The pancreas secretes insulin and glucagon, which regulate carbohydrate, fat, and protein metabolism. Insulin promotes glucose storage and fat synthesis, while glucagon increases glucose production and fatty acid availability for energy. Diabetes mellitus results from impaired metabolism due to insufficient insulin, with complications including hyperglycemia and hypoglycemia impacting overall health.

1. PANCREAS
SECRETE: INSULIN AND GLUCAGON
COMPOSED: ACINI AND ISLETS OF LANGERHANS
TYPES OF CELLS: ALPHA, BETA, DELTA, PP
ALPHA SECRETE GLUCAGON, BETA CELLS SECRETE INSULIN, DELTA CELLS
SECRETE SOMATOSTATIN, PP CELLS SECRETE PANCREATIC POLYPEPTIDE
INSULIN INHIBIT GLUCAGON, AMYLIN INHIBIT INSULIN, SOMATOSTATIN
INHIBIT INSULIN AND GLUCAGON
METABOLIC EFFECTS OF INSULIN
INSULIN IMPORTANT IN STORING EXCESS CARBOHYDRATE AS GLYCOGEN
IN LIVER AND MUSCLES, EXCESS CARBOHYDRATE MAY BE CONVERTED
INTO FATS AND STORED IN ADIPOSE TISUES AND AMINO ACIDS CONVERT
INTO PROTEIN AND INHIBIT BREAKDOWN OF PROTEIN

2. PANCREATIC ISLETS

3. EFFECT OF INSULIN ON CARBOHYDRATE METABOLISM
AFTER MEAL, GLUCOSE ABSORBED INTO BLOOD, CAUSES RAPID
SECRETION OF INSULIN, RAPID UPTAKE, STORAGE, USE BY MUSCLES,
ADIPOSE TISSUE AND LIVER
INSULIN PROMOTE MUSCLE GLUCOSE UPTAKE AND METABOLISM
MUSCLE MUCH DEPENDS ON FATTY ACIDS FOR ENERGY B/C RESTING
MUSCLE MEMBRANE IS SLIGHTLY PERMEABLE TO GLUCOSE, BUT AFTER
MEAL INSULIN SECRETED, PROMOTE GLUCOSE ENTRY INTO MUSCLE
CONDITIONS MUSCLE USE LARGE AMOUNT OF GLUCOSE
DURING EXERCISE, MUSCLE BECOME MORE PERMEABLE TO GLUCOSE
AFTER MEAL, BLOOD GLUCOSE CONC HIGH, PANCREAS SECRETE LARGE
QUANTITY OF INSULIN, RAPID TRANSPORT OF GLUCOSE INTO MUSCLES

4. STORAGE OF GLYCOGEN IN MUSCLE
MUSCLES NOT EXERCISING AFTER MEAL, GLUCOSE TRANSPORTED INTO
MUSCLE CELLS IN ABUNDANCE, MOST OF GLUCOSE STORE IN FORM OF
GLYCOGEN USED FOR ENERGY
INSULIN PROMOTE LIVER UPTAKE, STORAGE AND USE OF GLUCOSE
MOST IMPORTANT EFFECT OF INSULIN IS GLUCOSE STORED IN FORM
OF GLYCOGEN, WHEN BLOOD GLUCOSE CONC BEGINS TO FALL, INSULIN
SECRETION DECREASE AND LIVER GLYCOGEN SPLIT INTO GLUCOSE AND
KEEP BLOOD GLUCOSE CONC FALLING TOO LOW
INSULIN PROMOTE CONVERSION OF EXCESS GLUCOSE INTO FATTY
ACIDS AND INHIBIT GLUCONEOGENESIS IN THE LIVER: INSULIN
PROMOTE CONVERSION OF ALL EXCESS GLUCOSE INTO FATTY ACIDS
AND PACKED AS TRIGLYCERIDES IN LOW DENSITY LIPOPROTEIN AND
TRANSPORTED IN THIS FORM THROUGH BLOOD TO ADIPOSE TISSUE
AND DEPOSITED

5. INSULIN INHIBIT GLUCONEOGENESIS
DECREASE ACTIVITIES AND QUANTITIES OFLIVER ENZYMES REQUIRED
FOR GLUCONEOGENESIS
GLUCOSE UPTAKE AND USAGE BY BRAIN
BRAIN CELLS PERMEABLE TO GLUCOSE WITHOUT INTERMEDIATION OF
INSULIN, BRAIN CELLS ONLY USE GLUCOSE, ESSENTIAL TO MAINTAIN
BLOOD GLUCOSE LEVEL, WHEN BLOOD GLUCOSE FALL, DEVELOP
HYPOGLYCEMIN SHOCK, SEIZURE
EFFECT OF INSULIN ON CARBOHYDRATE METABOLISM IN OTHER
CELLS
INSULIN INCREASE TRANSPORT AND USAGE BY MOST OF CELLS,
TRANSPORT OF GLUCOSE TO ADIPOSE TISSUE PROVIDE SUBSTRATE FOR
GLYCEROL PORTION OF FAT, INSULIN PROMOTE DEPOSITION OF FAT

6. EFFECT OF INSULIN ON FAT METABOLISM
INSULIN PROMOTE FAT SYTHESIS AND STORAGE
INSULIN INCREASE UTILIZATION OF GLUCOSE AND DECREASE UTILIZATION
OF FATS AND PROMOTE SYNTHESIS OF FATTY ACID IN LIVER AND FORM
TRIGLYCERIDES AND STORED IN ADIPOSE TISSUE
INSULIN DEFICIENCY INCREASE USE OF FAT FOR ENERGY
IN ABSENCE OF INSULIN FAT BREAKDOWN, PLASMA CONC OF FREE FATTY
ACIDS RISE, LIVER CONVERSION INTO PHOSPHOLIPID AND CHOLESTEROL,
LEAD TO ATHEROSCLEROSIS
EXCESS USAGE OF FAT DURING INSULIN LACK CAUSE KETOSIS AND
ACIDOSIS
EXCESS FATTY ACIDS IN LIVER CONVERT INTO ACETOACETIC ACID, IN
ABSENCE OF INSULIN UTILIZATION OF ACETOACETIC ACID BY PERIPHERAL
TISSUE DEPRESSED

7. ACIDOSIS
ACETOACETIC ACID CONVERT INTO β HYDROXYBUTYRIC ACID AND
ACETONE (KETOSIS), SEVERE DIABETES ACETOACETIC ACID AND β
HYDROXYBUTYRIC ACID CAUSE ACIDOSIS, COMA, DEATH
EFFECT OF INSULIN ON PROTEIN METABOLISM AND GROWTH
INSULIN PROMOTES PROTEIN SYNTHESIS AND STORAGE AND PREVENT
DEGRADATION OF PROTEINS
INSULIN DEFICIENCY CAUSES PROTEIN DEPLETION AND INCREASED
PLASMA AMINO ACIDS
CATABOLISM OF PROTEINS INCREASE PLASMA AMINO ACIDS CONC, USED
FOR ENERGY OR SUBSTRATE FOR GLUCONEOGENESIS, INCREASED UREA
EXCREATION, WEAKNESS AND UNCONTROLLED FUNCTION OF ORGANS

8. INSULIN AND GROWTH HORMONE INTERACT SYNERGISTICALLY
INSULIN REQUIRED FOR PROTEIN SYNTHESIS, ESSENTIAL FOR GROWTH AS
GROWTH HORMONE, BOTH HORMONES PERFORM SPECIFIC FUNCTION
CONTROL OF INSULIN SECRETION
FACTORS INCREASE INSULIN SECRETION
INCREASE BLOOD GLUCOSE, FATTY ACIDS AND AMINO ACIDS
GASTROINTESTINAL HORMONES (GASTRIN, SECRETIN, CHOLECYSTOKININ,
GLUCOSE DEPENDENT INSULINOTROPIC PEPTIDE
OTHER HORMONES (GLUCAGON, GROWTH HORMONE, CORTISOL)
FACTORS INHIBITING INSULIN SECRETION
DECREASE BLOOD GLUCOSE, FASTING, SOMATOSTATIN, ɑ ADRENERGIC
ACTIVITY AND LEPTIN

9. GLUCAGON
SECRETED: ALPHA CELLS OF ISLETS OF LANGERHANS, BLOOD GLUCOSE
CONC FALL
HYPERGLYCEMIC HORMONE: INCREASE BLOOD GLUCOSE CONC
EFFECT ON GLUCOSE METABOLISM
BREAKDOWN OF LIVER GLYCOGEN, INCREASED GLUCONEOGENESIS IN
LIVER
GLUCAGON INCREASE GLUCONEOGENESIS
CAUSE HYPERGLYCEMIA BY INCREASE RATE OF AMINO ACIDS UPTAKE BY
LIVER CELLS, CONVERT INTO GLUCOSE
EFFECT ON FAT
ACTIVATE ADIPOSE CELL LIPASE, INCREASE FATTY ACIDS AVAILABILITY FOR
ENERGY, INHIBIT TRIGLYCERIDES STORAGE IN LIVER, PREVENT LIVER FROM
REMOVING FATTY ACIDS FROM THE BLOOD

10. REGULATION OF GLUCAGON SECRETION
 INCREASE BLOOD GLUCOSE INHIBIT GLUCAGON SECRETION
DECREASE BLOOD GLUCOSE CONS, INCREASE PLASMA CONC OF GLUCAGON,
INCREASE OUTPUT OF GLUCOSE FROM LIVER
INCREASE BLOOD AMINO ACIDS STIMULATE GLUCAGON SECRETION
GLUCAGON PROMOTE CONVERSION OF AMINO ACIDS INTO GLUCOSE
EXERCISE STIMULATE GLUCAGON SECRETION
PREVENT DECREASE BLOOD GLUCOSE CONC, INCREASE AMINO ACIDS IN EXERCISE, β
ADRENERGIC STIMULATION OF ISLETS OF LANGERHANS IN EXERCISE
SOMATOSTATIN INHIBIT GLUCAGON AND INSULIN SECRETION
SOMATOSTATIN: EXTEND PERIOD OF TIME FOR NUTRIENT ASSIMILATION INTO
BLOOD, DECREASE UTILIZATION OF ABSORBED NUTRIENT BY TISSUES

11. BLOOD GLUCOSE CONTROL
• BLOOD SUGAR CONC: 80-90 mg/100 ml, IN FASTING BEFORE BREAKFAST
• 120-140 mg/ 100 ml, DURING FIRST HOUR AFTER MEAL
• FEEDBACK SYSTEM FOR CONTROL OF BLOOD GLUCOSE CONC- CONTROL
LEVEL WITHIN 2 HOURS AFTER ABSORPTION OF CARBOHYDRATE
• IN STARVATION, GLUCONEOGENESIS FUNCTION OF LIVER, MAINTAIN
FASTING BLOOD GLUCOSE LEVEL
• WHEN BLOOD GLUCOSE RISES, RATE INSULIN SECRETION, TWO-THIRD
OF ABSORBED GLUCOSE STORED IN THE LIVER IN FORM OF GLYCOGEN
• WHEN BLOOD GLUCOSE CONC AND INSULIN SECRETION FALL IN
SUCCEEDING HOURS, LIVER RELEASES GLUCOSE INTO THE BLOOD
• INSULIN AND GLUCAGON FUNCTION FUNCTION AS FEEDBACK CONTROL
SYSTEM TO MAINTAIN NORMAL BLOOD GLUCOSE CONC

12. INSULIN SECRETION
• WHEN BLOOD GLUCOSE CONC RISE, DECREASE BLOOD GLUCOSE CONC
TOWARDS NORMAL
• BLOOD GLUCOSE CONC DECREASE, STIMULATE GLUCAGON
• NORMAL CONDITION: INSULIN FEEDBACK MECHANISM
• IN STARVATION OR EXERCISE: GLUCAGON MECHANISM
• IN SEVERE HYPOGLYCEMIA: DIRECT EFFECT ON HYPOTHALAMUS,
STIMULATES SYMPATHETIC NERVOUS SYSTEM, EPINEPHRINE SECRETED
BY ADRENAL MEDULLA FURTHER INCREASES GLUCOSE FROM LIVER
• IF PROLONGED HYPOGLYCEMIA: GROWTH HORMONE AND CORTISOL
SECRETED, DECREASE RATE OF GLUCOSE UTIZATION, UTILIZED FAT,
RETURN BLOOD GLUCOSE CONC TOWARDS NORMAL

13. DIABETES MELLITUS
• CARBOHYDRATE, FAT AND PROTEIN METABOLISM ARE IMPAIRED, DUE
TO LACK OF INSULIN OR DECREASED SENSITIVITY OF TISSUES TO
INSULIN
• TYPES OF DIABETES: TYPE I DIABETES- INSULIN DEPENDENT DIABETES
MELLITUS (LACK OF INSULIN), TYPE II DIABETES- NON INSULIN
DEPENDENT DIABETES MELLITUS (DECREASED SENSITIVITY OF
TISSUES TO INSULIN)
• ALTERED METABOLISM OF FOOD, PREVENT UPTAKE AND UTILIZATION
OF GLUCOSE, BLOOD GLUCOSE CONC RISES, FAT AND PROTEIN
UTILIZATION INCREASES

14. HYPOGLYCEMIA
BLOOD GLUCOSE CONC FALLS, SEIZURES, LOSS OF CONCIOUSNESS, IF
FURTHER LOWER CAUSE COMA
DIABETES INSIPIDUS: UNCOMMON DISORDER, IMBALANCE OF WATER
IN BODY
SYMPTOMS: EXTREME THIRST, EXCRETION OF LARGE AMOUNT OF
URINE
RATE OF FLUID EXCRETION BY KIDNEY CONTROL BY ADH (POSTERIOR
PITUITARY HORMONE)
CAUSE: DAMAGE OF PITUITARY GLAND, DEFECT IN KIDNEY TUBULE,
UNABLE TO RESPOND ADH

15. ENDOCRINE FUNCTIONS OF THE KIDNEYS
HORMONES: ERYTHROPOIETIN, CALCITRIOL AND RENIN
ERYTHROPOIETIN
STIMULI: LOW LEVELS OF OXYGEN IN THE BLOOD
TRAVELS: RED BONE MARROW
EFFECT: STIMULATES AN INCREASED PRODUCTION OF RED
BLOOD CELLS
RBC: OXYGEN CARRYING CAPACITY OF THE BLOOD

16. CALCITRIOL
ALSO CALLED: 1,25-DIHYDROXYCHOLECALCIFEROL, ACTIVE METABOLITE
OF VITAMIN D
PRODUCED: LIVER AND RENAL HYDROXYLATION OF VITAMIN D3
FUNCTION: STIMULATES CALCIUM UPTAKE BY THE SMALL INTESTINE,
PROMOTES MINERALIZATION OF NEW BONE
CONTROLLED: PARATHYROID HORMONE AND SERUM PHOSPHATE
CONCENTRATION

17. RENIN
ALSO KNOWN: ANGIOTENSINOGENASE
BODY'S RENIN-ANGIOTENSIN
ALDOSTERONE SYSTEM
CAUSE: INSUFFICIENT BLOOD FLOW TO THE
KIDNEYS ( DECREASE IN BLOOD VOLUME)
FUNCTION: CONVERSION OF PLASMATIC
ANGIOTENSINOGEN TO ANGIOTENSIN I
ANGIOTENSIN I
ANGIOTENSIN CONVERTING ENZYME TO
ANGIOTENSIN II
STIMULATES ALDOSTERONE SYNTHESIS AND
CAUSES INCREASE BLOOD VOLUME

18. THYMUS GLAND
TRIANGULAR, SOFT ORGAN
LOCATED: SUPERIOR OF HEART AND
POSTERIOR TO THE STERNUM
THYMOSIN HORMONE DURING FETAL
LIFE AND CHILDHOOD
FUNCTION: DEVELOPMENT OF T-
LYMPHOCYTES OR T CELLS
(EXTREMELY IMPORTANT TYPE OF
WBC)
T-CELLS: DEFEND THE BODY FROM
POTENTIALLY DEADLY PATHOGENS

19. HORMONAL EFFECT ON PHYSIOLOGY OF GROWTH
• GROWTH: COMPLEX PROCESS, COORDINATED ACTION OF SEVERAL HORMONES
• GROWTH HORMONE: STIMULATING BODY GROWTH, STIMULATE THE LIVER AND
OTHER TISSUES TO SECRETE IGF-I.
• IGF-I STIMULATES PROLIFERATION OF CHONDROCYTES (CARTILAGE CELLS),
RESULTING IN BONE
• DIRECT EFFECTS: GROWTH HORMONE BINDING ITS RECEPTOR ON TARGET CELLS.
FAT CELLS (ADIPOCYTES), GROWTH HORMONE STIMULATES AND BREAK DOWN
TRIGLYCERIDE AND SUPRESSES THEIR ABILITY TO TAKE UP AND ACCUMULATE
CIRCULATING LIPIDS.
• INDIRECT EFFECTS: ARE MEDIATED PRIMARILY BY A INSULIN-LIKE GROWTH FACTOR-
I (IGF-I), A HORMONE THAT IS SECRETED FROM THE LIVER AND OTHER TISSUES IN
RESPONSE TO GROWTH HORMONE. A MAJORITY OF THE GROWTH PROMOTING
EFFECTS OF GROWTH HORMONE IS ACTUALLY DUE TO IGF-I ACTING ON ITS TARGET
CELLS.