PSIO 303A Lecture Notes - Lecture 9: Insulin, Homeostasis, Vesicle Fusion

• School: University of Arizona
• Department: Physiology
• Course: PSIO 303A
• Professor: Eric Price, Steven Wright, Nick Delamere

Document Summary

Lecture 9 - molecular level of b-cell dysfunction in the. Major learning objectives of molecular level of b-cell dysfunction in the metabolic syndrome: Describe the two phases for dysfunction in the secretory capacity of pancreatic beta cells in the metabolic syndrome: a. b. Leading to a relative failure of the beta cell. Discuss the cellular mechanisms underlying the compensatory hyperinsulinemia and the relative. Defend whether a true dysfunction in the glucagon secretory mechanism if alpha-cells of the pancreas develop in the metabolic syndrome. For metabolic syndrome, the initiated symptom is added visceral obesity --> gradual increase in insulin resistance due to decreased insulin sensitivity. Re-visiting the development of the metabolic syndrome over time: Decrease in insulin sensitivity --> increase in insulin secretion [compensatory hyperinsulinemia]. This can be a benign response, until the system is on insulin production over-drive --> beta-cell dysfunction. Glucose excursions during meals in the transition to metabolic syndrome: impaired glucose tolerance (igt) and t2dm.