End Pancreas

Endocrine pancreas
‫بان جابر‬.‫د‬.‫م‬.‫أ‬
Pancreas is a gland, which has both
exocrine and endocrine cells, located
behind the stomach.
 1.Acinar cells produce an enzyme-rich

juice used for digestion (exocrine
product)
 2. Pancreatic islets (islets of

langerhans),1- 2 million islets in humans
islets of langerhans: include:
 •Beta (β) cells produce INSULIN
 • Alpha (α) cells produce GLUCAGON
 • Delta (δ) cells produce SOMATOSTATIN
 • F cells produce PANCREATIC POLYPEPTIDE
Insulin is a protein hormone composed from two
chains linked by disulfide bonds.
It synthesized as Preprohormone
During packaging in granules by golgi, proinsulin is
cleaved into insulin and C peptide.
C peptide had no biological activity, but secreted in
equimolar ratio with Insulin , Hence its
concentration in plasma directly reflects β–cells
activity.
Regulation of insulin secretion
Mechanism of glucose induced insulin
secretion
Mechanism of action insulin
Physiological actions of insulin
 1.On carbohydrate metabolism :
a. liver • Promotes glucose storage as glycogen
• Inhibits glycogenolysis
• Inhibits gluconeogenesis
b. muscle • Stimulates glucose uptake (GLUT4)
• Promotes glucose storage as glycogen
c. adipose tissue
• Stimulates glucose transport into adipocytes
• Promotes the conversion of glucose into
triglycerides and fatty acids
“ANTI-DIABETOGENIC”
2. On protein metabolism
• Facilitates amino acids entry into muscle cell
•Facilitates protein synthesis in ribosomes
• Inhibits proteolysis by decreasing lysosomal
activity.
3. On fat metabolism:
a. liver
• Anti ketogenic & Lipogenic
b. In fat cell
• Promotes storage of fat
• Inhibits lipolysis
• Promotes lipogenesis
4. On plasma k+ concentration
• Facilitates rapid entry of K+ into cell by
simulating Na-K ATPase activity .
Effects of Insulin: Insulin is an anabolic

hormone and its net effect is storage of
carbohydrates, proteins and fat. Therefore, it is
called Hormone of Abundance.
Glucagon
 Polypeptide hormone that is a potent
hyperglycemic agent .Produced by α cells
in the pancreas
Physiological actions of glucagon
•Stimulates glycogenolysis,
gluconeogenesis & inhibits glycogenesis
•Promotes lipolysis &ketogenesis
•Increases calorigenesis.
This hormone is secreted from:
1. Hypothalamus as hormone which inhibits growth hormone
secretion. Somatostatin is the same chemical
substance as growth hormone inhibitory hormone that is secreted in
the hypothalamus
2. D cells (δ-cells) in islets of Langerhans of pancreas
3. D cells in stomach and upper part of small intestine.
Somatostatin secretion is affected by same factors stimulating

insulin secretion
Functions:
•Inhibits secretion of insulin & glucagon
•Inhibits GI motility* & GI secretions
•Regulates feedback control of gastric emptying
 It Secreted from F cells of pancreas.
 It is a Polypeptide hormone Secreted in
response to food intake
 • Inhibits exocrine pancreatic secretion

 • Slows the absorption of food from the GI
tract.
DM
Is defined as a clinical syndrome characterized by sustained hyperglycemia
which may result due to lack of insulin secretion or to an excess of factors
that oppose its action. It may result from many environmental and
genetic factors often acting jointly. These abnormalities lead to
abnormalities in carbohydrate, protein and fat metabolism. Its major
effects include characteristic symptoms, ketoacidosis, progressive
microvascular diseases of retina and kidney, damage to peripheral nerves
and excessive arteriosclerosis.

The cardinal signs of DM are:
1.Hyperglycaemia:
- due to absence of effects of insulin.

2.Glucosuria: i.e loss of glucose in urine.
- when the blood glucose level becomes >
renal threshold (180 mg%).
3.Polyuria due to:
a)Excretion of glucose in urine.
b) osmotic pressure
of the blood drags water out of the cells towards the blood.
-This causes dehydration of the tissue cells.
4.Polydepsia:intense thirst due to dehydration.
5. Acidosis:
- Due to inhibition of carbohydrate
metabolism.
-The body depends on the fat metabolism
which supplies most of the energy needed.
-Uncontrolled diabetes  accumulation of
acetoacetic acid and beta hydroxybuteric
acid  acidosis.
6.Loss of weight and asthenia:
-Due to mobilization of fat and proteins for supply of energy.
7. cholesterol and TG in blood:

-early development of arteriosclerosis.
-8-Polyphagia – decreased activity of

- satiety center removes its inhibitory
- effect on feeding center in brain
Diagnosis
 • Demonstrating persistent hyperglycemia & glycosuria
 •Oral Glucose Tolerance Test (GTT)
 • Estimation of Fasting Blood Glucose (FBS) - Increase FBS in

more than two occasions confirms DM.
 HbA1c ??
Glycosylated Haemoglobin: When plasma glucose is episodically
elevated over time, small amounts of hemoglobin A is glycosylated
by non-enzymatic pathway to form HbAlc. Level of HbAlc is an index
of control of diabetes for 6 - 10 weeks before measurement.
 Treatment
 • Insulin therapy
 • Oral hypoglycemic agents
 • Life style modifications
Complications
• Microvascular – diabetic retinopathy,
diabetic nephropathy
• Macrovascular – Myocardial Infarction &
Stroke
• Diabetic neuropathy
• Chronic ulcer & gangrene formation due
to decreased resistance to infection

End Pancreas

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End Pancreas

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Endocrine pancreas

 1.Acinar cells produce an enzyme-rich

 2. Pancreatic islets (islets of

Effects of Insulin: Insulin is an anabolic

Somatostatin secretion is affected by same factors stimulating

 • Inhibits exocrine pancreatic secretion

Is defined as a clinical syndrome characterized by sustained hyperglycemia

which may result due to lack of insulin secretion or to an excess of factors

genetic factors often acting jointly. These abnormalities lead to

abnormalities in carbohydrate, protein and fat metabolism. Its major

effects include characteristic symptoms, ketoacidosis, progressive

microvascular diseases of retina and kidney, damage to peripheral nerves

and excessive arteriosclerosis.

- due to absence of effects of insulin.

-The body depends on the fat metabolism

which supplies most of the energy needed.

-Uncontrolled diabetes  accumulation of

acetoacetic acid and beta hydroxybuteric

7. cholesterol and TG in blood:

-8-Polyphagia – decreased activity of

 •Oral Glucose Tolerance Test (GTT)

 • Estimation of Fasting Blood Glucose (FBS) - Increase FBS in

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