SYNTHESIZING

INSULIN
Ngan Nguyen
Period: 4th
25 March 2015

WHAT IS INSULIN?
a chemical transported in the blood that controls

and regulates the activity of certain cells or in the

body
a hormone that regulates the amount of glucose

(sugar) in the blood

release a small amount of insulin into the body

EFFECT OF INSULIN
Feeling extreme thirst or hunger
Burry vision
Damage your nerves and kidneys
Low blood sugar
Fast heartbeat
Slowed healing of bruises

STRUCTURES OF INSULIN
The primary structure of insulin is made from two polypeptide
chains named subunit A and B. Subunit A consists of 21 amino
acids, whereas subunit B consists of 30 amino acids. These
chains are connected by two disulfide bridges. Insulin also
forms quaternary structure by creating diamers using
hydrogen bonds and hexamers by bonding with two zinc ions
(Bowen, 1999). Insulin The final product of insulin only
consists of 51 amino acids so it is quite small compared to
other proteins. Insulin's small size allows it to be a ligand for
other proteins appropriately named insulin receptors.

MECHANISM OF INSULIN ACTION

S Y N T H E S I S O F I N S U LI N
Two inactive precursors -> cleaved to form the
active hormone plus the C-peptide
C-peptide -> essential for proper insulin folding

I M P O RTA N T O F I N S U L I N
Without insulin, the blood glucose builds up in the
blood and the cells are starved of their energy
source.
Ketones can poison and kills cells if they build up
in the body over an extended period of time.
Can lead to serious illness or coma.

USEFULNESS
Help control the blood sugar
Help move blood sugar from blood stream into
cells
Cell in body change the food ingested into energy
Stimulate the live and muscle cells to take up
glucose from the blood

FUTURE
RESEARCH/DEVELOPMEN
T
Called glycemic awareness
Increased awareness of the exact blood glucose level
Strongly affected by local variables as site and depth of

injection ( heat of the skin, exercise of the muscle, etc)

Make all open-loop systems intrinsically inferior
insulin was first synthesized, diabetics needed to regularly

inject the liquid insulin with a syringe directly into their

bloodstream

A RT I F I C I A L S W E E T E N E R S
AFFECTS INSULIN LEVEL
The researcher want to determine whether insulin or blood sugar levels are affected

by the combination of sucralose and glucose.

Insulin levels also rose about 20 percent higher.
It could be detrimental because when people constantly secrete high levels of

insulin it can lead to type 2 diabetes.

Consuming artificial sweeteners could make people put on weight because

experiments on laboratory rats showed that those eating food sweetened with
artificial sweeteners ate more calories than their counterparts whose food was
sweetened with normal sugar.

I N S U L I N R E S I S TA N C E I N
U R E M I A M E D I AT E D BY P O S T
BINDING DEFECTS
The relative contributions of insulin binding versus post binding defects to this insulin

resistance are not known. Because insulin normally requires only a small portion of its receptors
to exert maximal biological effects on glucose uptake.
If post binding defects are present, however, then a decreased insulin response would be

expected at high insulin concentrations.

The steady state plasma insulin concentrations during the four insulin infusion protocols in the

uremic subjects were consistently higher than in the controls.

These results indicate that the in vivo dose-response curve relating plasma insulin

concentration to glucose metabolism was shifted to the right in uremic and failed to
normalize at high insulin levels.

U N D E R S TAN D I N G I T S AC T I O N
I N H E A LTH AN D D I S E A S E
The results of pancreas extirpation and pancreas grafting are best explained by
supposing that the islet tissue produce an Autacoid which passes into the blood stream
and effects carbohydrate metabolism and carbohydrate storage in such a manner that
there is no undue accumulation of glucose in the blood. Provisionally it will be
convenient to refer to this hypothetical substance as insuline.
Insulin is the prime controller of this process. When fasting hyperglycaemia
develops, as in diabetes mellitus, it could result from either over production of
glucose, through excess glycogenolysis and gluconeogenesis, or a failure of adequate
glucose uptake in the peripheral tissues (including the brain).