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Endocrinology > Carbohydrate Metabolism > Flashcards

Carbohydrate Metabolism Flashcards

1
Q

ATP is the main substrate for energy.

What can replenish ATP?

A
  1. Creatinine phosphate (muscle - short term)
  2. Anaerobic metabolism of CHO to lactate
  3. Aerobic metabolism of CHO, fat, and/or protein (mitochondria oxidation)
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2
Q

List the polysaccharides in the diet

A

Starch

Cellulose

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3
Q

List the disaccharides in the diet and what they’re composed of.

A

Maltose: glucose-glucose
Lactose: glucose-galactose
Sucrose: glucose-fructose

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4
Q

List the monosaccharides

A

Glucose
Galactose
Fructose

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5
Q

D-glucose

What does the D represent?

A

D-glucose refers to the way solution of glucose will rotate plane of polarised light to the right

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6
Q

a-D-glucose

What does the a represent?

A

alpha

refers to whether the -OH group is below (alpha) or above (beta) the C-atom

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7
Q

What type of bond holds together sucrose?

A

glucose-fructose

alpha-1,2-glycosidic bond

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8
Q

What type of bond holds lactose together?

A

Glycosidic bond

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9
Q

What kind of bond hols starch together

A

alpha-1,4-glycosidic bond

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10
Q

What is the process of CHO digestion?

A
  1. Mouth: salivary alpha-amylase
    - Starts digestion
    - Breaks down polysaccharides into mono- (glucose) and disaccharides, and dextrins
  2. Small intestine: pancreatic alpha-amylase
    - maltase: matose to glucose + glucose
    - sucrase: sucrose to glucose + fructose
    - lactase: lactose to glucose + galactose
  3. Active transport (SGLTs and GLUTs)
    - Monosaccharides in the blood.
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11
Q

What is the glycaemic index?

A

Rating system for foods containing carbohydrates

It shows how quickly each food affects your blood glucose levels when that food is eaten on its own

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12
Q

What is meant by high glycaemic index foods? And give some examples

A

High GI CHO foods are broke down quickly by your body and case a RAPID increase in blood glucose

E.g.:

  • Sugar and sugary foods
  • Sugary soft drinks
  • White bread
  • Potatoes
  • White rice
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13
Q

What is meant by low glycaemic index foods? And give some examples

A

Low/medium GI CHO foods are broken down more slowly and cause a gradual rise in blood glucose

E.g.:

  • Some fruit and vegetables
  • Whole grain foods, such as porridge oats
  • Beans, lentils
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14
Q

Give an example of an indigestible CHO

A

Cellulose

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15
Q

What is the transport and storage forms of CHO?

A 
Glucose = transport
Glycogen = storage
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16
Q

Which tissues depend on a constant supply of glucose and why?

A

Brain - other substrates cannot cross the blood-brain barrier

RBCs - lack mitochondria therefore cannot process any other substrate for energy release

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17
Q

What is normal serum glucose concentrations and how does this change after a meal?

A

Tightly regulated between 4-5mmol/L

Can rise to 8-12mmol/L after a meal

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18
Q

What hormones are principal in glucose homeostasis?

A

Insulin - released when glucose is high
Glucagon - release when glucose is low

Glucose can also be synthesised de novo by the liver to buffer plasma glucose

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19
Q

How is glucose transported into cells? And what is the mechanism of transport?

A

Down concentration gradient by facilitated diffusion via GLUTs 1-5

Against concentration gradient using energy provided by co-transport of sodium via SGLTs 1-2
- required in intestine to absorb from the gut lumen and in kidney to reabsorb from filtrate

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20
Q

What are the major sites and characteristics of SGLT1/2?

A

Major sites: intestinal mucosa and kidney tubules

Characteristics: Co-transport 1 molecule of glucose or galactose with 1 Na+

  • DOES NOT transport fructose
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21
Q

What are the major sites and characteristics of GLUT1?

A

Major sites: ubiquitous

Characteristics: high-affinity transporting glucose and galactose

  • DOES NOT transport fructose
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22
Q

What are the major sites and characteristics of GLUT2?

A

Major sites: liver, pancreatic B-cell, SI, kidney

Characteristics: transports glucose, galactose, and fructose

  • Low affinity/high capacity: glucose will only be transported across the membrane when it is in high concentration within the cell
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23
Q

What are the major sites and characteristics of GLUT3?

A

Major sites: brain, placenta, testes

Characteristics: Transports glucose and galactose (high-affinity)

  • DOES NOT transport fructose
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24
Q

What are the major sites and characteristics of GLUT4?

A

Major sites: Skeletal muscle, Cardiac muscle, adipocytes

Characteristics: this is the insulin-responsive glucose transporter with high affinity to glucose

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25
Q

What are the major sites and characteristics of GLUT5?

A

Major sites: SI and sperm

Characteristics: transports ONLY FRUCTOSE

  • DOES NOT transport glucose and galactose
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26
Q

What is the significance of GLUT4?

A

GLUT4 is the insulin-responsive transporter
Expressed on adipocytes and muscle only

  • In adipocytes: more glucose is transported and converted into TG/glycogen when [glucose]plasma is raised after a meal in response to increased insulin
  • In muscle: GLUT4 translocates in response to physical activity/exercise (independent of insulin) thus more glucose can be used for ATP production
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27
Q

List the fate of glucose within a cell

A
  1. ATP production - glycolysis, TCA, oxidative phosphorylation
  2. Storage as glycogen - glycogenesis
  3. Storage as lipid - from acetyl CoA after glycolysis
  4. Synthesis of sugars (pentoses) for RNA/DNA - Pentose Phosphate Pathway
  5. Can also form glycolipids and glycoproteins
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28
Q

What is the common step for all potential pathways of glucose fate?

A

First step:
Phosphorylation of glucose to glucose-6-phosphate

This is catalysed by hexokinases I-IV

  • Hexokinase IV: glucokinase- (expressed in b-pancreatic cells and liver ONLY)
  • Hexokinase I-III: expressed in all other tissue
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29
Q

What enzyme phosphorylates glucose to glucose-6-phosphate?

A

Hexokinases I-IV

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30
Q

What is hexokinase IV? And where is it expressed?

A

Glucose kinase

Expressed in: b-pancreatic cells and liver hepatocytes

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31
Q

What is the difference between Glucokinase and hexokinase

A

Glucokinase:

  • Expressed on b-cells of pancreas and hepatocyte sin liver
  • Has high Km (low affinity) - requires greater concentration to activate
  • Enzyme synthesis regulated

Hexokinase

  • Expressed on all other tissues
  • Has low Km (high affinity) - requires lower concentration to activate
  • is INHIBITED by glucose-6-phosphate (feedback inhibition)

On a graph (Y-axis: enzyme activity; X-axis: [glucose]):

  • Hexokinase will be the top line
  • Glucokinase will be the lower line
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32
Q

Where does the process of glycolysis occur? And what does it yield?

A

Cytoplasm

2 Pyruvate
2 ATP
2 NADH
4 H+

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33
Q

What is the committed step in glycolysis?

A

F6P –> F-1,6-BP

Via: Phosphofructokinase-1 (PFK-1) COMMITTED STEP

PFK-1 is inhibited by (downstream products):
ATP
Citrate

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34
Q

How does fructose enter glycolysis?

A

Fructose is converted to F1P by fructoKINASE

F1P is converted to DHAP and glyceraldehyde-3-phosphate - both are INTERMEDIATES for glycolysis

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35
Q

How does galactose enter glycolysis?

A

Galactose is converted into glucose-1-phosphate then to G6P

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36
Q

What is the fate of pyruvate generated by glycolysis?

A

Either:

  1. Anaerobic respiration: production of lactic acid
  2. Aerobic respiration
    - Converted to acetyl CoA in the mitochondria
    - Enzyme: PYRUVATE DEHYDROGENASE
    - Acetyl CoA used in the Krebs Cycle

*requires vitamin B1 (thiamine) as cofactor

37
Q

How many reactions of the Krebs cycle? And where does it take place

A

8

Mitochondria

38
Q 
How many ATPs are produced by:
NADH
FAHD2
GTP
?
A 
NADH:ATP = 1:3
FAHD2:ATP = 1:2
GTP:ATP = 1:1
39
Q

How many ATP molecules are generated from 1 glucose?

A

36 ATP molecules can be made per oxidised glucose molecule during cellular respiration
2 from glycolysis
2 from the Krebs cycle,
34 from the electron transport system

40
Q

What pathway is the source of ribose phosphate for synthesis of RNA and DNA?

A

Pentose phosphate pathway PPP

41
Q

What is the major product of the PPP? And what is it used for?

A

NADPH

  • lipid biosynthesis (e.g. liver, adrenal cortex, or lactating mammary glands): NADPH used in redox reactions required for synthesis of cholesterol, bile salts, steroid hormones, and triglycertides
  • Liver: also uses NADPH for hydroxylation reactions involved in the detoxification and excretion of drugs

Summary:
NADPH can be used for lipid biosynthesis and drug detoxification

42
Q

What is the committed step of pentose phosphate pathway?

A

Dehydrogenation pf G6P

43
Q

How much glucose is usually consumed?

List the tissues that depend mostly on glucose and the % of how much of the glucose they consume

A

200g

RBCs and Brain - 80%

44
Q

What is the name of the de novo pathway for glucose synthesis?

A

Gluconeogenesis

45
Q

What is the structure and bonds are found in glycogen?

A
  • Highly branched glucan
  • Branched polysaccharide of glucose
  • Contains 2 types of glycosidic bonds:
    1. alpha-1,4-linked glucose residues
    2. alpha-1,6-braches
46
Q

Where does glycogenesis occur?

A

Liver and muscle following a meal

47
Q

What induces the activation of glucokinase?

A

Continued consumption of a high-CHO diet

It is not inhibited by G6P like hexokinase is

48
Q

Through which transporter does glucose enter the liver following a meal? And what’s special about this transporter?

A

GLUT2

High-capacity, low affinity

49
Q

What happens to the excesses G6P in the liver after the glycogen stores have been replenished?

A
  • Glycolysis for energy

- Converted into FA and TAG and exported for storage in adipose tissue

50
Q

What is the regulatory enzyme for glycogenesis?

A

Glycogen synthase

51
Q

In glycogenolysis, which bind is removed first?

What enzyme facilitates this?

A

Abdundant external alpha-1,4-linked glucose residues

Glycogen phosphorylase

52
Q

What is the rate-limiting regulatory step in glucogenolysis?

A

Glycogen phosphorylase

Acting on alpha-1,4-bonds

53
Q

Describe the hormonal regulation of glycogenolysis? Inhibitors and activators

A

Activation:

  1. Glucagon - secreted from the a-pancreatic cells
    - initiated by hypoglycaemia
    - causes rapid activation of glycogenolysis
  2. Adrenaline - secreted from adrenal medulla
    - initiated by stress/hypoglycaemia
  3. Cortisol - secreted by the adrenal cortex
    - initiated by chronic stress
    - causes chronic activation

Inhibition:

  1. Insulin - secreted by b-pancreatic cells
    - response to hyperglycaemia
    - inhibits glycogenolysis
54
Q

What type of hormone is glucagon?

A

Peptide, secreted from pancreatic a-cells

55
Q

What is the primary function of glucagon?

A

Initiate glycogenolysis to maintain normoglycaeia

In response to hypoglycaemia

56
Q

What’s the half-life of glucagon in plasma?

A

5mins

57
Q

How does glucagon concentrations change:

a. During meals
b. Between meals
c. low-CHO diet

A

a. Decreases
b. Increases
c. Increases more

58
Q

What is the mechanism of action of glucagon?

A
  1. Glucagon binds to receptors on hepatocytes (GPCR)
  2. Increases cAMP
  3. Activation of PKA pathway
59
Q

List substrates of gluconeogenesis

A
  • lactate
  • pyruvate
  • glycerol
  • AAs
60
Q

When does gluconeogenesis become the primary sournce of glucose?

A

After 8hours of fasting

61
Q

Where is the energy for gluconeogenesis provided?

A

Metabolism of FAs from adipose tissue

62
Q

Where does gluconeogenesis occur?

A

Mainly in liver

Kidneys can contribute with prolonged starvation

63
Q

What is the pathway of gluconeogenesis?

A

*essentially the REVERSAL of GLYCOLYSIS

64
Q

What are the irreversible enzymes of glycolysis?

A
  1. glucokinase
  2. phosphofructokinase-1
  3. pyruvate kinase
65
Q

What are the irreversible enzymes of glycolysis? And how are these overcome in gluconeogenesis?

A

*essentially the REVERSAL of GLYCOLYSIS

  1. Pyruvate kinase
    - overcome by 2 enzymes:
    a) pyruvate carboxylase - PCOX (mitochondrial)
    b) PEPCK (cytoplasmic)
  2. phosphofructokinase-1
    - overcome by: fructose-1,6-bisphosphatase
  3. glucokinase
    - overcome by: glucose-6-phosphatase (ER)
66
Q

What is glucose-6-phophatase used for? And how is it stimulated? And what suppresses it?

A

This is the 3rd enzyme in gluconeogenesis
To overcome the irreverisble glucokinase action

Stimulated by: adrenaline and glucocortocoids (cortisol)
Suppressed by: insulin

67
Q

What is the intermediate formed in gluconeogenesis from pyruvate?

A

Oxaloacetate

68
Q

Can glucose be synthesised from FAs?

A

No

69
Q

What stimulates gluconeogenesis? And how?

A

Stimulated by: glucagon and adrenaline

  • Decrease glucokinase
  • Increase G6P and PEPCK

*effects is at level of gene expression

70
Q

Can muscle cells release glucose into circulation?

A

No

- They do not have glucose-6-phosphatase enzyme

71
Q

How can muscles contribute to gluconeogenesis

A

Releasing lactate which is transported to the liver

72
Q

How is glucose homeostasis controlled?

A

Anabolic: storing glucose - glycogenesis
- Insulin

Catabolic: releasing glucose - glycogenolysis and gluconeogenesis

  • Glucagon
  • Catecholamines ((nor)adrenaline)
  • Cortisol
  • GH
73
Q

List the main enzymes of gluconeogenesis

A
  1. Pyruvate carboxylase (PCOX) and PEPCK
  2. Fructose-1,6-bisphosphatase
  3. Glucose-6-phosphate
74
Q

What effect does insulin and glucagon have on gluconeogenesis?

A

Insulin: inhibit
Glucagon: activate

75
Q

On a high-CHO diet, what does insulin do with respect to enzymes?

A

Insulin induces gene transcription of:

  1. Glucokinase
  2. PFK
  3. Pyruvate kinase
  4. Glycogen synthase

*glycogenesis

76
Q

Pathway of insulin synthesis

A
  1. preproinsulin
    - peptidase
  2. proinsulin
    - endopeptidase
  3. insulin + c-peptide
  • occurs in eER
  • packaged into secretory vesicles in Golgi
77
Q

What is the name of the processes of insulin secretion?

A

Stimulus-secretion coupling in the

pancreatic b-cell

78
Q

Outline insulin signalling

A
  1. insulin binds to RTK (found primarily on liver, striated muscle, adipocytes)
  2. RTK phosphorylated
  3. Recruitment and phosphorylation of Insulin Receptor Substrates (IRS1-4)
  4. Activation of PIP3-PKB pathway
  5. Translocation of GLUT4 to surface
  6. Glycogen and FA syntehsis

PKB also inhibits:

  • lypolysis (adipose)
  • glucongeogenesis (liver)
79
Q

What are the plasma glucose concentrations:
Fasted
After meal

A

Fasted: 4-5mmol/L

After meal: 8-12mmol/L

80
Q

Glucose homeostasis

Effects of glucagon and adrenaline

A

Gluconeogenesis

  • Decrease glucokinase activity
  • Increase glucose-6-phoshphase and PEPCK activity
81
Q

Glucose homeostasis

Effects of insulin

A

Glycogenesis

  • Increase glucokinase activity
  • Decrease glucose-6-phosphatase and PEPCK activity
82
Q

Via what receptor is glucose taken up by adipose and muscle?

A

GLUT4

83
Q

List the 5 different classses of hypoglycaemic drugs

A
  1. Stimulate insulin secretion:
    - Sulphonylureas
  2. Act on incretin system:
    - GLP-1 receptor agonist
    - DPP-4 inhibitors
  3. Sensitise the peripheral tissues to insulin
    - Biguanides
    - Thiazolindinediones
  4. Decrease glucose absorption
    - SGLT2 inhibitors
    - inhibitors of alpha-glucosidase (acrabose )
84
Q

What’s the MOA of sulphonylureas?

Give an example

A

Increase insulin secretion

Inhibit K+-ATPsensitive channel

  • This closes the channel
  • Depolarises the membrane
  • Activate VGCC
  • Increases intracellular Ca2+
  • Stimulates exocytosis of insulin

E.g.: Tolbutamide

85
Q

What’s the MOA of biguanides?

Give an example

A

Increase peripheral insulin sensitivity

  • Mimics insulin by inhibiting hepatic gluconeogenesis
  • Mechanism of action uncertain but all involve inhibition of liver mitochondrial function
  • Reduces hepatic gluconeogenesis and decreases endogenous glucose production (glycogenolysis)
  • INHIBITS Glucose-6-phosphatase and PEPCK*

E.g.: Metformin (most common drug for T2DM)

86
Q

What’s the MOA of thiazolidinediones?

Give an example

A
  • Ligand for PPAR-gamma
  • PPAR-g is a transcription factor, stimulating
    expression of genes involved in triglyceride storage

*Stops inappropriate deposition of lipid in non-adipose
tissues (which leads to insulin resistance) – therefore
improves insulin sensitivity

E.g.: Pioglitazone

87
Q

List the GI hormones that potentiate insulin secretion

A
  1. Glycogen-like-peptide-1 (GLP-1)
  2. Gastric inhibitory peptide (GIP)
  3. Dipeptidyl Peptidase-4 (DPP-4) - inactivator of GLP1
88
Q

What’s the MOA of incretin mimics?

Give an example

A
  1. GLP-1 receptor agonist
    - increase insulin secretion
    - not cleaved by DDP-4
    - Injected

E.g.: Exenatide

  1. DDP-4 inhibitors
    - increase endogenous GLP1, therefore increases insulin secretion
    - oral drug

E.g.: Sidagliptin

89
Q

What’s the MOA of SGLT2 inhibitors?

Give an example

A
  • inhibit renal reabsorption of glucose from filtrate
  • decrease hyperglycaemia and BP

E.g.: Canagloflozin, dapagliflozin, empagliflozin
- EMPAREG and CANVAS RTCs: decreased CV mortality and hospitalisation due to CV events

Endocrinology (11 decks)

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