PMY 302 Lecture 45: Insulin and Oral Hypoglycemic Agents

• School: University at Buffalo
• Department: Pharmacology and Toxicology
• Course: PMY 302
• Professor: Bhattacharjee Arindam

Document Summary

We have drugs that can increase insulin secretion (we didn"t for thyroid hormones) Glucosidases: glucose uptake from the gi tract to tissues (pancreas, liver cell, adipose, muscle cells) Released in response to glucose, amino acids, hormones, and neurotransmitters. Release includes second messengers, ca++, gene transcription and glucose. Uptake by glut2 inhibits the atp dependent k+ channels which will metabolism then depolarization and opens ca2+ to release more ca2+ to secrete insulin. Camp and other gi hormones also increase insulin. Glucagon increases camp levels to augment glucose-stimulated insulin. Beta cell failure; cannot even synthesis insulin at all. Either the stored insulin from b cells cannot be secreted, insulin resistance. Sulfonylureas - glyburide, gly-ide insulin secretion between meals or alpha glucosidase inhibitors that do not act on beta cells. Insulin sparing: control of glucose without increasing fasting. Monotherapy or second line combination use with metformin. Moa: mimic atp action on k+ channels that depolarizes. Ae: hypoglycemia the cell to increase insulin secretion.