CARBS 1 Flashcards
Define monosaccharide
Simplest carbohydrate
- Cannot be hydrolysed into simpler forms
- can be 3C, 4C, 5C, 6C etc but simply bonded carbons
define dissacharides
- Two monosaccharides linked by glycosidic bond
- Alpha (U-shaped) or beta (Z-shaped) glycosidic bond: beta needs an enzyme to break down bond as its harder to break down (eg lactose—> lactase)
- alphas = anomeric OH below plane of ring
- beta = anomeric OH above plane of ring
What is an oligosaccharide
- 3-11 sugar residues
what are polysaccharides
- Many monosaccharides linked by glycosidic bond
- Most animals obtain their carbohydrates from the diet in these complex polysaccharide forms, then the process of digestion and absorption breaks these glycosidic bonds to release the constituent monosaccharide, glucose
how do glycosidic bonds form?
- occurs through: condensation between the hydroxyl group associated with the anomeric
carbon and - In case of disaccharides, another hydroxyl group on another monosaccharide.
normal glucose levels in humans and ruminants
- Monogastric eg. humans - 4-5 mM
- Ruminants eg sheep - 3-4 mM
what is hypoglycaemia
- <half normal values, fuel deprivation for brain ect.
- 2mM bad, 1mM really bad
What is Hyperglycaemia
- Extended elevation ≥ 10 mM in uncontrolled diabetes can lead to glycosylation of proteins (eg crystallins of lens)
What are the 4 major processes of glucose homeostasis
- Dietary carbohydrate intake ie substrate availability
- Main hormones: insulin, glycogen, adrenalin (hormone action)
- Tissue interrelationships eg role of liver, muscle, brain, fat
- Metabolic pathways: enzyme pathways, enzyme regulation
What occurs when animal just fed, short term shortage, medium term starvation and when exercising
- short term - just fed (day 1)
- Emphasis on storage of excess glucose as glycogen and excess carbon as fat
- Driven by insulin - Short term shortage
- Emphasis on mobilisation of glycogen stores
- Driven by glucagon - Medium term - starvation (2 days on)
- Emphasis on glucose sparing
- Gluconeogenesis for glucose dependent tissues
- Driven by glucagon - High demand - stress/exercise
- Emphasis on maximising glucose availability
- Driven by adrenalin
GLUT 1 location, Km and insluin repsonse
location: ethrocytes, brain, placenta, kidney
Km = 1 mM
no insluin repsonse
GLUT 2 location, Km and insluin repsonse
location - Liver, beta cell of pancreas, kidney
Km = 10-20mM
no insulin response
GLUT 3 location, Km and insluin repsonse
Location: brain, many tissues
Km = <1mM
No insulin response
GLUT 4 location, Km and insluin repsonse
location = muscle, heart, adipose tissue
Km = 5mM
IS insulin responsive
what occurs for GLUT 4 when insulin released and when no insulin? exercise?
- insulin released, causes transporters to migrate to cell membranes and absorb glucose
- Km = 5mM, if at homeostatic concentrations (5mM) goes at only half Vmax. If blood levels get higher, can absorb even more to decrease it
- when no insulin, no GLUT 4. So when starving, no glucose absorbed into muscle and adipose as no insulin produced
- muscle contraction during exercise causes muscle GLUT 4 migrate to membrane to absorb more glucose -> lasts 15 mins after exercise too
Why are GLUT 1 and 3 needed
- can’t speed up if blood glucose level gets really high
- but, can still function at very low levels of glucose so brain is prioritised during starvation (low levels), brain can still uptake glucose at low levels in blood
- not good at storing glucose though
why is GLUT 2 important
- liver -> crucial for protection against spikes of glucose when ingested
- works poorly at low concentrations, but very well at high concentrations
- livers stores heaps of glycogen, when no longer absorbing sugar from guts (no food left), release glycogen -> only when glucagon is released during “starvation”
GLUT transporter states when well fed (16mM) -> order and vmax
G1and3 = zero order, and at VMax
G4 = zero order, at vmax
G2 = first order, can still increase
GLUT transporter states when at homeostatic levels (5mM) -> order and vmax
G1 and 3 = zero order, vmax
G4 = first -> responsive, but insulin missing (not active)
G2 = zero oder, not absorbing much (liver should feed glucose into blood so this is good)
GLUT transporter states when Starvation (2mM) -> order and vmax
G1 and 3 = zero order, still getting glucose (almost at vmax)
G4 = first order -> low insulin signal so not absorbing much
G2 = first order -> liver not absorbing, needs to stay in blood
What do kinases, phosphrylases and phosphatases do?
- kinase = Any enzyme that adds phosphate using ATP as the phosphate donor
- Phosphorylase = Any enzyme that adds phosphate using inorganic phosphate [Pi] as the phosphate donor
- Doesn’t use an ATP - Phosphatase = Any enzyme that removes phosphate as inorganic phosphate [Pi]
how are metabolic pathways regulated :
- Substrate/product (stimulation/inhibition)
- Km/Vmax
- Allosteric effectors
- Stimulate or inhibit
- Effector concentration gives rapid change - Covalent modulation
- Stimulate or inhibit phosphate induces
conformational change
