SHEET L.02 SLIDE 1 (Carbohydrates) 2017
Clinical Biochem 2
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SHEET L.02 SLIDE 1 (Carbohydrates) 2017
In the previous lecture we talked about the importance of glucose inside our bodies , physiology of
glucose balance and began to talk about one of the disorders related to glucose homeostasis which is
Diabetes Mellitus in its different types .
In this lecture, we will talk about carbohydrates metabolism and disorders that come basically from the
disturbance of carbohydrates homeostasis.
In the next lecture, we will talk about determination of glucose in the body fluids and urinary albumin
concentration. Then, we will discuss one or two cases (how to look for and deal with numbers of the lab
tests and determine patient problems).
**Carbohydrates metabolism:
Glucose is a major component and energy source in our body, and we get glucose from many sources
such as:
1- Diet
2- Glycogenolysis  glycogen degradation
3- Gluconeogenesis from different precursors
*remember that our body doesn’t wait for the glucose gotten by our diet to be consumed then start
glycogenolysis and glyconeogenesis!! All of these sources are working together at the same time but,
one of them would be predominant (the major source) .
When we eat a carbohydrate meal, the most important source of glucose (the predominant source) is
that meal.
Once the glucose level gotten from diet is decreased (fasting state), the body tries to maintain glucose
level by using glycogen stored in the liver "glycogenolysis". If fasting state prolonged (starvation), our
body uses the muscular proteins to synthesize glucose "gluconeogenesis .”
Remember that: lipids are a good source of energy but need longer time for metabolism (slow process)
**it’s important to maintain glucose level between 70-180 mg/dL , and this level is controlled due to
different hormones :
1- Insulin  which is the most important hormone
2- Counter regulatory hormones ( glucagon, cortisol , growth hormone)  we call them "counter"
because their action is against insulin
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SHEET L.02 SLIDE 1 (Carbohydrates) 2017
**insulin function is lowering blood glucose concentration so; insulin will speed up any process that
removes glucose from the blood (like: lipids synthesis, proteins synthesis & entry of glucose into tissues
to store it as glycogen). On the other hand, insulin will slow down any process that adds glucose to the
blood (like: glycogenolysis & gluconeogenesis).
** our body can’t distinguish if glucose level is high or low ! it depends on insulin secretion  if the
insulin is secreted to the blood then the body will understand that glucose concentration is high.
Whereas, if no insulin was secreted then glucose concentration is low and our body needs glucose.
*Disorders related to glucose level abnormalities:
1- Hypoglycemia
2-Hyperglycemia (produced by D.M)
**Types of diabetes mellitus :
1- type 1 diabetes mellitus - more common in children and young adults
- Happened and discovered accidentally (in stressful conditions )
2-type 2 diabetes mellitus  appears gradually and usually at older age
3- Secondary diabetes mellitus  any disorder results from increased level of counter regulatory
hormones which cause hyperglycemia such as: Cushing syndrome (excessive production of cortisol that
increases glucose level in the blood)
4- Impaired glucose tolerance (called prediabetic)  people who are not normal but not diabetics as
well! They are in between.
**if prediabetic individuals change their lifestyle into healthy one they will go back to normal state.
Otherwise, they will become diabetics.
5- Gestational diabetes mellitus (GDM)  diabetes during pregnancy. Here we are talking about
diabetes that happens during pregnancy and only pregnancy! Not the individuals that had been
diagnosed having D.M before. (First recognition and onset happened during pregnancy)
-usually 1-5% of all pregnant ladies can develop GDM.
-GDM exposes both fetus and mother to different complications (we’ll talk about it later)
-30% of all pregnant women who have GDM can develop DM in the future. This means that our body
can’t deal well with the changes happened during pregnancy. (Similar to HTN during pregnancy, once
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SHEET L.02 SLIDE 1 (Carbohydrates) 2017
delivery happened everything backs to normal. and, in GDM once pregnancy terminated everything
backs to normal as well).
* long-term complications (microvascular changes) result from poor glycemic control for diabetic
individuals :
1- Vascular changes in the eye retinopathy
2- Kidney  nephropathy
3- In arteries arteriopathy
4- In neurons  neuropathy (the patient may lose the sensation, for example he won’t feel if his hands
are burnt due to close hot object)
-he might have a gangrene which is neuropathy, arteriopathy and an infection. That’s why he must
examine his eyes, legs and neurons continuously.
5- infections  diabetic individuals have a higher risk to be infected due to low immunity and blood
viscosity (Viscosity of blood comes from high conc. of glucose which impedes normal blood flow through
blood vessels >> blood flow for healing and repair is slower).
-UTI is the most common type of infections due to opportunistic bacteria that utilize glucose.
*it is not necessary that all diabetic patients have these complications, but their chance to happen
increases as period of the disease becomes longer or glucose level isn’t well-controlled.
*short-term complications : (classic signs and symptoms of D.M)
Polyuria, polydipsia , and polyphagia .
**kidney can reabsorb glucose in the tubules, but when glucose concentration goes high  kidney
transporters become saturated and glucose appears in the urine. So, loss of glucose causes polyphagia .
In addition, this condition causes osmotic diuresis results in fluids loss which leads to polydipsia &
polyuria .
when we lose fluids, the electrolytes "like Na+" also got lost which means further osmotic diuresis.
-
So, in most cases of uncontrolled D.M  glucosuria happens and causes osmotic diuresis that
leads to classical signs and symptoms of D.M !
Note: individuals have D.M may develop life threatening ketoacidosis , non-ketotic hyperglycemia , and
rarely lactic acidosis.
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*Again, the major source of energy is glucose, once its level decreases (during fasting) insulin will not be
released ! so, our body will try will any organs that can use energy sources other than glucose and use
them  mainly fatty acids are used (fatty acids will be released from adipose tissue and the cells which
have mitochondria are going to use fatty acids as another source of energy).
Remember that: the brain doesn’t utilize fatty acids as a source of energy bc the can’t enter the brain .
so, the major sources of energy for the brain are glucose and ketone bodies only.
*other tissues oxidize F.A through mitochondria then enter krebs cycle which increases level of acetyl
coA to obtain energy (acetyl coA is converted into ketone bodies released into the blood).
Depending on what we said , tissues are divided into 3 categories :
1- use only glucose
2- can use ketone bodies (such as : brain)
3-can use free fatty acids
**remember that the body uses another source of energy only when insulin level is low .
-WHY a type-1-D.M patient might have ketoacidosis ???
In type 1 D.M there is a problem in insulin secretion and when the patient didn’t take the insulin dose
the body will understands this as there is a decrease in glucose level (bc in normal case : no insulin
secretionmeans low glucose level) so it will start to break down F.A which leads to ketone bodies
production "KETOACIDOSIS".
*ketoacidosis causes :
1- ketonuria ketone bodies in the urine
2-hedydration
3-acidosis  due to acidic ketone bodies
4- hyperkalemia
**Hyperkalemia :
Due to acidosis, H+ enters inside the cells to balance the PH. On the other hand, K+ inside the cells goes
out which leads to potassium depletion inside the cells , and an increased level in the blood !
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-if we gave the patient an insulin dose to treat ketoacidosis, both glucose and K+ will enter the cell
causing K+ depletion, so wehave to give him K+ supplements as well .
*again, in case of starvation we need to maintain :
1-ketone bodies for the brain
2-glucose & keep it in normal level
3- other sources such as fatty acids
-in case of ketoacidosis , the state becomes worse because ketone bodies pooled without any use!
**all the cells basically don’t need insulin for glucose utilization , but some tissues that store glucose
(such as: liver, muscles , and adipose tissue) need transporters stimulated by insulin.
Notes:
-
our body can tolerate starvation for months.
Once ketone bodies areformed , this means that the body is using F.A as a source of energy .
*according to D.M guideline :
Diabetic  FBG> 126mg/dL
Prediabetic between 110-126mg/dL
Normal FBG <110mg/dL
Random should be less than 200mg/dL
*Oral glucose tolerance test (OGTT) : we challenge the body by a load of glucose the follow its behavior.
-normal situation: no glucose in urine
-after 2 hrs, blood glucose conc. backs to baseline
- in diabetic patient: glucose con in the blood is higher than normal level and needs longer time
(around 2 hours) to back to normal/original state.
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**in type 2 D.M , patients will never have ketoacidosis state bc the problem is mainly in the response to
insulin. So , insulin in the body is enough to inhibit lipolysis and ketone bodies production , but not
enough to keep glucose level in control .
-
Type 2 D.M patients develop hyperosmolar non-ketotic coma causes marked hyperglycemia ,
means glucose level may reach 900mg/dL!! This high conc. increases osmolarity m so our body
tries to keep fluids but osmotic diuresis induces body fluid loss .
*These balance-maintenance trials from the body results in different symptoms and conditions such as:
Cerebral dehydration due to glucosuria and leads to coma.
Treatment: 1- lowering blood glucose conc.
2- fluids intake( return body fluids that are lost!)
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Anwar Asfour
Samar Almazone
Sara’a Alrayushi
Sahar ALazzam
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