ENDOCRINE PANCREAS

DIFFERENCE BETWEEN EXOCRINE AND ENDOCRINE GLANDS

Secrete their essential product by way of a duct to some environment external to itself, either inside the body or on a surface of the body.

EXAMPLES• Salivary Glands• Tear Glands• Anal Glands• Stomach Pit

Secrete their products, hormones, directly into the blood rather than through a duct.

EXAMPLES• Pituitary Gland,• Pineal Gland,• Thyroid Gland,• Adrenal Gland,• Pancreas,• Testes &Ovary, etc,. 

• Glandular Organ• Size: 6-9 inches• Weight: 3 ounces (85 gm)• Position: partially behind the stomach• Color: Grayish-pink• STRUCTURE Head concavity of

duodenum Body base if

stomach Tail abutting the

spleen

• HETEROCRINE GLAND

Exocrine Tissue Endocrine Tissue99%

1%

MICROSCOPIC ANATOMY

HORMONES OF ENDOCRINE PANCREAS

α alpha cells secrete glucagon (increase glucose in blood),β beta cells secrete insulin (decrease glucose in blood),Δ delta cells secrete somatostatin (regulates/stops α and β cells) andPP cells, or γ (gamma) cells, secrete pancreatic polypeptide

MECHANISM OF GLUCAGON ACTION

• Main target tissues: liver, muscle, and adipose tissue• Glucagon prevents hypoglycemia by cell production

of glucose• Liver is primary target to maintain blood glucose levels Gluconeogenesis Glycogenolysis

REGULATION OF GLUCAGON INCREASE• Increased blood glucose levels inhibit glucagon release.• Amino acids stimulate glucagon release (high protein,

low carbohydrate meal).• Stress: epinephrine acts on alpha cells, increasing

glucagon release (increases availability of glucose for energy).• Insulin inhibits glucagon secretion.

INSULIN FROM BETA CELLS• ACTS ON TISSUES (ESPECIALLY LIVER, SKELETAL MUSCLE, ADIPOSE) TO

INCREASE UPTAKE OF GLUCOSE AND AMINO ACIDS.

• WITHOUT INSULIN, MOST TISSUES DO NOT TAKE IN GLUCOSE AND AMINO ACIDS WELL

REGULATION OF INSULIN RELEASE

• MAJOR STIMULUS: INCREASED BLOOD GLUCOSE LEVELS

• AFTER A MEAL, BLOOD GLUCOSE INCREASES

• IN RESPONSE TO INCREASED GLUCOSE, INSULIN IS RELEASED

• INSULIN CAUSES UPTAKE OF GLUCOSE INTO TISSUES, SO BLOOD GLUCOSE LEVELS DECREASE.

• INSULIN LEVELS DECLINE AS BLOOD GLUCOSE DECLINES

Glucose homeostasis

Figure 26.8

Insulin

Beta cellsof pancreas stimulatedto release insulin intothe blood

Bodycellstake up moreglucose

Blood glucose leveldeclines to a set point;stimulus for insulinrelease diminishes

Liver takesup glucoseand stores it asglycogen

High bloodglucose level

STIMULUS:Rising blood glucoselevel (e.g., after eatinga carbohydrate-richmeal) Homeostasis: Normal blood glucose

level(about 90 mg/100 mL)

STIMULUS:Declining bloodglucose level(e.g., afterskipping a meal)

Alphacells ofpancreas stimulatedto release glucagoninto the blood

Glucagon

Liverbreaks downglycogen and releases glucoseto the blood

Blood glucose levelrises to set point;stimulus for glucagonrelease diminishes

Type I Diabetes Mellitus IDDM b cells of the islets of Langerhans are destroyed by autoimmune

attack which may be provoked by environmental agent.Glucose cannot enter the adipose cells.Increased blood [glucagon].

TYPE II DIABETES MELLITUS NIDDMSlow to develop.Genetic factors are significant.Occurs most often in people who are overweight.Decreased sensitivity to insulin or an insulin resistance.

GESTATIONAL DIABETESSome pregnant women require more insulin than their body can produce.

IMPAIRED GLUCOSE TOLERANCE AND PREDIABETESIt is a condition in which blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes. Patients are at high risk of developing type 2 diabetes.

INSULINOMA

SOMATOSTATINSecreted by D cells of the pancreatic islets.Inhibits the secretion of several hormones including GH, TSH, Insulin, Glucagon and gastrinProduces decrease in blood glucose concentration

PANCREATIC POLYPEPTIDESecreted by PP cells in the endocrine pancreas predominantly in the head of the pancreasTriggered by protein rich meals, fasting, exercise, and acute hypoglycemia.Inhibited by SomatostatinExact biological role is uncertainPhysiological effect: Inhibition of contraction of gall bladder & pancreatic enzyme secretion.