carbohydrate metabolism

Carbohydrates Glucose supply

- structure
- properties
- tissue dependence
Glut

GLycogenesis
>
Glucose Glycogen
ne
← PPP g Glycogenolysis
NADPH
Glycolysis Glyconeogenesis
w
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NADH Lactate
Pyruvate

y
Shuttles
Mitochondrial Wall

Oxidative n

Phosphorylation e TCA v

b
ATP
 carbohydrate metabolism
blood
regulating glucose
1. “Know the homeostatic blood glucose concentrations and the range of hypo/hyperglycaemic blood
glucose concentrations in animals”.
- monogastrics (humans) - 4-5 mM. (readily absorbed).
- ruminants (sheep) - 3-4 mM. (lower bc lower glucose availability as it must ferment).
- hypoglycaemia:
- half normal values, brain struggles.
- hyperglycaemia:
- higher than 10 mM - enzymes become too conditioned to processing sugar, stop doing it as
much, causing diabetes.

2. “Define carbohydrates, monosaccharides, disaccharides, oligosaccharides and polysaccharides.”

- sugars / saccharides, names end in -ose.
- consist of carbon, hydrogen & oxygen, sometimes nitrogen (amino sugars).
- in a hydroxide group (OH) and aldehyde or ketone.
- monosaccharides: simplest forms, one sugar.
- disaccharides: two sugars. (two monosacch. joined by glycosidic bond, eg sucrose).
- oligosaccharides: 3 to 11 sugars.
- polysaccharides: many sugars.

3. “Understand the nature of a glycosidic bond, and the consequences for enzyme action and specificity.”
- a glycosidic bond combines saccharides.
- formed by -OH of carbon, and second compound (monosacch, amine, etc).
- second group OH: O-glycosidic bond.
- second group amine: N-glycosidic bond.
- enzymes are highly specific for each bond.

Processes of glucose homeostasis:

1. Carbohydrate intake (substrate availability).
- in ruminants, glucose isn’t immediately consumed, so they evolved lower glucose levels.
2. Hormones (insulin, glucagon, adrenalin)
3. Tissue interrelationships (liver, muscle, brain, fat).
4. Metabolic activity. (enzyme pathways/regulation).
 4. “List the names and tissue locations of the glucose transporters (GLUC).”
- glucose uptake is via GLUT transporters (proteins).
location km insulin responsive ?

GLUT1 erythrocyte, brain, placenta, 1 mM (low - kinda No

kidney constant)
GLUT2 liver, pancreas b-cell, kidney 10-20 mM (high - L

No
only if sub. high)
< 1 mM (low -
GLUT3 brain, many tissues only if sub. high) No
5 mM (not too Yes (GLUT4 transfers
GLUT4 muscle, heart, adipose tissue high, med. sub?)
glucose into cell).

5. “Distinguish the properties of the glucose transporters in terms of their Km and control.”
* homeostasis As
homeostasis:

I-
- Glut1+3 constant use by brain.
-

zero order

- GLUT2 some glucose storage.

order 1+3 brain CNS
- GLUT4 little absorption into liver,
glut
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zero

muscle fat
only when in dangerous levels.
gutta
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E
or Horder glut
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liver
glucose
lvliveractsas sponge
+ when full glatt activated
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moving glucose out of blood

into muscle Ifat '

.in plasma
glucose conc
starvation - overfed

- GLUT1+3: glucose transport into cells. (always high as brain needs glucose).
- GLUT2: remove glucose from plasma (highly active when well fed).
- GLUT4: glucose transport into cells (influenced by glucose, most active when well fed).
- pancreas absorbs glucose and releases insulin in response to activate GLUT4, reduce glucose.
6. “Describe the glucose dependence of the major tissues and how the GLUT transport proteins
interact with this dependence.”
- erythrocytes (GLUT1): no mitochondria, can’t produce glucose, must be provided with by GLUT1.
- brain/nervous tissue (1+3): glucose dependent.
- type 2 muscle (4): few mitochondria, limited oxygen supply., needs glucose.
- liver (2): acts as a glucose sink, removing glucose from plasma into liver.