Insulin Flashcards
The beta cell of the pancreas produce:
- Somatostatin
- Amylin
- Insulin only
- Glucagon and amylin
- Amylin.
Although the beta cells produce insulin, it is not the only thing that they produce, therefore 3 is wrong
Alpha cells produce glucagon
Delta cells produce somatostatin
What is the structure of active insulin?
2 peptides, A and B chain, held by disulfide bonds
What is the role of C peptide?
C peptide is important in stimulating axonal repair, Na+/K+ pump and promoting renal filtration.
Excess C peptide would result in:
inflammation of the endothelia of blood vessels causing impaired vascular tone and cardiovascular disease
This happens because it deposits there and causes macrophages to turn to foam cells and induce T-medicated inflammation and smooth muscle proliferation
Lack of C-peptide results in:
- Neuropathy (due to poor axonal repair)
- cardiovascular disease (because of impaired Na+/K+ pump and nitric oxide release which impairs vascular tone)
- renal disease (because glomerular filtration is inhibited by poor vascular tone)
What is the dominant mechanism for stimulating insulin release?
- Sugar metabolism: Glut 2 -> glucokinase -> glycolysis, TCA, resp chain make ATP and
- ATP/NAD(P)H close the K+ channel, depolarize the membrane
- Calcium channel opens
- Ca2+ flux causes insulin vesicle fusion with plasma membrane, release to ECF
Which vitamins affect insulin secretion and how?
Vitamins A, D, and biotin will all increase gene expression of insulin and enzymes required to stimulate the release of insulin
If you have a low carb, high protein diet, will insulin still be released?
Yes, but to a lesser extent. Amino acids are not as potent of a stimulant to the beta cell. They must be converted to alpha keto acids before being fed to krebs to produce ATP in the cell, close K+ channels, open Ca2+ channels and induce degranulation
In a low carb, high protein and fat diet, will insulin still be released and how does fat affect this?
Yes, but to a lesser extent. Protein and fats are not as potent of stimulators. long chain fats can stimulate insulin.
What would happen if you thought about food all day long?
Parasympathetic stimulation of the b cell via ACh would activate PLC to IP3 to release
calcium from the ER, bind to insulin vesicles and cause release.
When insulin engages a muscle cell, it can release pre-formed GLUT4,
activate glycogen synthase, and stimulate transcription. Describe the
basics of insulin receptor signaling to support these processes.
The insulin receptor is a tyrosine kinase, who forms a dimer and
autophosphorylates upon insulin binding. The insulin receptor substrate is a scaffold protein who is activated upon insulin receptor phosphorylation. Active IRS recruits several kinases, which can induce independent outcomes.
Describe the intracellular action to release GLUT4
The insulin receptor substrate (activated by autophosphorylation of an enzyme linked receptor) recruits a kinase that activates phospholipase C. Phospholipase C converts a membrane component to IP3 and DAG. DAG then activates protein kinase B (AKA Akt), which releases preformed GLUT4.
How does metformin bypass insulin signaling and cause release of GLUT 4?
Metformin activates protein kinase B (Akt) independently, bringing GLUT4 to the surface.
If the liver has GLUT2, how does insulin regulate liver glucose?
- activates glycolysis
- activates glycogen synthase/glycogenesis
- inhibits gluconeogenesis
How does insulin affect lipids in the liver?
- increases enzymes for TG and cholesterol formation
- activates ACCase for fatty acid biosynthesis
- inhibits fatty acid metabolism
