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GOVERNMENT HOMOEOPATHIC
MEDICAL COLLEGE AND HOSPITAL
BHOPAL (M.P.)
TOPIC
ENDOCRINE
FUNCTIONS OF PANCREAS
DATE: 27-02-2019 TIME :4:30pm TO 5:30pm
GUIDED BY:
DR. PREMNIDHAN PAL CHOWDHURY
(H.O.D. PHYSIOLOGY)
LECTURE DELIVERED BY:
DR.SANDEEP SINGH
(BHMS, PG SCHOLAR) Mob no. 9340034627
email id:
singh.sandeep659@gmail.com
ENDOCRINE FUNCTION OF
PANCREAS
INSULIN
GLUCAGON
SOMATOSTATIN
INTRODUCTION
The pancreas is about 6 inches long
and sits across the back of the
abdomen, behind the stomach in the
upper left abdomen. The head of the
pancreas is on the right side of the
abdomen and is connected to the
duodenum (the first section of the
small intestine) through a small tube
called the pancreatic duct. The
narrow end of the pancreas, called the
tail, extends to the left side of the
body.
Functions of the Pancreas
 Exocrine Function:
 The pancreas contains exocrine glands that
produce enzymes important to digestion. These
enzymes include TRYPSIN and CHYMOTRYPSIN
proteins; AMYLASE carbohydrates; and LIPASE
to break down fats.
 Endocrine Function:
 The endocrine component of the pancreas
consists of islet cells (islets of Langerhans)
that create and release
important hormones directly into the
bloodstream.
ISLET OF LANGERHANS
HUMAN PANCREAS CONTAIN ABOUT ONE TO
TWO MILLIONS ISLETS CELL
THERE ARE FOUR TYPE OF ISLETS OF
LANGERHANS
 Alpha-cells or α-cells SECRETE GLUCAGON
Beta cells (β cells) SECRET INSULIN
Delta cells (δ-cells or D cells) SECRETE
SOMATOSTATIN
F CELLS OR PP CELLS SECRETE PANCREATIC
POLYPEPTIDE
INSULIN
SOURCE OF SECRETION
BETA CELLS OF ISLETS OF LANGERHANS
CHEMISTRY ANDHALF LIFE
IT IS A POLYPEPTIDE WITH 51 AMINO ACIDS BIOLOGICAL
HALF LIFE IS 5 MINUTES
the time required for the body to eliminate half of an
administered dose of any substance by regular physiological
processes
SYNTHESIS
IT IS SYNTHESISED IN ROUGH ENDOPLASMIC
RETICULUM OF BETA CELLS.
PREPROINSULIN PROINSULIN INSULIN
METABOLISM
IT IS DEGRADED IN LIVER AND KIDNEY BY CELLULAR ENZYME
CALLED INSULIN PROTEASE.
ACTION OF INSULIN
ON CARBOHYDRATE METABOLISM
IT IS THE ONLY ANTI DIABETIC HORMONE SECRETED IN
BODY ,I.E. IT REDUCES BLOOD GLUCOSE LEVEL BY
FOLLOWING ACTION
--INCREASE THE TRANSPORT AND UPTAKE OF GLUCOSE BY
CELLS:
INSULIN FASCILITATESTHE TRANSPORT OF GLUCOSE FROM
BLOOD INTO THE CELLS BY INCREASING THE PERMEABILITY
OF CELL MEMBRANE TO GLUCOSE. GLUCOSE IS
TRANSPORTED IN CELLS BY THE HELP OF GLUCOSE
TRANSPORTERS ( GLUT).
GLUT 4 IS INSULIN SENSITIVE AND IS LOCATED IN
CYTOPLASMIC VESICLES.
WHEN INSULIN RECEPTOR COMPLEX IS
FORMED IN THE MEMBRANE OF CELL
THE GLUT4 ARE ATTRACTED TOWARDS
THE MEMBRANE AND GLUT4 IS
RELEASED INTO THE MEMBRANE. NOW
IT STARTS TRANSPORTING GLUCOSE
MOLECULE FROM EXTRACELLULAR
FLUID INTO CELLS.
CELLS WHERE GLUCOSE IS METABOLISED
( LIVER, MUSCLE, AND ADIPOSE TISSUE )
WHERE NOT METABOLISED ( BRAIN
EXCEPT HYPOTHALAMUS, RENAL
TUBULES, MUCOUS MEMBRANE OF
INTESTINE, RBCs.
1. PROMOTES PHERIPHERAL UTILIZATION
OF GLUCOSE
2. PROMOTES STORAGE OF GLUCOSE-
GLYCOGENESIS STORAGE OF GLUCOSE
INTO GLYCOGEN IN MUSCLES AND
LIVER
3. INHIBTS GLYCOGENOLYSIS.
BREAKDOWN OF GLYCOGEN INTO
GLUCOSE
4. INHIBITS GLUCONEOGENSIS:
FORMATION OF GLUCOSE FROM
PROTEINS BY INHIBITING THE
RELEASE OF AMINO ACIDS.
ON PROTEIN MTABOLISM
IT INCREASE THE SYNTHESIS OF FATTY ACIDS
AND STORAGE OF PROTEIN AND INHIBITS THE
CELLULAR UTILIZATION OF PROTEINS BY:
 INCREASES THE PERMEABILTY OF CELL
MEMBRANE FOR AMINO ACID
PREVENT PROTEIN CATABOLISM
ON FAT METABOLISM
INSULIN STIMULATE THE SYNTHESIS OF FAT
AND STORAGE OF FAT
REGULATION OF INSULIN
SECRETION
ROLE OF BLOOD GLUCOSE LEVEL
ROLE OF PROTEIN
ROLE OF LIPID
ROLE OF GASTROINTESTINAL HORMONE
GASTRIN, SECRETIN
APPLIED PHYSIOLOGY
DEVELOPS DUE TODEFICIENCY OF HORMONE
INSULIN
TYPES
a) TYPE 1 DIEBETS MELLITUS: DUE TO DEFICIENCY
OF INSULIN DUE TO DESTRUCTION OF BETA
CELLS OF ISLETS F LANGERHANS. USUALLY
DEVELOPS BEFORE 40 YEARS OF AGE.
CAUSE ; VIRAL INFECTION, CONGENITAL
DISORDER,
AUTOIMMUNE DISEASE
b) TYPE 2 DIABETS MELLITUS : DUE TO INSULIN
RESISTANCE
CAUSE : GENETIC DISORDER, LIFE STYLE , STRESS.
SIGN AND SYMPTOMS OF
DIABETES MELLITUS
1. INCREASED BLOOD GLUCOSE LEVEL(NORMAL
80-100mg/dl) fasting
2. Loss of glucose in urine ( glucosuria)
3. Polyuria and polydipsia:
4. Polyphagia : intake of excessive food
5. Acetone BREATHING
6. KUSSMAUL BREATHING: INCREASE RATE
AND DEPTH OF RESPIRATION
7. COMA
COMPLICATION
1. HYPERTENSION
2. MYOCARDIAL INFARCTION
3. DIABETIC RETINOPATHY
4. DIABETIC NEPHROPATHY
5. DIABETIC NEUROPATHY
DIAGNOSTIC TEST
FASTING BLOOD GLUCOSE LEVEL
POSTPRANDIAL BLOOD GLUCOSE
GLUCOSE TOLERANCE TEST
GLYCOSYLATED HEMOGLOBIN
GLUCAGON
SOURCE OF SECRETION:
ALPHA CELLS OF ISLET OF LANGERHANS
CHEMISTRY AND HALF LIFE:
IT IS A POLYPEPTIDE CONTAIN 29 AMINO ACIDS.
HALF LIFE IS 3 TO 6 MINUTES.
METABOLISM:
ABOUT 30% DEGRADED IN LIVER AND 20% IN
KIDNEY. 50 % DEGREDED IN BLOOD BY
ENZYME SERINE AND CYSTEINE PROTEASES.
ACTION OF GLUCAGON
ON CARBOHYDRATE:
IT INCREASES THE BLOOD GLUCOSE LEVEL
BY INCRESING GLYCOGENOLYSIS
BY INCREASING GLUCONEOGENESIS
ON PROTEIN METABOLISM:
INCREASES THE TRANSPORT OF AMINO ACIDS
INTO LIVER CELLS.
ON FAT METABOLISM:
IT SHOWS LIPOLYTIC AND KETOGENIC ACTIONS.
KETOGENIC MEANS FORMATION OF KETONE
BODIES.
REGULATION OF GLUCAGON
SECRETION
ROLE OF BLOOD GLUCOSE LEVEL :
DECREASE IN BLOOD GLUCOSE LEVEL INCREASES THE
SECRETION
ROLE OF AMINO ACID LEVEL
INCREASE IN AMINO ACID INCREASE THE SECRETION
WHICH IN TURN INCREASE THE CONVERSION OF AMINO
ACID INTO GLUCOSE.
ROLE OF OTHER FACTOR
EXERCISE
STRESS
GASTRIN INCRESES THE SECRETION
CHOLECYSTOKININ
CORTISOL
FACTORS THAT INHIBITGLUCAGON SECRETION
ARE:
SOMATOSTATIN
INSULIN
FREE FATTY ACIDS
KETONES
SOMATOSTATIN
SECRETED FROM
HYPOTHALAMUS
D CELLS OF ISLETS OF LANGERHANS
D CELLS IN STOMACH AND UPPER PART OF SMALL
INTESTINE
CHEMISTRY & HALF LIFE:
IT IS A POLYPEPTIDE. AND HAVE HALF LIFE OF 2 TO 4
MIN.
METABOLISM:
DEGRADED IN LIVER
ACTION OF SOMATOSTATIN
INHIBIT BOTH GLUCAGON AND INSULIN
DECREASES THE MOTILITY OF STOMACH,
DUODENUM AND GALLBLADDER.
REDUCES SECRETION OF GASTRIC HORMONE
IT INHIBIT SECRETION OF GROWTH HORMONE
AND TSH FROM ANTERIOR PITUITARY.
THUS KNOWN AS
GROWTH HORMONE INHIBITORY HORMONE(
GHIH)
THANK YOU

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Pancreas

  • 1. GOVERNMENT HOMOEOPATHIC MEDICAL COLLEGE AND HOSPITAL BHOPAL (M.P.) TOPIC ENDOCRINE FUNCTIONS OF PANCREAS DATE: 27-02-2019 TIME :4:30pm TO 5:30pm
  • 2. GUIDED BY: DR. PREMNIDHAN PAL CHOWDHURY (H.O.D. PHYSIOLOGY) LECTURE DELIVERED BY: DR.SANDEEP SINGH (BHMS, PG SCHOLAR) Mob no. 9340034627 email id: singh.sandeep659@gmail.com
  • 4. INTRODUCTION The pancreas is about 6 inches long and sits across the back of the abdomen, behind the stomach in the upper left abdomen. The head of the pancreas is on the right side of the abdomen and is connected to the duodenum (the first section of the small intestine) through a small tube called the pancreatic duct. The narrow end of the pancreas, called the tail, extends to the left side of the body.
  • 5. Functions of the Pancreas  Exocrine Function:  The pancreas contains exocrine glands that produce enzymes important to digestion. These enzymes include TRYPSIN and CHYMOTRYPSIN proteins; AMYLASE carbohydrates; and LIPASE to break down fats.  Endocrine Function:  The endocrine component of the pancreas consists of islet cells (islets of Langerhans) that create and release important hormones directly into the bloodstream.
  • 6. ISLET OF LANGERHANS HUMAN PANCREAS CONTAIN ABOUT ONE TO TWO MILLIONS ISLETS CELL THERE ARE FOUR TYPE OF ISLETS OF LANGERHANS  Alpha-cells or α-cells SECRETE GLUCAGON Beta cells (β cells) SECRET INSULIN Delta cells (δ-cells or D cells) SECRETE SOMATOSTATIN F CELLS OR PP CELLS SECRETE PANCREATIC POLYPEPTIDE
  • 7. INSULIN SOURCE OF SECRETION BETA CELLS OF ISLETS OF LANGERHANS CHEMISTRY ANDHALF LIFE IT IS A POLYPEPTIDE WITH 51 AMINO ACIDS BIOLOGICAL HALF LIFE IS 5 MINUTES the time required for the body to eliminate half of an administered dose of any substance by regular physiological processes SYNTHESIS IT IS SYNTHESISED IN ROUGH ENDOPLASMIC RETICULUM OF BETA CELLS. PREPROINSULIN PROINSULIN INSULIN
  • 8. METABOLISM IT IS DEGRADED IN LIVER AND KIDNEY BY CELLULAR ENZYME CALLED INSULIN PROTEASE. ACTION OF INSULIN ON CARBOHYDRATE METABOLISM IT IS THE ONLY ANTI DIABETIC HORMONE SECRETED IN BODY ,I.E. IT REDUCES BLOOD GLUCOSE LEVEL BY FOLLOWING ACTION --INCREASE THE TRANSPORT AND UPTAKE OF GLUCOSE BY CELLS: INSULIN FASCILITATESTHE TRANSPORT OF GLUCOSE FROM BLOOD INTO THE CELLS BY INCREASING THE PERMEABILITY OF CELL MEMBRANE TO GLUCOSE. GLUCOSE IS TRANSPORTED IN CELLS BY THE HELP OF GLUCOSE TRANSPORTERS ( GLUT). GLUT 4 IS INSULIN SENSITIVE AND IS LOCATED IN CYTOPLASMIC VESICLES.
  • 9. WHEN INSULIN RECEPTOR COMPLEX IS FORMED IN THE MEMBRANE OF CELL THE GLUT4 ARE ATTRACTED TOWARDS THE MEMBRANE AND GLUT4 IS RELEASED INTO THE MEMBRANE. NOW IT STARTS TRANSPORTING GLUCOSE MOLECULE FROM EXTRACELLULAR FLUID INTO CELLS. CELLS WHERE GLUCOSE IS METABOLISED ( LIVER, MUSCLE, AND ADIPOSE TISSUE ) WHERE NOT METABOLISED ( BRAIN EXCEPT HYPOTHALAMUS, RENAL TUBULES, MUCOUS MEMBRANE OF INTESTINE, RBCs.
  • 10. 1. PROMOTES PHERIPHERAL UTILIZATION OF GLUCOSE 2. PROMOTES STORAGE OF GLUCOSE- GLYCOGENESIS STORAGE OF GLUCOSE INTO GLYCOGEN IN MUSCLES AND LIVER 3. INHIBTS GLYCOGENOLYSIS. BREAKDOWN OF GLYCOGEN INTO GLUCOSE 4. INHIBITS GLUCONEOGENSIS: FORMATION OF GLUCOSE FROM PROTEINS BY INHIBITING THE RELEASE OF AMINO ACIDS.
  • 11. ON PROTEIN MTABOLISM IT INCREASE THE SYNTHESIS OF FATTY ACIDS AND STORAGE OF PROTEIN AND INHIBITS THE CELLULAR UTILIZATION OF PROTEINS BY:  INCREASES THE PERMEABILTY OF CELL MEMBRANE FOR AMINO ACID PREVENT PROTEIN CATABOLISM ON FAT METABOLISM INSULIN STIMULATE THE SYNTHESIS OF FAT AND STORAGE OF FAT
  • 12. REGULATION OF INSULIN SECRETION ROLE OF BLOOD GLUCOSE LEVEL ROLE OF PROTEIN ROLE OF LIPID ROLE OF GASTROINTESTINAL HORMONE GASTRIN, SECRETIN
  • 13. APPLIED PHYSIOLOGY DEVELOPS DUE TODEFICIENCY OF HORMONE INSULIN TYPES a) TYPE 1 DIEBETS MELLITUS: DUE TO DEFICIENCY OF INSULIN DUE TO DESTRUCTION OF BETA CELLS OF ISLETS F LANGERHANS. USUALLY DEVELOPS BEFORE 40 YEARS OF AGE. CAUSE ; VIRAL INFECTION, CONGENITAL DISORDER, AUTOIMMUNE DISEASE b) TYPE 2 DIABETS MELLITUS : DUE TO INSULIN RESISTANCE CAUSE : GENETIC DISORDER, LIFE STYLE , STRESS.
  • 14. SIGN AND SYMPTOMS OF DIABETES MELLITUS 1. INCREASED BLOOD GLUCOSE LEVEL(NORMAL 80-100mg/dl) fasting 2. Loss of glucose in urine ( glucosuria) 3. Polyuria and polydipsia: 4. Polyphagia : intake of excessive food 5. Acetone BREATHING 6. KUSSMAUL BREATHING: INCREASE RATE AND DEPTH OF RESPIRATION 7. COMA
  • 15. COMPLICATION 1. HYPERTENSION 2. MYOCARDIAL INFARCTION 3. DIABETIC RETINOPATHY 4. DIABETIC NEPHROPATHY 5. DIABETIC NEUROPATHY
  • 16. DIAGNOSTIC TEST FASTING BLOOD GLUCOSE LEVEL POSTPRANDIAL BLOOD GLUCOSE GLUCOSE TOLERANCE TEST GLYCOSYLATED HEMOGLOBIN
  • 17. GLUCAGON SOURCE OF SECRETION: ALPHA CELLS OF ISLET OF LANGERHANS CHEMISTRY AND HALF LIFE: IT IS A POLYPEPTIDE CONTAIN 29 AMINO ACIDS. HALF LIFE IS 3 TO 6 MINUTES. METABOLISM: ABOUT 30% DEGRADED IN LIVER AND 20% IN KIDNEY. 50 % DEGREDED IN BLOOD BY ENZYME SERINE AND CYSTEINE PROTEASES.
  • 18. ACTION OF GLUCAGON ON CARBOHYDRATE: IT INCREASES THE BLOOD GLUCOSE LEVEL BY INCRESING GLYCOGENOLYSIS BY INCREASING GLUCONEOGENESIS ON PROTEIN METABOLISM: INCREASES THE TRANSPORT OF AMINO ACIDS INTO LIVER CELLS. ON FAT METABOLISM: IT SHOWS LIPOLYTIC AND KETOGENIC ACTIONS. KETOGENIC MEANS FORMATION OF KETONE BODIES.
  • 19. REGULATION OF GLUCAGON SECRETION ROLE OF BLOOD GLUCOSE LEVEL : DECREASE IN BLOOD GLUCOSE LEVEL INCREASES THE SECRETION ROLE OF AMINO ACID LEVEL INCREASE IN AMINO ACID INCREASE THE SECRETION WHICH IN TURN INCREASE THE CONVERSION OF AMINO ACID INTO GLUCOSE. ROLE OF OTHER FACTOR EXERCISE STRESS GASTRIN INCRESES THE SECRETION CHOLECYSTOKININ CORTISOL
  • 20. FACTORS THAT INHIBITGLUCAGON SECRETION ARE: SOMATOSTATIN INSULIN FREE FATTY ACIDS KETONES
  • 21. SOMATOSTATIN SECRETED FROM HYPOTHALAMUS D CELLS OF ISLETS OF LANGERHANS D CELLS IN STOMACH AND UPPER PART OF SMALL INTESTINE CHEMISTRY & HALF LIFE: IT IS A POLYPEPTIDE. AND HAVE HALF LIFE OF 2 TO 4 MIN. METABOLISM: DEGRADED IN LIVER
  • 22. ACTION OF SOMATOSTATIN INHIBIT BOTH GLUCAGON AND INSULIN DECREASES THE MOTILITY OF STOMACH, DUODENUM AND GALLBLADDER. REDUCES SECRETION OF GASTRIC HORMONE IT INHIBIT SECRETION OF GROWTH HORMONE AND TSH FROM ANTERIOR PITUITARY. THUS KNOWN AS GROWTH HORMONE INHIBITORY HORMONE( GHIH)