Week 4: CHO

Glycemic index; glucose vs starch: different CHO cause different spikes in blood glucose.

Fructose and metabolism:

location: mainly liver

• can also occur in the liver, kidney and small intestine

Fructose is mainly used for liver glycogen

• beneficial for active people; a small amount will be coverted into lactate and glucose.

• unfavourable for sedentary individuals as it can lead to TAG synthesis, lipid accumulation due to inactivity which can lead to insulin deficiencies and issues like type 2 diabetes.

fructose uptake is not insulin dependent unlike glucose

Summary:

• GLUT-1 diffuses glucose into astrocytes, also the main passage from glucose into the brain: insulin independent

• GLUT-2 diffuses glucose form the blood into the liver: insulin independent

Glucose in the blood triggers insulin release, insulin binds to receptors and triggers glucokinase to create a concentration gradient, glucose enters into the liver and glucokinase adds a phosphate group onto the glucose to then be either synthesise glycogen or be put back into the blood by removing the phosphate group with enzyme glucose-6-phosphatase

• GLUT-3 diffuses glucose in neurons: insulin independent

• GLUT-4 used in skeletal muscle: insulin dependent / insulin independent

Glucose enters through GLUT-4 after insulin binds to the receptor and causes hexokinase to stimulate reactions and keep the concentration gradient.

BASICALLY:

Liver:

• Transporter: GLUT-2

• Enzyme: Glucokinase

• insulin promotes glycogen synthesis for storage

• Enzyme to remove phosphate group: Glucose - 6 - Phosphatase

Skeletal Muscle:

• Transporter: GLUT-4

• insulin promotes glycogen synthesis for storage

• Enzyme: Hexokinase

Brain:

• transporter: GLUT-3 (neuron), GLUT-1 (blood brain barrier, astrocyte)

• insulin promotes glycogen synthesis for storage

• enzyme: hexokinase

GLYCOGEN SYNTHESIS:

Glycogen synthesis: once glucose 6 phosphate is created, the enzyme mutase converts it into glucose 1 phosphate by changing its structure, reactions with UTP and UDP lead to glycogen synthase to ultimately convert glucose into glycogen

insulin activates protein phosphatase (remover of phosphate group) meaning glycogen can then be made

Adrenaline and calcium ions inactivate the glucose as they increase the release of kinase A which adds a phosphate group

SUMMARY - glycogen breakdown and synthesis enzymes:

glycogen synthase

role: active attatched UDP-glucose to glycogen (no phosphate gorup)

protein phosphatase:

role: removes phosphate group making glycogen synthase active

stimulated by: insulin

Protein Kinase A:

role: adds phosphate group making glycogen synthase inactive

stimulated by: calcium ions, adrenaline and glucagon

Glycogen phosphorylase active form:

role: breaks down glycogen to glucose-1-phosphate

inhibited by: high levels of G-6-P and ATP

Glycogen Phosphorylase phosphatase:

role: removes phosphate making glycogen phosphorylase inactive

stimulated by: insulin

inhibited by: high AMP

Glycogen phosphorylase kinase:

role: adds phosphate making glycogen phosphorylase active

stimulated by: clacium ions, adrenaline and glucagon

glycogen synthesis and breakdown: hormones

adrenaline: flight or fight, stimulates the breakdown of glycogen

insulin: released after CHO ingestion, reduces the breakdown of glycogen and stimulates storage

glucagon: released after periods of no food, stimulates breakdown and inhibits storage

glycolytic enzymes in muscle:

• hexokinase

• glycogen phosphorylase

• phosphofructokinase

• pyruvate kinase

• lactate dehydrogenase

• pyruvate dehydrogenase

TCA cycle functions:

• decarboxylation of acetyl-coA

• ATP production

• FADH2 production

• NADH production

Amino acid breakdown, fat breakdown, carbohydrate breakdown feeds into the TCA cycle.

Electron transport chain:

1. 4 large complexes

2. electrons pass from electron donors to electron acceptors

3. each electron acceptor wants the electron more than the last one

4. final =

Gluconeogenesis: liver (kidneys)

• fatty acids can not restore glucose of the liver as it would be inneficcient

• pyruvate to OAA, if there is lots of acetyl co a coming from fatty acids,

  acetyl co a inhibits acetyl dehydrogenase due to the increase of fatty acids giving acetyl coa, this means pyruvate has to go in a difeferent way, it will be converted into oxaloacetate, this is sent out of the mitochondria into the cytoplasm and is using the malatatepaspartate shuttle