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Regulation of Blood Glucose Level 
Dr. Shabeena Patel
What goes wrong when the concentration 
decreases? 
Hypoglycaemia 
The symptoms associated 
with low blood sugar 
are: 
tiredness, confusion, 
dizziness, headaches, 
mood swings, muscle 
weakness, tremors, 
irreversible CNS 
damage, coma, death
What goes wrong when the concentration 
increases too far? 
Hyperglycaemia 
The symptoms include: 
Excessive thirst; frequent urination; 
fatigue; unexplained weight loss; 
vision problems, such as blurring; 
increased susceptibility to infections 
Dibetes mellitus
We eat food containing carbohydrates
Fundamental regulation / 
Autoregulation 
• Hormones: 
• Insulin 
• Glucagon 
Organs: Liver 
Skeletal muscles 
Pancreas 
Adipose tissue
ROLE 
OF 
LIVER
Role of liver and Sk muscle
Role of the Pancreas 
1. Digestion – secretes digestive enzymes 
2. Metabolism 
• Regulation 
• Carbohydrates 
• Lipids 
• Proteins 
• Produces primary messengers (hormones) 
• Insulin 
• Glucagon
Role of adipose tissue
Glucose transporters 
Organ Glucose transporter Classification 
Brain GLUT1 Glucose dependent 
Erythrocyte GLUT1 Glucose dependent 
Adipocyte GLUT4 Insulin dependent 
Muscle GLUT4 Insulin dependent 
Liver GLUT2 Glucose sensor 
GK  - cell GLUT2 Glucose sensor 
Gut GLUT3-symporter ---- Sodium dependent 
Kidney GLUT3-symporter ---- Sodium dependent
• 51 amino acids 
• 2 chains linked by disulfide bonds 
• 5800 Dalton molecular weight
MECHANISM 
OF INSULIN 
SECRETION
ADIPOSE 
TISSUE AND 
MUSCLES
insulin stimulates the synthesis of an enzyme 
(glucokinase) (low affinity to glucose) [ in the 
liver] 
•Required to ‘trap’ glucose in the cell (only 
when glucose concentration is high)
Most Cells 
 Protein synthesis 
Insulin 
Control Muscle 
 Glucose uptake 
 Glycogen synthesis 
Adipose  triglycerides 
 Glucose uptake 
 Glycerol production 
 Triglyceride breakdown 
Liver 
 Glucose uptake 
 Glycogen synthesis 
 Fatty acid synthesis 
 Glucose synthesis 
Brain 
No effect 
Gastrointestinal 
hormones 
Pancreas 
Beta cells 
Feedback 
 amino 
acids 
 glucose 
 Insulin  Triglyceride synthesis 
Amino 
acids 
Blood 
glucose
Glucagon 
Control 
Adipose 
 Triglyceride breakdown 
 Triglyceride storage 
Liver 
 Glycogen breakdown 
 Glucose synthesis 
 Glucose release 
Brain 
No effect 
Pancreas 
Alpha cells 
Exercise 
Feedback 
 Fatty acids 
 Blood glucose 
Epinephrine 
(stress) 
Amino acids
Glucocorticoids 
• 1)Increase blood glucose: 
• i) Peripheral tissues :increase protein catabolism 
• Decrease uptake and utilization of glucose 
• ii)Liver : Increase amino acid uptake 
• Increase the transaminase activity 
• Increase gluconeogenesis 
• + Pyruvate carboxylase 
• + PEP carboxykinase 
• + Fructose -1,6-biphosphatase 
• +Glucose-6- phosphatase
• 2)Liver: Increase liver glycogen 
• + glycogen synthase activity 
Glucocorticoids are catabolic to the peripheral 
tissues but anabolic to the liver
+ ACTH 
synthesis 
Glucocortico 
id syn
Anterior pituitary hormones 
• 1)Growth hormone: 
• i)Decreases glucose uptake in tissues 
• ii)Increase liver gluconeogenesis 
• Chronic administration may lead to diabetes 
mellitus due to stimulation and exhaution of 
beta cells 
• 2)ACTH: Stimulates glucocorticoids synthesis 
• Raise blood glucose level
Thyroid hormones 
• Raise blood glucose levels 
• i)Increase hepatic glycogenolysis 
• ii)Increase sensitivity of tissues to catecholamines 
• iii)Increases destruction of insulin 
• iv) Increase absorption of hexoses from intestine 
• v) Increase peripheral tissue protein catabolism
Adipose tissue as endocrine gland
Causes of hyperglycemia 
• 1)Diabetes mellitus 
• 2)Hyperactivity of thyroid, pituitary and 
adrenals 
• 3)Emotional stress 
• 4)diffuse pancreatic diseases 
• 5)Sepsis 
• 6)Asphyxia
Hypoglycemia 
• 1)Overdosage of insulin 
• 2)Insulinoma 
• 3)Hypoactivity of thyroids –myxodema,cretinism 
• Pituitary gland 
• Adrenals- Addisons disease 
• 4)Severe liver diseases 
• 5)Glycogen storage diseases

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Seminar blood glucose regulation

  • 1. Regulation of Blood Glucose Level Dr. Shabeena Patel
  • 2. What goes wrong when the concentration decreases? Hypoglycaemia The symptoms associated with low blood sugar are: tiredness, confusion, dizziness, headaches, mood swings, muscle weakness, tremors, irreversible CNS damage, coma, death
  • 3. What goes wrong when the concentration increases too far? Hyperglycaemia The symptoms include: Excessive thirst; frequent urination; fatigue; unexplained weight loss; vision problems, such as blurring; increased susceptibility to infections Dibetes mellitus
  • 4. We eat food containing carbohydrates
  • 5.
  • 6.
  • 7. Fundamental regulation / Autoregulation • Hormones: • Insulin • Glucagon Organs: Liver Skeletal muscles Pancreas Adipose tissue
  • 9. Role of liver and Sk muscle
  • 10. Role of the Pancreas 1. Digestion – secretes digestive enzymes 2. Metabolism • Regulation • Carbohydrates • Lipids • Proteins • Produces primary messengers (hormones) • Insulin • Glucagon
  • 11. Role of adipose tissue
  • 12.
  • 13.
  • 14. Glucose transporters Organ Glucose transporter Classification Brain GLUT1 Glucose dependent Erythrocyte GLUT1 Glucose dependent Adipocyte GLUT4 Insulin dependent Muscle GLUT4 Insulin dependent Liver GLUT2 Glucose sensor GK  - cell GLUT2 Glucose sensor Gut GLUT3-symporter ---- Sodium dependent Kidney GLUT3-symporter ---- Sodium dependent
  • 15. • 51 amino acids • 2 chains linked by disulfide bonds • 5800 Dalton molecular weight
  • 16. MECHANISM OF INSULIN SECRETION
  • 17.
  • 19.
  • 20. insulin stimulates the synthesis of an enzyme (glucokinase) (low affinity to glucose) [ in the liver] •Required to ‘trap’ glucose in the cell (only when glucose concentration is high)
  • 21. Most Cells  Protein synthesis Insulin Control Muscle  Glucose uptake  Glycogen synthesis Adipose  triglycerides  Glucose uptake  Glycerol production  Triglyceride breakdown Liver  Glucose uptake  Glycogen synthesis  Fatty acid synthesis  Glucose synthesis Brain No effect Gastrointestinal hormones Pancreas Beta cells Feedback  amino acids  glucose  Insulin  Triglyceride synthesis Amino acids Blood glucose
  • 22.
  • 23.
  • 24.
  • 25.
  • 26. Glucagon Control Adipose  Triglyceride breakdown  Triglyceride storage Liver  Glycogen breakdown  Glucose synthesis  Glucose release Brain No effect Pancreas Alpha cells Exercise Feedback  Fatty acids  Blood glucose Epinephrine (stress) Amino acids
  • 27.
  • 28.
  • 29. Glucocorticoids • 1)Increase blood glucose: • i) Peripheral tissues :increase protein catabolism • Decrease uptake and utilization of glucose • ii)Liver : Increase amino acid uptake • Increase the transaminase activity • Increase gluconeogenesis • + Pyruvate carboxylase • + PEP carboxykinase • + Fructose -1,6-biphosphatase • +Glucose-6- phosphatase
  • 30. • 2)Liver: Increase liver glycogen • + glycogen synthase activity Glucocorticoids are catabolic to the peripheral tissues but anabolic to the liver
  • 31.
  • 32. + ACTH synthesis Glucocortico id syn
  • 33. Anterior pituitary hormones • 1)Growth hormone: • i)Decreases glucose uptake in tissues • ii)Increase liver gluconeogenesis • Chronic administration may lead to diabetes mellitus due to stimulation and exhaution of beta cells • 2)ACTH: Stimulates glucocorticoids synthesis • Raise blood glucose level
  • 34.
  • 35. Thyroid hormones • Raise blood glucose levels • i)Increase hepatic glycogenolysis • ii)Increase sensitivity of tissues to catecholamines • iii)Increases destruction of insulin • iv) Increase absorption of hexoses from intestine • v) Increase peripheral tissue protein catabolism
  • 36. Adipose tissue as endocrine gland
  • 37.
  • 38.
  • 39.
  • 40.
  • 41.
  • 42. Causes of hyperglycemia • 1)Diabetes mellitus • 2)Hyperactivity of thyroid, pituitary and adrenals • 3)Emotional stress • 4)diffuse pancreatic diseases • 5)Sepsis • 6)Asphyxia
  • 43. Hypoglycemia • 1)Overdosage of insulin • 2)Insulinoma • 3)Hypoactivity of thyroids –myxodema,cretinism • Pituitary gland • Adrenals- Addisons disease • 4)Severe liver diseases • 5)Glycogen storage diseases