glucose the life saver

1. INSULIN REGULATION AND METABOLISM

2.  When insulin is secreted into the blood , it
circulates almost entirely in an unbound form ,
because it has a plasma half life of approximately 6
minutes it is cleared from the circulation.
Within 10 to 15 minutes, insulin that is not bound
with receptors in the target cell is degraded by the
enzyme.
Insulin is mainly in the liver to a lesser extent in the
kidneys and muscles and slightly in
most other tissues.

3. INSULIN RECEPTOR

4.  Combination of four subunits held together by disulphide
 two extracellular alpha subunits lie entirely outside the
cell, has insulin-binding site.
 Two trans-membrane beta subunits penetrate through
the membrane, protruding into the cytoplasm.
 Tyrosine kinase protein kinase is an example of enzyme-
linked receptor.
 Tyrosine kinase, in turn, causes phosphorylation of
multiple other intracellular enzymes, including a group
called insulin receptor substrate (IRS)

5. INSULIN SIGNALING

6.  Insulin binding to its receptor stimulates intrinsic tyrosine
kinase activity, leading to receptor auto-phosphorylation
and the recruitment of intracellular signaling molecules
such as insulin receptor substrates.
 IRS and other adaptor proteins initiate a complex cascade
of phosphorylation and de-phosphorylation reactions,
resulting in the widespread metabolic and mitogenic
effects of insulin.

7.  Activation of phosphodiacetyl-3-kinase pathway
stimulates translocation of glucose transporters to the
cell surface.
 Activation of other insulin receptor signaling pathways
induces glycosine synthesis, protein synthesis,
lipogenesis, and regulation of various genes.

8. REGULATION OF INSULIN SECRETION

9.  CHEMICAL REGULATION
 mainly by glucose entry in the cell, other nutrients, amino
acids, fatty acids, and ketone bodies.
 Note :- glucose induces a brief pulse of insulin output
within two minutes.
 Glucose and other nutrients are more effective when
given orally than cause they generate chemical signals in
creatins from the gut which acts directly on beta cells.
 Immediate release of insulin.

10. β - CELLS
D - CELLS
α - CELLS
 HORMONAL REGULATION
 intra-isolate paracrine interactions between the hormones
produces by isolates of Langerhans.
GLUCAGON SOMATOSTATIN

11.  NEURAL REGULATION
Isolated of the Lung or Hands are the richly innervated by
both Adrenergic and the cholinergic Nerve.
α -2 Adrenergic Receptors inhibit the Insulin release.
β-2 Adrenergic and the Vagal Nerve enhance the Insulin
release.
Note, any condition that activate the sympathetic branch of
the Anus, such as the Hypoxia. Hypoglycemia, Hypothalmia
separates the secretion of the Insulin by the extubation of the
α -2 receptor.

12.  CONTENT :-
 Growth hormone corticosteroids thyroxine modify insulin
release in respone to glucose.
 PGE has shown to inhibit insulin release.

13. EFFECTS OF INSULIN

14.  Immediately after a high carbohydrate meal, the
high blood pressure glucose causes the rapid
secretion of the insulin.
 The insulin in turn causes rapid uptake, storage, and
use of glucose by almost all tissues of the body, but
especially by the muscles, adipose tissue, and the
liver.

15.  EFFECTS OF INSULIN ON THE MUSCLE
 Insulin promotes muscle glucose uptake and
metabolism.
 during much of the day , muscle tissue depends not on
the glucose, but on the fatty acid for its energy.
 The resting muscle membrane is only slightly
permeable to the glucose without the influence of
insulin.

16.  Under the two conditions, the muscle do use large
amount of the glucose.
1. During the moderate or the heavy exercise, the exercise
muscle fiber become more permeable to the glucose.
These usage of the glucose does not require large
amount of the insulin, because insulin contraction
increase. Transportation of the glucose transporter 4,
GLUT4, from the intracellular storage depend to the cell
membrane, which in turn facilitate diffusion of the
glucose into the cell.
2. Second, during the few hours after a meal, the blood
glucose concentration is high, and the pancreas is
secreting large quantity of insulin, causing the rapid
transport of the glucose into the muscle.

17.  EFFECTS OF THE INSULIN ON THE LIVER
1. Insulin inactivates the liver phosphorylase, the
principal enzyme that causes liver glycogen to split into
the glucose. This inactivation prevents breakdown of the
glycogen that has been started in the glucose.
2. Insulin enhances uptake of glucose from the blood by
the liver cell by increasing the activity of the enzyme
glucokinase.

18. 3. Insulin stimulates glycogen synthesis, which
promotes the glycogen synthesis.
4. In the liver, insulin decreases the rate of
gluconeogenesis by decreasing the activity of the
enzyme that promotes gluconeogenesis.

19. EFFECTS OF THE INSULIN ON THE ADIPOSE
TISSUE
Insulin has other essential effects that are required for
the fat storage in the Adipose Tissue.
1. Insulin inhibits the effect of the hormone sensitive
lipase that causes hydrolysis of the triglycerides stored in
the fat cell.
This inhibits the release of the fatty acid from the
Adipose Tissue into the circulating blood.

20. 3.Insulin promotes triglyceride formation in the liver cell that
is transported to the Adipose Tissue and deposited there.
4. Insulin increases the transport of the K plus ion into the
Adipose Tissue cell
2.Insulin promotes glucose transport through a cell
membrane into a fat cell. Similar to the muscle cell, some of
this glucose is then used to synthesize a minute amount of
the fatty acid.

21. Effect of the insulin deficiency on the fat and protein
metabolism
This occurs even normally between male when the secretion of insulin is
minimal, but it becomes extreme in the diabetes melitus when the
secretion of insulin is almost zero.
1. Insulin deficiency causes lipolysis of the storage fat and the release of
free fatty acids. This is because the enzyme hormone sensitive lipase in
the fat cell becomes strongly activated.
2. Insulin deficiency increases plasma cholesterol in the lipid
concentration. These two substances are discharged into the blood
along with the excess triglyceride form. The high concentration of
cholesterol promotes the development of atherosclerosis in people with
several diabetes.

22. 3. Insulin deficiency causes protein depletion and the
increased plasma amino acid. Virtually all protein
storage comes to a halt when insulin is not available.
The catabolism of the protein increases, protein
synthesis is stopped, and large quantities of the amino
acids are jumped into the plasma.

23. EFFECT OF THE INSULIN ON GROWTH
1. It may alter cellular nutrition to increase nutrient
uptake and the utilization.
2. Insulin may exert a direct anabolic action via either the
insulin or type 1 IgF receptor.
3. Insulin may modulate the release of the IgF or other
growth factor from the fetal tissue.

24.  Insulin has a physiological inhibitory effect on the
growth hormone releasing in the healthy human.
Insulin is therefore a physiological regulator of
the fetal growth and acts in part by stimulating
the cellular uptake of the glucose and its
preferential use for oxidation metabolism in the
fetal tissue.
 GH antagonizes insulin acts via the various
molecular pathways.