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GI > GI - metabolism > Flashcards

GI - metabolism Flashcards

1
Q

There are three control steps to glycolysis. What are the enzymes involved in these?

A

hexokinase (converts glucose to glucose-6-phosphate); phosphofructokinase (converts fructose-6-phosphate to fructose-1,6-biphosphate); and pyruvate kinase (the last step of glycolysis, which produces pyruvate).

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2
Q

What would inhibit glycolysis?

A

The products of glycolysis itself - i.e. ATP, or glucose-6-phosphate. Also glucagon - as if you have low blood sugar, you don’t want to break any more down.

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3
Q

What would stimulate glycolysis?

A

AMP. This signals that cell energy is low.

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4
Q

Why is the first step of glycolysis a control step?

A

It’s not reversible, and it ‘commits’ the glucose to the cell, as once it is made into glucose-6-phosphate it can’t leave the cell.

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5
Q

What are the products of glycolysis alone?

A

2 x NADH and 2 x ATP (ATP net gain)

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6
Q

If you take into account the energy which the NADHs can yield later on, what’s the energy produced by glycolysis

A

5-7 ATP per glucose

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7
Q

What is the energy yield of one molecule of glucose (aerobic respiration)

A

30-32 ATP

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8
Q

What are the products of aerobic respiration?

A

Lactate (which can leave the cell - pyruvate can’t); and NAD+. NAD won’t be getting made by oxidative phosphorylation as there’s no O2 to accept the electrons. So aerobic respiration provides a workaround, it gets shut of all the pyruvate, and keeps things going with a supply of NAD+.

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9
Q

What is the key control enzyme in glycogen synthesis?

A

glycogen synthase

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10
Q

What two things are needed as well, for glycogenesis?

A

UDP (a carrier for glucose); and TYROSINE.

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11
Q

What is the enzyme needed for glycogenolysis?

A

Glycogen phosphorylase.

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12
Q

What is the difference between glycogen usage in muscles and glycogen usage in the liver?

A

Glycogen broken down in the muscle can ONLY be used in that cell. There is no glucose-6-phosphatase, so it can’t be converted all the way back to glucose. The liver can remake glucose from glycogen though, key for maintaining BGL.

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13
Q

What is the MAIN location in the body of fatty acid synthesis?

A

The liver.

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14
Q

What are two other body sites of fatty acid synthesis?

A

Breast tissue and adipose tissue.

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15
Q

What is the cell location of fatty acid synthesis?

A

The cell cytosol.

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16
Q

What is the start point for fatty acid synthesis?

A

Acetyl CoA

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17
Q

What enzyme is at the control point of fatty acid synthesis?

A

Acetyl CoA carboxylase

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18
Q

What can the liver do with fatty acids?

A

It can package them into VLDLs, which can move in the blood to be stored or used elsewhere in the body.

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19
Q

Can Acetyl CoA leave mitochondria?

A

No - it can’t cross the membrane. It can leave as citrate, though.

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20
Q

What does it mean if cellular levels of AMP are high?

A

Cell energy is LOW.

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21
Q

What does a high level of AMP cause to happen?

A

Synthesis pathways are stopped and energy yielding pathways are stimulated.

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22
Q

How does glucagon slow down glycogenesis?

A

It stimulates phosphorylation of enzymes. When glycogen synthase is phosphorylated, it is inactivated, so glycogenesis stops.

23
Q

How does glucagon stimulate glycogenolysis?

A

It stimulates phosphorylation of enzymes. When glycogen phosphorylase is phosphorylated, it is activated, so glycogenolysis is activated.

24
Q

Why are ketone bodies formed in metabolism?

A

If fat is being used for fuel, this forms Acetyl CoA. When Acetyl CoA overloads the Krebs cycle, ketone bodies are formed.

25
Q

What organ especially can make use of ketone bodies for fuel?

A

The brain

26
Q

What 4 things need cholesterol?

A

Bile, hormones, vitamin D, cell membranes

27
Q

What gene transcription is inhibited by cholesterol? (Which in turn inhibits cholesterol synthesis).

A

SREBP

28
Q

Why do we end up with too much circulating cholesterol?

A

Because we can only excrete less than 5% in faeces

29
Q

List three diseases which are linked to excess lipids

A

CHD, alzheimers, steatohepatitis

30
Q

Where does cholesterol synthesis take place?

A

in the smooth ER, in cytosol, of LIVER

31
Q

Which important enzyme is involved in cholesterol synthesis, and is inhibited by statins?

A

HMB CoA reductase

32
Q

What’s another product of the cholesterol synthesis pathway?

A

Isoprenoids

33
Q

What is the intermediate substance in the isoprenoid / cholesterol synthesis pathway?

A

Mevalonate

34
Q

What’s the problem with too many ketone bodies?

A

They are weak acids, so can lead to ketoacidosis.

35
Q

what is the ‘reverse’ of glycolysis, and what are the control steps? (3)

A

the first one involving pyruvate (pyruvate kinase), the one which makes fructose-6-phosphate from fructose-1,6-bisphosphate (phosphofructokinase) and the last one which turns glucose-6-phosphate into actual glucose (hexokinase)

36
Q

what other substance is moved from the liver to the muscle and keeps transamination going?

A

the glucose-alanine cycle.

37
Q

what activates the urea cycle?

A

high levels of amino acids

38
Q

why does alcohol make you hungry?

A

when it gets metabolised (to acetaldehyde then acetate), lots of NAD is used up. this pushes the reactions lactate –> pyruvate towards lactate (yields NAD) and glyceraldehyde-3-P –> glycerol towards glycerol (also yields NAD). So less glucose can be made and BGL drops.

39
Q

What are the control points in the Krebs cycle?

A

There are three. Citrate synthase (makes 6C citrate) and the two dehydrogenase steps where a carbon atom is lost.

40
Q

Why does diabetic ketoacidosis happen?

A

The body doesn’t ‘see’ the glucose in the bloodstream. Gluconeogenesis keeps on happening, which results in an overflow of Acetyl CoA (from fatty acid breakdown) and the oxaloacetate getting used up (as the Krebs cycle has been busy). Ketone bodies are made from the Acetyl CoA, which results in ketoacidosis.

41
Q

What is an ATP uncoupler?

A

A compound like 2-4-DNP will dilute the proton gradient of oxidative phosphorylation and less ATP can be made. Heat is generated instead. Newborns use thermogenin to do this when they get cold.

42
Q

what is the embryological origin of hepatocytes?

A

endoderm

43
Q

what is the embryological origin of Kuppfer and haematopoetic cells?

A

mesoderm (from the future diaphragm)

44
Q

what makes most of foetal blood?

A

the liver. after birth this function is shifted to the bone marrow.

45
Q

what is meconium. describe it.

A

the first bowel movement of the newborn. it should be dark green as the liver started producing bile in week 12. if it isn’t green this might indicate annular pancreas (incomplete rotation of the buds and malformation) which has compressed the duodenum.

46
Q

why do many newborns have neonatal jaundice and what is the therapy for this?

A

they relied on the mother to remove bilirubin, and they don’t have enough GLUCURONOSYLTRANSFERASE to conjugate their own bilirubin. Blue light helps it go by oxidising the bilirubin to a water soluble form.

47
Q

what is kernicterus?

A

excess unconjugated bilirubin crosses the BBB and causes brain damage. this can happen if neonatal jaundice isn’t treated (with phototherapy)

48
Q

what is another, rarer cause of neonatal jaundice?

A

biliary atresia. the liver successfully conjugates bilirubin but there’s no way for it to get out (as the bile duct is obliterated). it won’t cause kernicterus.

49
Q

what is the embryonic derivation of the pancreas

A

it’s from the endoderm - two outpocketings of the GI tube which eventually fuse.

50
Q

what is the uncinate process of the pancreas formed from?

A

the ventral bud

51
Q

what is the head, body and tail of the pancreas formed from?

A

the dorsal bud

52
Q

what can cause obstruction, ulcer or haemorrhage, usually in the stomach and duodenum?

A

ectopic pancreatic tissue. can occur in lungs too.

53
Q

what is the embryonic origin of the SPLEEN

A

the MESODERM.

GI (5 decks)

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