NS 3310 1st Edition Lecture 14Outline of Past LectureI. Glycosylated Hemoglobin (A1c)II. Progression of DiabetesOutline of Current LectureI. Review for PrelimCurrent LectureI. Review for Prelim- GPCR: glucagon and incretin hormones GIP and GLP-1 are examples. Ligand binds to the receptor and activates adenylate cyclase, which converts ATP to cAMP. cAMP activates PKA and EPAC2. PKA has many downstream targets. - Insulin does not use GPCR. Insulin is an anabolic hormone that is often associated with diabetes. Insulin activates a number of proteins. Insulin receptor activates IRS, which activates PI3K and then AKT. Insulin makes proteins, lipids, stores more glycogen and stimulates glycolysis. It increases glycogen synthesis via GSK, increases glycolysis via GK, lipids increase via citrate, protein synthesis regulated by mTOR.- In beta cells, glucose comes in through GLUT2, activates GK, and undergoes glycolysis and then TCA cycle in mitochondria. Electron gradient across inner membrane drives thegeneration of ATP. The generation of ATP is important for insulin exocytosis.- UCP protein causes dissipation of heat, reducing ATP productionThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.- Know organs of digestive tract, cell types in stomach- Small intestine: duodenum, jejunum, ileum- Sphincter of Oddi controls the regulation of secretions into the duodenum from the gallbladder and pancreas- Cholesterol can make bile acid, steroids, vitamin D- Cholesterol comes from acetyl-coA- FXR and RXR in
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