Lab 17: Glucose Tolerance
Role of Pancreas in Regulation of Blood Glucose:
fasting causes decreases glucose
Sensor & Integrating Center: Pancreatic islets monitor blood glucose
sense an decrease of glucose and cause:
beta cells in pancreatic islets to decrease insulin secretion
alpha cells in pancreatic islets to increases glucagon secretion
Effectors: Skeletal muscle, liver cells, and adipocytes
increase in glucagon stimulates:
causes Glycogenolysis in the liver, releasing glucose into the blood
promotes gluconeogenesis in liver (the production of glucose from non-carbohydrate sources), to make up for low glucose levels
increases plasma concentration
decrease in insulin causes removal of glucose transporters in liver and muscle cells
causes Glycogenolysis in skeletal muscle cells only (hydrolysis of glycogen into glucose)
also promotes ketogenesis (formation of ketone bodies from fatty acids)
also promotes hydrolysis of fat and protein
hydrolysis of glycogen, fat, and protein causes changes in blood levels:
increase in blood glucose
increase in amino acids in blood
increase in fatty acids in blood
increase in ketone bodies
absorption of a meal increase glucose
Sensor & Integrating Center: Pancreatic islets monitor blood glucose
sense an increase of glucose and cause increase in beta cells secretion and decrease in alpha cells secretion
beta cells in pancreatic islets increases insulin secretion
alpha cells in pancreatic islets to decreases glucagon secretion
hormones (insulin and glucagon) are just messengers
Effectors: Skeletal muscle, liver cells, and adipocytes
increase in insulin and decrease in glucagon causes insertion of glucose transporters in liver and muscle cells
promotes glucose uptake by tissues, forming glycogen to be stored in liver and skeletal muscle, promoting glycogenesis
if run out of space for glycogen storage, promotes formation of fat, and protein
promotion of glycogen, fat, and protein causes changes in blood levels:
decrease in blood glucose
due to glycogen being stored in liver and skeletal muscle
decrease in amino acids in blood
due to formation of protein
decrease in fatty acids in blood
due to formation of fat
decrease in ketone bodies
Diabetes Mellitus
Diabetes Mellitus: disease where body either does not produce enough insulin or does not respond adequately to insulin, resulting in abnormally high blood glucose levels
Type 1 Diabetes Mellitus: pancreas secretes little to no insulin in response to glucose load
Type 2 Diabetes Mellitus: tissue no longer responds adequately to circulating insulin
glucose tolerance test: help diagnose type 1 and type 2 diabetes and examines how well body responds to glucose load, demonstrating negative feedback loop for glucose levels
in lab, examine homeostatic regulation of blood sugar levels in normal fasted individuals
expected results:
after ingesting glucose, significant increase in blood glucose
followed by return to baseline
Possible Errors to Experiment:
subjects did not fast
malfunction with equipment
errors made by experimenters
Diabetes insipidus: disease characterized by failure of posterior pituitary to produce ADH, resulting in inadequate reabsorption of water by kindeys and production of copious amounts of urine
Definitions:
glycogenesis: generations of glycogen from glucose, stimulated by insulin
gluconeogenesis: generation of glucose from non-carbohydrate molecules such as amino acids and lactic acid
glycogenolysis: hydrolysis of glycogen to glucose
ketone bodies: substance derived from fatty acids and used as fuel by muscle and brain
ketoacidosis: type of metabolic acidosis caused by excessive production of ketone bodies