1 / 26

GLUCAGON

GLUCAGON. GLUCAGON. Glucagon: is secreted when “Glucose is GONE” Peptide hormone made of 29 amino acids. MW: 3485 Has several functions that are dramatically opposite to Insulin

kato-witt
Download Presentation

GLUCAGON

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. GLUCAGON

  2. GLUCAGON • Glucagon: is secreted when “Glucose is GONE” • Peptide hormone made of 29 amino acids. • MW: 3485 • Has several functions that are dramatically opposite to Insulin • One injection of purified glucagon can have profound Hyperglycemic effects! Therefore, it is also called the HYPERGLYCEMIC HORMONE!

  3. GLUCAGON • SYNTHESIS: in the alpha cells of the Islets of Langerhans. Preproglucagon (158 AA) ↓ Glucagon + Major proglucagon fragment (in the alpha cells)

  4. GLUCAGON METABOLISM • Circulates without binding to carrier proteins. • Plasma half-life: 5 minutes • 25% of the Glucagon is destroyed during passage through the Liver. • Glucagon also degraded by the kidneys & the plasma peptides.

  5. ACTIONS OF GLUCAGON The physiological role of Glucagon is to stimulate hepatic production & secretion of glucose. It accomplishes this by: • Glycogenolysis • Increased Gluconeogenesis NOTE: • Muscle DOES NOT respond to Glucagon. • It exerts its effects on the Liver and Adipose tissues.

  6. Mechanism of Glycogenolysis Glucagon activates adenylyl cyclase in the hepatic cell membrane ↓ Formation of cyclic adenosine monophosphate (cAMP) ↓ Protein kinase regulator protein is activated ↓ Protien kinase is activated ↓ Phosphorylase b kinase is activated ↓ Phosphorylase b is converted into phosphorylase a ↓ Promotes degradation of Glycogen into Glucose-1-phosphate ↓ Glucose-1-phosphate is dephosphorylated ↓ Glucose is released from the liver

  7. MECHANISM OF GLUCONEOGENESIS • It increases the rate of amino acid uptake by the liver cells. • It then stimulates the conversion of many amino acids to Glucose. ↓ This is achieved by activating many enzymes required for AA transport & gluconeogenesis.

  8. OTHER EFFECTS: • It activates adipose cell lipase→ increased quantities of fatty acids are made available. • It inhibits storage of TG in the liver → this prevents the liver from removing fatty acids from the blood! • It increases the blood flow in some tissues such as kidneys. • Enhances bile secretion. • Inhibits gastric acid secretion.

  9. REGULATION OF GLUCAGON SECRETION • Increased blood glucose concentration is the most potent factor: It INHIBITS Glucagon secretion • Increased amino acids stimulate Glucagon secretion (same effect as on INSULIN!) • Decrease in fatty acid levels stimulate Glucagon secretion (opposite to the effect on Insulin). • Somatostatin inhibits Glucagon & Insulin secretion • Exhaustive exercise stimulates Glucagon secretion

  10. What happens when you take a protein only diet? • Glucagon release is stimulated by plasma amino acids. This pathway prevents hypoglycemia after ingestion of a pure protein meal. • If a meal contains protein but no carbohydrate, amino acids absorbed from the food cause insulin secretion. Even though no glucose has been absorbed, insulin-stimulated glucose uptake increases, and plasma glucose concentrations fall. • Unless something counteracts this process, the brain’s fuel supply is threatened by hypoglycemia. Co-secretion of glucagon in this situation prevents hypoglycemia by stimulating hepatic glucose output. • As a result, although only amino acids were ingested, both glucose and amino acids are made available to peripheral tissues.

  11. Glucagon Dominates in Fasting State Metabolism Figure 21-14: Endocrine response to hypoglycemia

  12. The Balance b/w insulin & Glucagon • Over-riding concern is glucose homeostasis : – must maintain sufficient levels for use by brain – other tissues adjust to other energy sources as necessary. Insulin is known as the “Hormone of Feasting”, while Glucagon is known as the “Hormone of Fasting”.

  13. Muscle: Fed State Glucose from circulation (Active muscle) Pyruvate Glycogen Glucose (Inactive muscle)

  14. Muscle: Fasting State 1st uses own glycogen stores 2nd absorbs fatty acids and ketone bodies Glycogen Glucose Pyruvate Fatty Acids and Ketone Bodies from Circulation Acetyl CoA

  15. Liver: Fed State Glucose from circulation Pyruvate Glycogen Glucose Fatty Acids released to Circulation Acetyl CoA

  16. Adipose: Fed State Glucose from circulation Pyruvate Glycogen Glucose Fatty Acids Acetyl CoA Triacylglycerol (Fat) Fatty Acids from Circulation

  17. Adipose: Fasting State Pyruvate Glycogen Glucose Fatty Acids and glycerol Acetyl CoA Triacylglycerol (Fat) Fatty Acids and glycerol released to circulation

  18. somatostatin

  19. SOMATOSTATIN • Secreted by the Delta cells of Islets of Langerhans • Polypeptide containing only 14 AA • Extremely short half life of 3 minutes • All matters related to food ingestion increase its secretion: -increased blood Glucose -increased fatty acids -increased amino acids -increased concentrations of GI hormones

  20. ACTIONS OF SOMATOSTATIN • It has paracrine function locally within the Islets of langerhans where it depresses the secretion of both Insulin & Glucagon • It decreases the motility of stomach, duodenum & gall bladder • It decreases both secretion & absorption in the GIT Principal role is to extend the period of time over which the food nutrients are absorbed into the blood by slowing its passage through the GIT!

More Related