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Transcript
Physiology lec.9
The dr. starts the lec. Talking about “black Sunday“ and he end early so this lec. Could
be short
starting to review the previous lec. we will talk about diabetes mellitus


In these patients there is a disturbance in all food components (I.e. lipids
proteins, lipids and carbs).
As we we know diabetes mellitus is a disease in which the patient have high
blood sugar (hyperglycemia): high conc of free fatty acids and amino acids.
This high blood sugar indicates that glucose cannot enter the cell so it stays at the
blood and these cells try to use another sources for energy.



Proteins is one source for energy but using proteins(protein catabolism) increase
the level of a.a. in blood .
Lipids is another source to supply the body with its needs
Lipid catabolism
increase free fatty acids
ketone bodies
(acetoacetic acid, acetone and hydroxypotelic acid)
acidosis occur
Diabetes mellitus patients also excrete too much water from their body and that
will lead to dehydration and depletion of electrolyte (like Na+ ion) so sodium will
be replaced by hydrogen and acidosis occur.
Note: also the body use lipids and proteins (mainly lipids) its imp to know that not all the
cells utilize lipids and proteins at the same way there is some differences according to
the type of the cell and its function.(some cells prefer free fatty acids and others prefer
amino acids but in general free fatty acids first).
From above we can notice that diabetes mellitus lead to acidosis and also to
dehydration than to coma and consequently death.
Coma not only occurs in the case of hyperglycemia, it might also seen in
the cases of hypoglycemia.
Another type of diabetes we explained before is Diabetes insipidus, what about it?
Diabetes insipidus (DI) is a condition characterized by excessive thirst and excretion
of large amounts of severely diluted urine and caused by a deficiency of
arginine vasopressin (AVP), also known as antidiuretic hormone (ADH). Any way it will
be discussed in pathology next year as the dr. said
Now there are 2 types of diabetes mellitus:
Type 1 diabetes (insulin-dependent diabetes mellitus):
1.
2.
3.
4.
5.
6.
7.
8.
Usually genetic.
Appear in children and may be babies
Result from pathology of the islet β cells of pancreas.
They have normal body weight.
Little or no insulin in plasma of these patients
As a consequence there is increase in insulin level in the plasma
High glucose in plasma: hyper glycemia
They have normal insulin sensitivity.
Type 2 diabetes (non-insulin-dependent diabetes mellitus, maturity(obesity)onset diabetes mellitus):
1. Might be occurring coz of genetic but that would be very rare and does not
represent the general case of this type.
2. There is insulin ( and some times high level of it in blood) but there is some
abnormality in the insulin receptors (either these receptors are structurally
abnormal or decreased in number)
3. Occur mostly after the age of 40 and increasingly common with age(in obese old
age and sometimes in young people)
4. Type 2 diabetics are almost always over-weight, weight control is very imp in
these patients coz obesity alone coq the insulin receptors to become less
sensitive to insulin.
5. High plasma glucose , reduced sensitivity
6. These patients to produce more insulin they take some kind of tablets that
stimulate more and more secretion of insulin and even they may use insulin
directly to normalize blood glucose level.
7. These diabetics are usually not organized people, they eat everything and
anything (like mansaf and konafa).
Obesity
Obesity is a medical condition, the weight is 20 percent above the desired weight ,in
which excess body fat has accumulated to the extent that it may have an adverse effect
on health, leading to reduced life expectancy and/or increased health problems.
Now there is two ways to now if you are obese or not


First by body mass index:
Body mass index (BMI),is a measurement which compares weight and height,
defines people as overweight (pre-obese) if their BMI is below 25 :normal
,between (25 – 30) kg/m2 :overweight , and obese if it is greater than 30 kg/m2.
We can calculate it by dividing the weight over square the height(in meters)

Second is by measuring the waist circumference and it must be less than half of
your height.
Also this way is very simple it still very imp coz the most dangerous obesity
resides in waist ,it kills.
Obesity depends on the size of cells not their number.
Now let’s talk about the risks of being obese
1. cardiovascular disease
2. hypertension
3. pulmonary diseases
4. non-insulin dependent diabetes mellitus (type 2 diabetes)
5. varicose veins
6. gallbladder diseases
7. cancers: eg.breast,uterus.
Glucagon

Glucagon is a hormone , secreted by alpha cells of the pancreas that raises
blood glucose levels its effect is opposite that of insulin, which lowers blood
glucose levels.



Its main effect is on the liver (the most important organ in glucose homeostasis),
causes the liver to convert stored glycogen into glucose, which is released into
the bloodstream.
Glucagon also stimulates the release of insulin, so that glucose can be taken up
and used by the tissues.
Actions of glucagon on the target tissues are:
1- glycogenolysis in the liver
2- inhibition of glycogen synthesis in the liver
3- gluconeogenesis in the liver
4- lipolysis in adipose tissue
5- stimulation of insulin release from the β cells of pancreas
6- stimulation of catacolamin release
7- positive inotropic effect on the heart
Just to clarify some of the terms above:
Glycogenolysis (also known as "Glycogenlysis") is the conversion of glycogen polymers
to glucose monomers.
Gluconeogenesis: The formation of glucose, especially by the liver, from noncarbohydrate
sources, such as amino acids. Also called glyconeogenesis.
Lipolysis: the breakdown, splitting up or decomposition of fat.
Inotropic affect: affecting the force of muscular contractions; commonly applied to drugs that
increase contractility of cardiac muscle.
 stimulatory factors of glucagon are :
1)
2)
3)
4)



hypoglycemia
increase in amino acid concentration
epinephrine and norepinephrine
acetylcholine
inhibitors factors are:
1. insulin
2. somatostatin
3. increase fatty acid concentration
we should know that it’s the most potent hyperglycemic hormone (other
hyperglycemic hormones are GH,cortisol,adrenaline and thyroid hormones)
In exercise glucose is high, insulin is low.


maximum carbs concentration is 700gm,mainly in the liver and muscle
cells,that’s the problem that the body doesn’t have high level of carbs .
study the figure in the last slides I guess to know about the role of the liver as
well as the glucose coming from and to the liver and other cells.
done by : siraj al-3nizi