week3-L6-intro to Diabetes Mellitus Flashcards
GLUT4
highly insulin responsive common in muscle and adipocytes, recruited by insulin to uptake glucose
effects of insulin of cell metabolism
fed state
increase protein synthesis and inhibit protein breakdown and gluconeogenesis
effects of glucagon on cell metabolism
fasting state
opens channels to allow transport of pyruvate lactate
increase breakdown of proteins
increase gluconeogenesis
fuel stores
carbohydrate, fat and proteins
effects on insulin of adipocytes
increase activity of LPL lipoprotein lipase
increase Glycerol and NEFA intake to form triglyceride and inhibit triglyceride breakdown
NB cortisol and GH breakdown triglyceride during fast state
why short responsive time?
due to double circulation of the GI and hepatic portal circulation
gluconeogenesis
contribute to 25% hepatic glucose output HGO 10h after fasting
triglyceride into Gly-3P to glucose
brain fuel
glucose or ketone bodies
ketone bodies regulation
insulin inhibition
glucagon stimulate conversion of fatty acyl CoA into ketone bodies due to low glucose present for brain supply
hepatic glycogenolysis
conversion of liver glycogen store to glucose to increase the HGO
difference between glycogen in liver and muscles
only liver glycogen store can be broken down to glucose
hormone acting of muscle cells
cortisol and GH inhibit the glucose uptake but insulin hormone increase the uptake of glucose
fasted state process
increase lipolysis, proteinolysis glycogenolysis and gluconeogenesis to increase the HGO and prolonged state results in increase ketogenesis; low insulin to glucagon
fed state process
increase lipogenesis, protein synthesis and glycogen store
decrease proteinolysis and gluconeogenesis
high insulin to glucagon ratio
diabetes
too high blood glucose the the body cannot overcome