PSIO 303A Lecture Notes - Lecture 11: Insulin Resistance, Glycogenesis, Glycogenolysis

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

Document Summary

Lecture 11 - excess hepatic glucose production in the. Lecture objectives for excess hgp in the metabolic syndrome: Define the time course of hgp in the metabolic syndrome. Discuss contributions of defects in insulin secretion and action responsible for excessive hgp in the metabolic syndrome. Discuss the significance of alterations in glucagon secretion that contribute to excessive hgp in the metabolic syndrome. Defend whether the glucagon:insulin ratio is an accurate way of estimating hgp in the metabolic. At some point we see an increase in glucagon production (this is counterintuitive) --> pathophysiological. Remember, glucagon does the opposite of inulin to provide more glucose in the cytoplasm of cells. Reminder from past two lectures on the role of insulin and glucagon in hgp: Early onset of dm - hgp seems normal, however as the disease progresses --> greater levels of hgp from liver. Normally, insulin inhibits lipolysis --> decrease of ffa into bloodstream.