2. Islet cell structure α cell : glucagon β cell : insulin
δcell : somatostatin
δcell
α cell
β cell

3. Principal actions of insulin
Its net effect is to promote the storage of carbohydrate, protein and fat. It is therefore appropriately called the “ hormone of abundance”.
70 mg/dl
300 mg/dl
(Glucosurea)

4. Consequences of insulin deficiency
NORMAL
DIABETIC

5. Disturbances in protein metabolism
INSULIN DEFICIENCY

6. Dehydration

7. Insulin
lipodystrophy

8. Chronic neuropathy:
Trophic ulceration

9. Gangrene

10. Gangrene with infection

11. Insulin allergy

12. Glucagon Synthesis and secretion of glucagon ⊕ ⊕ ○ Glucagon ⊕
Amino acids ⊕
Glucose
FFA
Ketoacid ○
Glucagon ⊕

13. Actions of glucagon
Plasma: Glucose ↑ Amino acids ↓ Free fatty acids↑

14. Diabetic retinopathy – Microvascular complication

15. Hormones of the pancreatic islets
Pancreas, Liver & Nutrient
Liver : the central organ in
nutrient traffic

16. Endocrine regulation of carbohydrate metabolism
Insulin
Glucagon
Somatostatin --- inhibit the secretion of insulin & glucagon
Epinephrine --- cyclic AMP increased, [Ca+2] increased  hepatic
glucose output increased.
5. thyroid hormone : (1) increases the absorption of glucose from the intestine
(2) cause hepatic glycogen depletion
(3) accelerate the degradation of insulin
6. glucocorticoids --- diabetogenic effect
7. growth hormones --- inhibition of glucose
phosphorylation  decrease utilization

17. In Summary Insulin Glucagon
Is released by B-cells in the Islets of Langerhans in the pancreas.
Responds to high levels of blood sugar; is released when someone has a meal and needs to store extra energy.
Lack of insulin or response to insulin leads to diabetes.
Is released by a-cells in the Islets of Langerhans in the pancreas.
Responds to low levels of blood sugar; is released when someone hasn’t eaten or requires extra energy
Basically, glucagon is the opposite of insulin.