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Pancreas as endocrine organ:
Glucose homeostasis & Insulin

        Nermeen Bastawy
      Physiology Department
       Faculty of Medicine
         Cairo University
F




60%       25 %
Pro insulin
Ribosomes   ER /Golgi   Golgi/Granules
Mechanism of insulin release
• Phases :
 1st phase: rapid, short, glucose dependent
 2nd phase: slow,sustained, glucose independent
• Oscillation pattern:
  every 5 min.
Insulin receptors & effects


                       K, aa




Na/K ATpase   IRS
Glucokinase
Lipase                     GLUT4
(Glucose transporters (9
2ry active transp.   Facilitated Diffusion
GROWTH & METABOLISM

• Proteins & growth (anabolic(
• CHO : insulin sensitive tissues
( muscle, adipose, liver(
• Fat & KB
INSULIN
                -- lipase    Adipose




                       FFA
Glucose



               ATP
GLUT2


      GK

G6P           ATP
                                 TG & VLDL
  GS
                        lipase

                                  FFA
              Lipase



                       Hs-
                                  Adipose
                       Lipase
+ ???Insulin & K
• Insulin  K shift into the cells by ++ Na/K
  ATPase. That's why insulin is used in the
  treatment of hyperkalemia.
• Hyperkalemia: more K will enter beta cell
  ++ insulin secretion
• Hypokalemia more K will leave beta cell
   -- insulin secretion.
• Why diuretics are contraindicated in DM?
Control of insulin secretion


• Hypothalamus/pituitary? NOT
• Feed back? Glucose / Insulin
• +++/- - - - ?
FOOD    Hs   ANS    K+ cAMP
Insulin
                     Max



          Basal

          70   100   300
           Glucose mg %
Control of insulin secretion


• Hypothalamus/pituitary? NOT
• Feed back? GLUCOSE/Insulin
• +++/- - - - ?
FOOD    Hs   ANS    K+ cAMP
How dose food ++ insulin secretion?

 W is better stimulant 4 insulin
 secretion: oral or IV glucose?
Control of insulin secretion


• Hypothalamus/pituitary? NOT
• Feed back? GLUCOSE/Insulin
• +++/- - - - ?
FOOD    Hs   ANS    K+ cAMP
Glucagon
• Pancreas (A cells)
• GIT & brain ( A & L cells)
• Actions:
1. Oppose insulin
2. ++ insulin, GH, SS secretion
3. +ve inotrope.
• Regulation : Food Hs ANS
   stress & exercise glucocorticoids
Somatostatin

• GIT & Pancreas ( D cells)
• ++ by food & GIT hormones
• -- all hormones & GIT motility &
  secretions
Important Qs
• Why exercise is benefit for DM?
It lower blood by ++ cAMP-kinase w moves
   GLUT4.
• Why diuretics are contraindicated in DM?
K is important for insulin secretion, so
Diuretics -- K+  -- insulin secretion
Mechanism of Glucostasis
1. Liver (glycogenesis, glycogenolysis,
   gluconeogenesis).

2. Hormonal mechanism
• Insulin / glucagon
• Catecholamine, GH & cortisol
70-100 mg%




Glycogenolysis
Mechanism of Glucostasis
1. Liver
2. Hormonal mechanism
• Insulin / glucagon
• Catecholamine, GH & cortisol
++ energy sources :
 ++ glucose (glycogenolysis,
   gluconeogenesis with IR)
++ FFA, KB & aa
Pancrease
Pancrease

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Pancrease

  • 1. Pancreas as endocrine organ: Glucose homeostasis & Insulin Nermeen Bastawy Physiology Department Faculty of Medicine Cairo University
  • 2.
  • 3.
  • 4.
  • 5.
  • 6. F 60% 25 %
  • 7.
  • 9. Ribosomes ER /Golgi Golgi/Granules
  • 10.
  • 11. Mechanism of insulin release • Phases :  1st phase: rapid, short, glucose dependent  2nd phase: slow,sustained, glucose independent • Oscillation pattern: every 5 min.
  • 12.
  • 13. Insulin receptors & effects K, aa Na/K ATpase IRS Glucokinase Lipase GLUT4
  • 14. (Glucose transporters (9 2ry active transp. Facilitated Diffusion
  • 15. GROWTH & METABOLISM • Proteins & growth (anabolic( • CHO : insulin sensitive tissues ( muscle, adipose, liver( • Fat & KB
  • 16. INSULIN -- lipase Adipose FFA Glucose ATP
  • 17. GLUT2 GK G6P ATP TG & VLDL GS lipase FFA Lipase Hs- Adipose Lipase
  • 18. + ???Insulin & K • Insulin  K shift into the cells by ++ Na/K ATPase. That's why insulin is used in the treatment of hyperkalemia. • Hyperkalemia: more K will enter beta cell ++ insulin secretion • Hypokalemia more K will leave beta cell  -- insulin secretion. • Why diuretics are contraindicated in DM?
  • 19. Control of insulin secretion • Hypothalamus/pituitary? NOT • Feed back? Glucose / Insulin • +++/- - - - ? FOOD Hs ANS K+ cAMP
  • 20. Insulin Max Basal 70 100 300 Glucose mg %
  • 21. Control of insulin secretion • Hypothalamus/pituitary? NOT • Feed back? GLUCOSE/Insulin • +++/- - - - ? FOOD Hs ANS K+ cAMP
  • 22. How dose food ++ insulin secretion? W is better stimulant 4 insulin secretion: oral or IV glucose?
  • 23. Control of insulin secretion • Hypothalamus/pituitary? NOT • Feed back? GLUCOSE/Insulin • +++/- - - - ? FOOD Hs ANS K+ cAMP
  • 24. Glucagon • Pancreas (A cells) • GIT & brain ( A & L cells) • Actions: 1. Oppose insulin 2. ++ insulin, GH, SS secretion 3. +ve inotrope. • Regulation : Food Hs ANS stress & exercise glucocorticoids
  • 25. Somatostatin • GIT & Pancreas ( D cells) • ++ by food & GIT hormones • -- all hormones & GIT motility & secretions
  • 26. Important Qs • Why exercise is benefit for DM? It lower blood by ++ cAMP-kinase w moves GLUT4. • Why diuretics are contraindicated in DM? K is important for insulin secretion, so Diuretics -- K+  -- insulin secretion
  • 27. Mechanism of Glucostasis 1. Liver (glycogenesis, glycogenolysis, gluconeogenesis). 2. Hormonal mechanism • Insulin / glucagon • Catecholamine, GH & cortisol
  • 29. Mechanism of Glucostasis 1. Liver 2. Hormonal mechanism • Insulin / glucagon • Catecholamine, GH & cortisol ++ energy sources : ++ glucose (glycogenolysis, gluconeogenesis with IR) ++ FFA, KB & aa

Editor's Notes

  1. FOODS: glucose, aa, K +,
  2. FOODS: glucose, aa, K+ insulin ++ Na/K pump  --- K +,
  3. FOODS: glucose, aa, K+ insulin ++ Na/K pump  --- K +,