BIOL122 Lecture Notes - Lecture 6: Diabetic Ketoacidosis, Kidney Disease, Gluconeogenesis
Diabetes Mellitus:
Definition: Chronic disorder of carbohydrate, fat and protein metabolism due to
defective/ deficient insulin secretion
Types of Diabetes:
1.) Type 1:
2.) Type 2: non obese
Gestational diabetes:
• Elevated BGL’s in pregnancy
• Increased growth hormone and placental hormones
• Beta cells cannot compensate
• Increased risk of type 2 diabetes
Normal pancreas:
• Contains cells known as islets of Langerhans
• Cells of the islets include:
- B cells secrete and synthesis insulin
- A cells secrete and synthesise glucagon
- Others
Normal insulin synthesis:
• Insulin synthesised by beta cells of pancreas
Normal insulin storage:
• Insulin stored in beta cells of pancreas
Normal insulin release:
• Insulin release from pancreases is triggered by increased BGL’s biphasic
release of insulin
• Other factors can promote or inhibit insulin release but not synthesis e.g.
hormones and drugs
Why do we need insulin:
- Brain requires glucose at all times
- Glucose is supplied to bloodstream via GI tract and liver
- Glucose requires a transporter to move it from blood into cells
- These transporters are known as glucose transport units (GLUTs)
- GLUTs are tissue specific
- GLUTS move from inner cell to plasma membrane to ‘pick-up’
glucose from the blood stream
- Some GLUTs are insulin- responsive (so they only work in the
presence of insulin)
- Other GLUTs are non- insulin responsive (they work without
insulin)
What happens when insulin binds to insulin receptors
- Insulin is a large peptide molecule
- Insulin binds to insulin receptors on target tissues
- Target tissues include liver, muscle and fat
- Receptor- bound insulin triggers certain GLUTs
- GLUTs ‘pick up’ glucose from blood; hence decreasing BGLs
Major effects of insulin on the body:
Effects of insulin on carbohydrate metabolism:
• Liver: e.g. stimulates glycogen synthesis
• Muscle: e.g. stimulates glycogen synthesis
• Adipose tissue: e.g. stimulates formation of glucose to fat to fatty acids to
triglycerides
• Effects of insulin on protein metabolism: e.g. stimulates protein synthesis
• Effects of insulin on adipose tissue: e.g. stimulates fatty acid synthesis
Document Summary
Definition: chronic disorder of carbohydrate, fat and protein metabolism due to defective/ deficient insulin secretion. Increased growth hormone and placental hormones: beta cells cannot compensate. Normal pancreas: contains cells known as islets of langerhans, cells of the islets include: Insulin release from pancreases is triggered by increased bgl"s biphasic release of insulin: other factors can promote or inhibit insulin release but not synthesis e. g. hormones and drugs. Glucose is supplied to bloodstream via gi tract and liver. Glucose requires a transporter to move it from blood into cells. These transporters are known as glucose transport units (gluts) Gluts move from inner cell to plasma membrane to pick-up" glucose from the blood stream. Some gluts are insulin- responsive (so they only work in the presence of insulin) Other gluts are non- insulin responsive (they work without insulin) What happens when insulin binds to insulin receptors. Insulin binds to insulin receptors on target tissues. Target tissues include liver, muscle and fat.
