycogen
C. Muscle has a very low glucose 6-phosphatase activity
D. It is not possible for glucose in the cytoplasm of muscle cells to pass through GLUT-1 or GLUT-4 transporters into the bloodstream
E. Muscle hexokinase is not inhibited by a build-up of G6P, so glucose trapping is always really fast.
C. Muscle has a very low glucose 6-phosphatase activity
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88. Adipose Tissue Lipolysis: Which statement regarding lipolysis is FALSE?
A. Lipolysis is activated by hormones that cause a rise in cAMP in fat cells
B. Lipolysis is the hydrolysis of stored triacylglycerol in adipose tissue
C. For every three molecules of fatty acids released during lipolysis, one molecule of glycerol is also released
D. Lipolysis occurs when Hormone Sensitive Lipase (HSL) is phosphorylated
E. Fatty acids are bound to albumin before being released from the adipocyte into the bloodstream
E. Fatty acids are bound to albumin before being released from the adipocyte into the bloodstream
(I think the bind to albumin IN the blood)
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71. Nitrogen Flux: We are in daily nitrogen balance when:
A. The daily intake of amino acids match what is lost as urea each day
B. The amount of protein that is degraded each day is less than 1% of our total body protein pool
C. The amount of protein that is made each day is less than 1% of our total body protein pool
D. Every day, we lose an equal amount of protein in our faeces as we do in our urine
E. Every day, the amount of nitrogen lost in the faeces matches the amount of protein ingested
A. The daily intake of amino acids match what is lost as urea each day
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62. What best represents the distribution of ENDOGENOUSLY made fat to body tissues?
a) Chylomicrons
b) VLDL
c) LDL
d) all of the above
e) none of the above
b) VLDL
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31. The main substrate for fatty acid synthesis is acetyl CoA. What statement about the formation and use of this acetyl CoA is CORRECT?
A It is made by glycolysis in the cytoplasm
B It needs to be transported out of the mitochondria
C It is made by the Krebs Cycle
D It is made when PDH is switched off
E none of the above
B It needs to be transported out of the mitocondria
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92. What statement regarding ketone bodies is TRUE?
A. All tissues can make ketone bodies
B. Cells do not need to express the enzymes that catalyse beta-oxidation in order to oxidise ketone bodies
C. Only the brain can use ketone bodies
D. During oxidation, ketone bodies are decarboxylated to acetone then acetyl CoA
E. Ketone bodies require carnitine to cross the plasma membrane
B. Cells do not need to express the enzymes that catalyse beta-oxidation in order to oxidise ketone bodies
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42. Pentose Phosphate Pathway (PPP): What is the relationship between the PPP & lipogenesis?
A PPP provides pyruvate for lipogenesis
B PPP acts as a buffer for glucose, regulating lipogenesis
C PPP provides reductant for lipogenesis
D Excess glucose goes into the PPP, signaling lipogenesis
E don’t know
C PPP provides reductant for lipogenesis
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15. Glycemic Index: Only one of the following foods can have a GI. Which?
a) vodka
b) water melon
c) steak
d) lentils
e) none of the above
d) lentils
Fructose doesn't contribute to GI, as GI measures BG response. Safe to assume water melon has no glucose (only fructose).
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8. In what form do we get most of our carbohydrate?
a) sucrose
b) starch
c) fructose
d) monomeric glucose
e) none of the above
b) starch
