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Summary Medical Biochemistry
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Medical Biochemistry notes directly from the lectures and course material, integration with laboratory practicals and workgroups.
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Medical BiochemistryCARBOHYDRATE AND GLUCOSE METABOLISM
Priority of the body: to give glucose to the brain, most pathways are designed to transport
glucose to the brain. Each day 160-200 g of glucose are used. 120-150g are used by the
brain for ten hours, the brain does gluconeogenesis but not via fatty acids because they
cannot cross the myelin sheets, and so they use ketone bodies but only after a few days.
Stereo-isomers sugars: differ in the position of OH and H in usually only one position, and
since they are different they need different enzymes, because they don’t fit the same ones.
They normally form ring structures from a linear one, and the carboxyl group can either be
up (beta) and down (alpha) and the body prefers the beta.
D and L forms, depending on which way they close the ring, D is the one we can use in our
body because L is the mirror image and it doesn’t fit the enzyme, so the tridimensional
structure is very important to determine if we can use these carbohydrates.
We initially got them in food, plants, lactose, starch, sucrose.
Polymers have many branches so they need many enzymes to break at the branch point.
Alpha-amylase degrades the alpha 1,4 bonds in the polymers. You want to get the glucose
as fast as possible digested so you start already in the mouth with the salivary
alpha-amylase.
Digestion of complex carbohydrates: after the mouth, the monosaccharides are taken up in
the intestine, after passing through the stomach.
Fiber is a kind of carbohydrate we cannot digest, such as cellulose, because it has beta 1,4
bonds that we can’t break. Our intestinal flora uses it and promotes a normal digestive tract.
Uptake: by passive transport, using a concentration gradient, but sometimes you want to
transport against the gradient in order not to waste any glucose, so against it is active
transport, which requires energy. In the intestinal epithelial we have active transport
because even though it’s full of glucose we want more to fill the whole human body.
Lactose intolerance: they lack the enzyme to break the bond between glucose and
galactose, beta 1,4, so they can't break the milk sugar, and in many societies babies don’t
drink milk anymore after 2-3 yo, so they lose the ability to make it, but luckily bacteria can.
Galactosemia: inability to break the galactose and it might be life-threatening. If you have
high levels you store it in other forms, not normally made, that can be lethal. There is the
classical galactosemia, when you lack galactose 1-phosphate uridylyltransferase (GALT)
that transforms galactose 1-phosphate into glucose 1-phosphate. Or you can have non
classical galactosemia, which is when you lack galactokinase that phosphorylates galactose
into galactose 1-phosphate.
Fructosemia: same thing but with the fructose sugar, you lack the enzyme that converts the
fructose into products that can be inserted inside the glycolysis pathways. Fructokinase
deficiency is not very severe, but it is for Aldolase B.
Glycogen metabolism: high branched molecular structure, found in the muscle, liver, and
the reason why you store glucose in glycogen form is that you can degrade this very fast
cause of the many enzymes that do it, and with these molecules you don’t need as many
enzymes as with the glucose, so you don’t go in a state of unbalanced homeostasis.
Glucose from glycogen the muscles take up, they use it for themselves during exercise,
instead the liver can take it up and can give it back, regulating the blood concentration. This
is because the muscle lacks the enzyme to turn the glucose back to glycogen.
,Glycogen synthase: it transforms glucose 1-P into glycogen, and from this you can
generate the glycogen. It just adds new sugars on the branches or also linear, and when
they get too long, this enzyme cuts it off and adds a branch. Having more sites where to add
staff makes it faster.
Phosphorylase: this is the one that degrades glycogen into glucose 1-P. It chops the
branches and adds them to the linear part.
Blood glucose concentration: regulated by insulin (sugar level high) and glucagon
(sugar level low). Glucagon is released when fasting, leading to activation of glycogen
phosphorylase, meaning that glycogen is degraded into glucose. Insulin is released to make
storage, leading to glycogen synthase activation. Epinephrine also gives signals to the liver
to respond to stress and exercise.
Muscles are instead not responsive to glucagon, but it is for epinephrine, activity and insulin.
This means that when there are high levels of sugar in the muscles they will use it, but if
there is not only the liver is the one that makes glucose for the rest of the body.
Glucagon and Epinephrine lead to G protein activation, which leads to a cascade of
phosphorylation of enzymes, such as the activation of protein kinase A. This activates the
phosphorylase to break down, so this pathway doesn’t happen with insulin, because you
don’t want it to break.
Muscles: respond to exercise, so to the Calcium used for muscle contraction, and this leads
to activation of glycogen phosphorylase. There is regulation by insulin and glucagon (only for
the liver) so the phosphorylation is controlled by hormones, but also the allosteric in the
muscles, inside the cells themselves, to respond to internal demands, so they use
metabolites that come from the inside. This just changes the conformation of an enzyme to
make it more active, or also give non active conformations. In the muscles this division is
common, but in the liver is mostly phosphorylation.
Blood glucose level: different tissues have different metabolic capacities.
The liver can make the ketone bodies but it cannot use them, because there won’t be
anything left for the brain.
,Homeostasis: insulin is released from pancreas after a meal, so when
the glucose in the blood is high, this leads to glucose going into the
tissues and cells but also glucose being transformed into glycogen in
the liver. Glucagon is released during meal and glycogen is transformed
into glucose in the liver, which pours it in the blood.
Insulin production suppresses glucagon production, so they are never
high together.
Glucagon regulation is more intricate than insulin, because it can also
be stimulated by amino acids and nerve action.
In case of a low carb diet, amino acids are used to make glucose from
the brain or you will start to break down your muscles.
Almost all tissues use fatty acid pathways but not the brain.
Insulin is regulated by glucose level in beta-cells in the pancreas. ATP production by them
makes so that the insulin is released into the bloodstream, and if the insulin response is low
you become glucose intolerance or diabetic.
To test this they make you eat a lot of glucose with an empty stomach and measure the level
after a bit of time and if still really high it means you lack insulin.
The uptake rate by facilitated diffusion follows enzyme kinetics. This includes Km which is
the substrate concentration when the speed is half of the Vmax. This says something about
how active the pumps for the facilitated transport are, and a high Km means low affinity and
vice versa, this because when the substrate is at a low level and you still have a high speed
it means that the affinity is higher.
GLUTs are glucose transporters, and different tissues have different ones with different
affinities. For instance, the liver has a lower affinity one, because it only needs to take the
, glucose up when it’s there and not all the time as the blood that needs to bring it to the brain
too. The muscles have a insulin - sensitive transporter GLUT4, because you have a lot of
muscles and if all of them fill the glycogen storage up every time they encounter it then there
won’t be enough left for the brain, and also they work when the insulin is high meaning that
they take it up when there is a lot and use it for themselves. The brain instead has a high
affinity system because it’s the first one that needs it.
Glucokinase: it has a high Km, low affinity and High Vmax. Liver and pancreas mostly use
this, sparing glucose for the brain and muscles, but when there are high levels of it, then it
uses it to make glycogen.
Hexokinase: low Km, high affinity and low Vmax, used by all other cells.
Hexokinase is always at Vmax, while glucokinase is not, it depends on the glucose
concentration.
Glucose-6P inhibits hexokinase, but not glucokinase, meaning that when there is glucose
the liver works, while the hexokinase doesn’t depend on it. In fact, when there is glucose-6P
it means there is enough glucose for the cells so they can’t stop making it. Instead, the liver
can take it up more to make storage, so it doesn’t want the making of glucose-6P to stop
going on. Liver takes up all excess glucose, because it can convert it into glycogen and
make the storage, while the muscles and other cells have a limit.
Gluconeogenesis: it’s the process where the glucose is made via different pathways and
all this depends on glucagon. For instance, from amino acids you take the ammonium ion
NH4+ which goes into the urea cycle and exits, or you take carbon skeletons which go into
the making of glucose.
Only the liver has the G6Pase to transform the G6P into glucose, so
it can release it back into the blood.
After a protein enriched meal, the glucagon release is induced,
leading to gluconeogenesis, because you don’t introduce much
glucose but more nitrogen, while after a high carbohydrate meal the
insulin is high because you already have a lot of glucose. Especially,
the body has a preference for the alanine to make pyruvate.
When you make Acetyl CoA you cannot go back to the pyruvate, so
it cannot be turned back into glucose, but yes into glycerol so
another form of energy, but not glucose never. This is why the brain
cannot use the fatty acids, because they go directly into the TCA
cycle via Acetyl CoA, but the brain can only use glucose and not any
other form of energy storage.
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