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Endocrine > Carbohydrate Metabolism > Flashcards

Carbohydrate Metabolism Flashcards

1
Q

How is the energy for anabolic processes provided?

A

by hydrolysis of ATP.

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2
Q

How can ATP be replenished?

A

Creatine Phosphate (muscle and nervous tissue - short term).
Anaerobic metabolism of CHO to lactate.
Aerobic metabolism of CHO, fat and/or protein in mitochondria.

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3
Q

List the 3 classes of CHO found in the diet and examples?

A

Polysaccharides - starch, cellulose.
Dissacharides - maltose, sucrose and lactose.
Monosaccharides: glucose and fructose.

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4
Q

What is the difference between D and L-glucose? What do they stand for?

A

They have the same formula but arranged in a different way.
Dextro and laevo.
laevo is not found naturally.

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5
Q

What links glucose monomers in disacchrides?

A

a-1,2 glycosidic bonds.

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6
Q

What is sucrose composed of?

A

glucose + fructose.

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7
Q

What is lactose composed of?

A

glucose + galactose.

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8
Q

How is starch broken down?

A

Via salivary alpha amylase in the mouth and pancreatic alpha amylase.

Starch is broken down to glocose, dissacharides and dextrins.

These are further broken down by maltase, lactase and sucrase in the small intestine brush border.

There is no CHO digestion in the stomach.

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9
Q

What affects the speed at which a starch is digested?

A

Raw foods have not be broken up at all in cooking process e.e intact starch granules and plant cell wall structure.
May be hard for enzymes to break down if in a tightly packed structure e.g. raw potato.
Dietary fibre slows absorption as gut contents become more viscous.
CHO foods containing high at may cause delayed gastric emptying so influences food being passed to intestine.

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10
Q

What is glycaemic index and what is the difference between high and low?

A

How quickly a food effects your blood glucose level.

High GI means there is a rapid blood glucose increase.
Low GI takes longer to get the glucose from that food so is slower.

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11
Q

Why cant cellulose be digested?

A

As glucose monomers are linked by Beta-1,4 glycosidic bonds which we dont have enzymes to break.
Some gut microflora can help digestion, but no significant calories are found in cellulose for humans.

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12
Q

What is the transport and storage form of CHO?

A

Transport - glucose

Storage - glycogen

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13
Q

Where is glycogen stored?

A

Striated muscle and liver.

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14
Q

What tissues rely on glucose in blood? Why?

A

RBC’s as they have no mitochondria.
The brain as it contains a lot of lipid, but is unable to get lipid from the blood stream due to the nature of the blood-brain barrier as lipid is transported as lipoprotein or with albumin.
Also though the brain may use it to make neurotransmitters as many NT’s are metabolites of glucose.
Testis.
Brown adipose.

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15
Q

What are normal levels of glucose in the fed state and fasted state?

A

Fasted: 4-5mM/L
Fed: 8-12mM/L

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16
Q

What 2 hormones are involved in glucose homeostasis?

A

Insulin (fed state) and glucagon (fasted state).

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17
Q

Where can glucose be synthesised? What is it synthesised from?

A

The liver can synthesise glucose from lipids, lactate and amino acids via gluconeogenesis.

The kidney can also synthesise glucose but only in extreme starvation.

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18
Q

How is glucose transported into tissues?

A

Into cells via transporters then down a concentration gradient (facilitated diffusion) but GLUT1-5 transporters. They form a pore in the plasma membrane.

Can also be transported against a concentration gradient usuing energy provided by cotransport of sodium via SGLUT1 and 2. This is required in the intenstine to absorb all food and get al calories.
Also important in the kidney to allow all glucose in filtrate to be transported back to the blood.

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19
Q

What transporter do all cells have to transport glucose? What else does it transport?

A

GLUT1 (also transports galactose).

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20
Q

What does GLUT5 transport? Where is it found?

A

Fructose.

Small intestine and sperm.

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21
Q

What is CLUT3’s function and where is it found?

A

Transports glucose and galactose. It is the primary transporter for neurons.
Found in the brain, placenta and testes.

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22
Q

What is GLUT2’s function and where is it found?

A

Transports glucose, galatose and fructose. Liver, pancreatic B cells, Small intestine and kidney. Can act as a glucose sensor in B cells as it has a low affinity for glucose.

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23
Q

What is GLUT4’s function and where is it found?

A

Insulin-responsive glucose transporter. Means more glucose can be transported in (and converted to triglyceride of glycogen) when plasma [glucose] is raised after a meal.
In muscle GLUT4 translocates in response to exercise so more glucose can be used for ATP production.

Skeletal and cardiac muscle. Adipocytes.

24
Q

How is glucose (re)absorbed in cells of the small intestine and PCT?

A

The Na+/K+ pump causes outside the cell to have high Na+ and inside to have high K+. IT uses ATP to maintain gradient.
As there is high Na+ outside, glucose can be co-transported with Na into the cell via SGLT-1/2.
The GLUT transporters can then transport glucose out to capillaries via facilitated diffusion.

25
Q

What is plasma glucose used for?

A

Glycogen in muscle.
Uptake by tissues.
Synthesis of fatty acids and triglycerides.
Stored as glycogen in the liver (reversible).
Synthesis of pentoses (important in DNA and RNA).

26
Q

What is the fate of glucose within a cell?

A

ATP production: Glycolysis, TCA cycle & oxidative phosphorylation.
Storage as glycogen.
Storage as lipid: From Acertyl-CoA after glycolysis.
Synthesis of sugars for RNA/DNA: Pentose Phosphate pathway.
Minor fraction to synthesise glycolipids and glycoproteins.

27
Q

What ‘traps’ glucose in a cell?

A

Phosphrylation to glucose-6-phosphate by glucokinase (hexokinase 4).

28
Q

Where is glucokinase found?

A

Expressed by B-cells of the pancreas and liver.
Has a high affinity (Km).
ITs synthesis is regulated.

29
Q

Where is hexokinase 1-3 found?

A

All tissues (except pancreas and liver B-cells).
Has a low affinity (Km).
It is inhibited by feedback inhibition when there is enough G-6-P.

30
Q

Compare the kinetics of glucokinase and hexokinase?

A

Hexo is higher initially then becomes saturated quickly.
Gluco becomes activated at higher glucose concentrations.
Physiologically we are usually in the range both can work.

31
Q

How many ATP does glycolysis yield?

A

Uses 2 and produces for so 2 NET gain.

32
Q

Outline the 2 main steps in glycolysis.

A

Glucose -> Glucose-6-phosphate via Glucokinase.

> Fructose-6-phosphate -> Fructose-1,6-bisphosphate via Phosphofructokinase.

Ends with pyruvate.

33
Q

What determines whether G6P from glucokinase is used for glycolysis or other purposes?

A

Citrate (downstream products).

34
Q

In glycolysis how is NADH used under aerobic and anaerobic conditions?

A

Aerobic: NADH is used to make more ATP in mitochondria.

Anaerobic: Lactate is formed and no further ATP is produced.

35
Q

What converts pyruvate to lactate?

A

Lactate dehydrogenase.

36
Q

What is Coenzyme A made of?

A

B vitamins that you can synthesis yourself.

37
Q

How many ATP does the aerobic Krebs cycle generate?

A

36 ATP.

38
Q

What does the pentose phosphate pathway synthesise?

A

Fatty acids

Nucleotides by formation of ribose-5-phosphate (RNA, DNA)

39
Q

Outline the process of glycogensis?

A

Glucose –GLUCOKINASE–> G6P G1P -> UDP-Glucose–GLYCOGEN SYNTHASE–> Glycogen + UDP

40
Q

Outline the process of glycogenolysis?

A

Glycogen –GLYCOGEN PHOSPHORYLASE–> G1P G6P

41
Q

Define gluconeogenesis?

A

Synthesis of glucose from a noncarbohydrate (nonhexose) source.

42
Q

What can be used for gluconeogenesis?

A

Lactate
Pyruvate
Glycerol
Certain amino acids (only in extreme starvation).

43
Q

Why are glucokinase, PFK and pyruvate kinase not reversible enzyme?

A

As they need ATP.

44
Q

Why is the liver the only organ that can do gluconeogenesis?

A

As it has enzymes to overcome the irreversible reactions of glycolysis.

45
Q

What enzyme is used instead of glucokinase in gluconeogenesis?

A

Glucose-6-phosphatase.

46
Q

What enzyme is used instead of phosphofructokinase in gluconeogenesis?

A

Fructose 1,6-bisphosphatase.

47
Q

Where is glucose-6-phosphatase found? how does it work?

What regulates its expression?

A

The lumen of the ER
Has transporters to move glucose-6-phosphate into the lumen, and converts it to Glucose + Pi.
Glucose and Pi are moved out the lumen by transporters.
Adrenaline and glucocorticoids stimulate it.
Insulin suppresses it.

48
Q

What enzyme is used instead of pyruvate kinase in gluconeogenesis?

A 
Pyruvate carboxylase (pyruvate -> oxaloacetate)
and Phosphoenolpyruvate Carboxykinase (PEPCK - Oxaloacetate -> Phosphoenolpyruvate).
49
Q

What stimulates gluconeogenesis and what is its action?

A

Glucagon and adrenaline: Decreases glucokinase, increase G6Pase and PEPCK activity.

50
Q

How would the results of the glucose tolerance test differ in those of a healthy person, and someone with DM?

A

Normally, blood glucose will be elevated after ingestion of a fixed dose of glucose, but within 2 hours, the concentration should have returned to normal (4-6mmol/L).
In a patient with DM, ingestion of the same dose will result in an abnormally high concentration of glucose which is sustained for a much longer period of time.

51
Q

When can glucose be detected in urine?

A

When blood glucose concentration exceeds 11mmol/L.

52
Q

Why would diabetic patient have a plasma glucose concentration of >11mM when waking up?

A

As they have an increased glucasgon:insulin ration, resulting in increased glucose formation.

53
Q

What do patients with DM have nocturnal polyuria?

A

Due to increased levels of glucose in plasma, thus increased levels of glucose excreted into the kidney tubule.

54
Q

Why do patients with T1DM often lose weight while eating plenty?

A

As they do not produce insulin so glucose cant be transported into cells - cells starve and have to utilise fat and protein to generate energy resulting in loss of fat and muscle bulk.

55
Q

What hormones/neurotransmitters could influence the glucose tolerance test?

A

(Nor)adrenaline probably only one to have a quick enough effect. It can counteract insulin function by promoting lipolysis, gluconeogenesis and glycogenolysis. This may be produced due to nerves of the test.

Cytokines: Only act locally.
Costisol: Stress hormone that acts by influencing gene transcription - wouldnt act quick enough to affect test.

56
Q

When would insulin concentration peak in the glucose tolerance test?

A

Just after glucose concentration has peaked. Usually within 30 minutes after ingestion.

57
Q

Revise the functions of insulin?

A

Acts on liver: stimulates glycogensis, inhibits gluconeogenesis.
Muscle: Stimulates glycogenesis.
Adipose: Stimulates TAG synthesis, inhibits lipolysis.

Endocrine (11 decks)

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