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College of pharmacy
Insulin
Prepared by
*karmand salih
*Miran mustafa
*Niga taymoor
*Frishta Ahmad
*Nigar muhammad
*Hawar Ezzat

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Introduction
Insulinis apeptid hormon, produced by beta cell of the pancreas , and is
central to regulating carbohydrate and fat metabolism in the body. Insulin
causes cells in the liver, skeletal muscle, and fat tissue to absorb glucose
from the blood. In the liver and skeletal muscles, glucose is stored as
glycogen, and in fat cells (adipocytes) it is stored as triglycerides.
Insulin is produced in the pancreas and released when any of several
stimuli are detected,, These stimuli include ingested protein and glucose
in the blood produced from digested food.,Insulin initiates a signal
transduction, which has the effect of increasing glucose uptake and
storage. Finally, insulin is degraded, terminating the response.
insulin is provided within the body in a constant proportion to remove
excess glucose from the blood, which otherwise would be toxic. When
blood glucose levels fall below a certain level, the body begins to use
stored sugar as an energy source through glycogenolysis, which breaks
down the glycogen stored in the liver and muscles into glucose, which
can then be utilized as an energy source. As a central metabolic control
mechanism,
Diabetes mellitus, or simply diabetes, is a group of metabolic diseases in
which a person has high blood sugar, either because the pancreas does not
produce enough insulin, or because cells do not respond to the insulin that
is produced, This high blood sugar produces the classical symptoms of
polyuria (frequent urination), polydipsia (increased thirst) and
polyphagia (increased hunger)
Type 1 DM results from the body's failure to produce insulin, and
currently requires the person to inject insulin or wear an insulin pump.
This form was previously referred to as "insulin-dependent diabetes
mellitus" (IDDM) or "juvenile diabetes".
Type 2 DMresults from insulin resistancea condition in which cells fail
to use insulin properly, sometimes combined with an absolute insulin
deficiency. This form was previously referred to as non insulin-dependent
diabetes mellitus (NIDDM) or "adult-onset diabetes
The third main form, gestational diabetes occurs when pregnant women
without a previous diagnosis of diabetes develop a high blood glucose
level. It may precede development of type 2 DM.

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Insulin stops the use of fat as an energy source by inhibiting the release
of glucagon With the exception of the metabolic disorder diabetes
mellitus and metabolic syndrome..
Biosynthesis of Insulin
Insulin is synthesized in significant quantities only in beta cells in the
pancreas. The insulin mRNA is translated as a single chain precursor
called preproinsulin, and removal of its signal peptide during insertion
into the endoplasmic reticulum generates proinsulin.
Proinsulin consists of three domains: an amino-terminal B chain, a
carboxy-terminal A chain and a connecting peptide in the middle known
as the C peptide. Within the endoplasmic reticulum, proinsulin is exposed
to several specific endopeptidases which excise the C peptide, thereby
generating the mature form of insulin. Insulin and free C peptide are
packaged in the Golgi into secretory granules which accumulate in the
cytoplasm.
When the beta cell is appropriately stimulated, insulin is secreted from
the cell by exocytosis and diffuses into islet capillary blood. C peptide is
also secreted into blood, but has no known biological activity.

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Hypoglycemia
is an abnormally diminished content of glucose in the blood, The term
literally means "low sugar blood".,It can produce a variety of
symptomsand effects but the principal problems arise from an inadequate
supply of glucose to the brain,, resulting in impairment of function
(neuroglycopenia)., Effects can range from mild dysphoria to more
serious issues such as seizures, unconsciousness, and (rarely) permanent
brain damage or death
The most common forms of hypoglycemia occur as a complication of
treatment of diabetes mellitus with insulin or oral medications.
Hypoglycemia is treated by restoring the blood glucose level to normal
by the ingestion or administration of dextrose or carbohydrate foods. In
more severe circumstances, it is treated by injection or infusion of
glucagon.,Recurrent hypoglycemia may be prevented by reversing or
removing the underlying cause, by increasing the frequency of meals,
with medications like diazoxide, octreotide, or glucocorticoids, or by
surgical removal of much of the pancreas.
Oral Hypoglycemic Agent: Oral hypoglycemic drugs are used only in the
treatment of type 2 diabetes which is a disorder involving resistance to
secreted insulin. Type 1 diabetes involves a lack of insulin and requires
insulin for treatment.Oral hypoglycemic agents include
1-Biguanides
2-Prandial glucose regulator: Example(Repaglinide)
3-SulfonylureasType :
a-first generationExample: (Chlorpropamide,Tolbutamide)
b-Second generationExample : (Gliclazide,Glibenclamide,Glipizide)
c-Third generation Example : ( Glimepiride)
4--α- glucosidase inhibitors Example : (Acarbose)
5-Thiazolidinediones Example : (Rosiglitazone,Pioglitazone)

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Discussion
In this experiment we wont to know the effect of insulin on a mouse
which was fasted for 24 hrs & the effect of Glucagon ,Also to know the
effect of glucose on a mouse which was take adequat nutrent .
When we inject the 6 IU of insulin by i.p in to the mouse which was
fasted for 24 hrs the sing and symtom of hypoglycemia was apear
such as hunger ,tachycardia ,tremor,convulsion, Hypoglycemia
occurs when your blood sugar (glucose) level falls too lowbecause the
mouse was fasted so the level of glucose was decreased
And insulin it self decrease the glucose, Insulin inhibits breakdown
of triglycerides in adipose tissue and gluconeogenesis in the liver.
Insulin acts on target cell via membrane-bound tetrameric
receptorwith tyrosine kinase activity
When we observe the symptom of convulsion we inject the glucagon
to increase the blood glucose and return the mouse to normal the
mechanism of action of glucagon is
Glucagon binds to the glucagon receptor, a G protein-coupled receptor,
located in the plasma membrane. The conformation change in the
receptor activates G proteins, a heterotrimeric protein with α, β, and γ
subunits. When the G protein interacts with the receptor, it undergoes a
conformational change that results in the replacement of the GDP
molecule that was bound to the α subunit with a GTP molecule. This
substitution results in the releasing of the α subunit from the β and γ
subunits. The alpha subunit specifically activates the next enzyme in the
cascade, adenylate cyclase.
Adenylate cyclase manufactures cyclic adenosine monophosphate (cyclic
AMP or cAMP), which activates protein kinase A (cAMP-dependent
protein kinase). This enzyme, in turn, activates phosphorylase
kinase,which, in turn, phosphorylates glycogen phosphorylase, converting
into the active form called phosphorylase A. Phosphorylase A is the
enzyme responsible for the release of glucose-1-phosphate from
glycogen polymers
When we inject glucose to the mouse which was taked adequat nutrent
the sing of hyperglycemia was apear such as tachycardia

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The result was not good this is may be because of :
*mouse may not be fasted
*Site of administration
*packaging of drug