Pancreatic Hormones
• Glucagon
• Insulin
Pancreas
13-34
Islets of Langerhan (Pancreatic Islets)
Pancreas Histology
Pancreatic Hormones, Insulin &
Glucagon Regulate Metabolism
Figure 22-8: Metabolism is controlled by insulin and glucagon
Insulin Stimulates Cellular Glucose Uptake
Adipocytes
Liver
Insulin
Insulin
Intestine & Pancreas
Skeletal Muscle
Insulin
Glucagon and Insulin
Actions of Insulin on the Liver
• Stimulates glucose uptake
• Stimulates glycogenesis
• Stimulates glycolysis
• Stimulates HMP shunt activity
• Inhibits glycogenolysis
• Inhibits gluconeogenesis
• Stimulates lipogenesis
• Inhibits lipolysis
• Stimulates cholesterol synthesis
• Increases VLD lipoprotein
• Increases potassium and phosphate uptake
Actions of Insulin on Muscle
• Stimulates glucose uptake
• Stimulates glycogenesis
• Stimulates glycolysis
• Inhibits glycogenolysis
• Inhibits FFA uptake and oxidation
• Stimulates proteogenesis
• Inhibits proteolysis
• Stimulates uptake of potassium, phosphate and
•
magnesium
Increases blood flow
GLUCAGON
Alpha cells
Hypoglycemia =
glucagon secretion
Actions
increased glycogenolysis
increased gluconeogenesis
Result = normoglycemia
hypoglycemia (<90mg%)
alpha cells secrete glucagon
( -)
negative
feedback
liver cells:
increase glycogenolysis
increased gluconeogenesis
increased blood glucose
normoglycemia (>90mg%)
INSULIN
Beta cells
Hyperglycemia =
insulin secretion
Actions
increased glucose uptake
increased glycogenesis
increased lipogenesis
hyperglycemia (<110mg%)
beta cells secrete insulin
( -)
negative
feedback
increased glucose uptake into body cells
increase glycogenesis
(skeletal muscle, liver)
increased lipogenesis
decreased blood glucose
Result = normoglycemia
Diabetes mellitus
normoglycemia (<110mg%)
Normal
Insulin
Glycerol
Lipolysis
Free fatty acids
Synthesis
Free fatty acids
LPL
Glucose
Insulin
Triglyceride
Type 1 Diabetes Mellitus
Glycerol
Lipolysis
Free fatty acids
Synthesis
Free fatty acids
LPL
Glucose
Triglyceride
Diabetes Mellitus
•
•
This is a disease caused by elevated glucose levels
2 Types of diabetes:
Type I diabetes (10% of cases)
Type II diabetes (90% of cases)
Type I Diabetes (10% of cases)
• Develops suddenly, usually
before age 15
• Caused by inadequate
production of insulin because T
cell-mediated autoimmune
response destroys beta cells
• Controlled by insulin injections
Type II diabetes (90% of cases)
• Usually occurs after age 40 and in
obese individuals
• Insulin levels are normal or
elevated but there is either a
decrease in number of insulin
receptors or the cells cannot take it
up.
• Controlled by dietary changes and
regular exercise
•
Glucose homeostasis
Insulin
Beta cells
of pancreas stimulated
to release insulin into
the blood
High blood
glucose level
STIMULUS:
Rising blood glucose
level (e.g., after eating
a carbohydrate-rich
meal)
Body
cells
take up more
glucose
Liver takes
up glucose
and stores it as
glycogen
Homeostasis: Normal blood glucose level
(about 90 mg/100 mL)
Blood glucose level
rises to set point;
stimulus for glucagon
release diminishes
Figure 26.8
Blood glucose level
declines to a set point;
stimulus for insulin
release diminishes
Liver
breaks down
glycogen and
releases glucose
to the blood
STIMULUS:
Declining blood
glucose level
(e.g., after
skipping a meal)
Alpha
cells of
pancreas stimulated
to release glucagon
into the blood
Glucagon
Type 2 diabetes: patophysiology
Exxagerated lipolysis
I
I
Beta Cell
Dysfunction
Insulin
Pancreas
I
Decreased Glucose
Uptake
Insulin Resistance
FOOD
Storage In Fat Depots
Inhibition of Lipolysis
I
I
Insulin
Secretion
Insulin
Pancreas
Restrain of
HGO
I
Insulin Effects
Uptake of glucose
‫‪Prevention of obesity‬‬
‫قال صلى هللا عليه وسلم (ما مأل آدمي وعاء شرا من بطنه‪ ،‬بحسب‬
‫ابن آدم لقيمات يقمن صلبه‪ ،‬فان كان البد فاعال فثلث لطعامه وثلث‬
‫لشرابه وثلث لنفسه)‪ .‬رواه أحمد والترمذي‬