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Bio 203 metabolism
metabolism review
Question | Answer |
---|---|
insulin promotes anaboloic or catabolic events? | anobolic |
cortisol stimulates | gluconeogenesis |
glycogenolysis promoted by | glucagon, epi, cortisol |
lipolysis stimulated by | epi, cortisol |
protein catab (deamination) promoted by | cortisol |
how do diabetics (Type I) end up in DKA? | glucose up in blood, down in cell *normally goes to Krebs, but if don't have insulin, can't make ATP *lack of insulin promotes lipolysis (cells starving, break down lipids, protein) *acetyl CoA builds up and is converted to ketone bodies form (acids) |
Acidosis effects neuronal cells | slows down NS, life threatening |
tx for DKA | admin insulin, monitor glucose & pH levels *watch K levels which will move into cell --> hypokalemia |
signs of DKA | fruity breath smell from ketone bodies |
Actions of insulin in general | *facilitates glucose into cell *speed glycogenesis *increase uptake aa, pro synth *speed lipogenesis *slow glycogenolysis *slow gluconeogenesis |
feedback of insulin | creates decreased blood glucose --> inhibit further release of insulin |
in CAD, we have chol, triglyc, WBC, and platelets clogging vessel called | plaques |
Total chol, HDL, LDL, VLDL & triglycerides in lab measures for | total cholesterol values |
hormones, cell wall, myelin sheath, Vit D synth | what we need cholesterol for |
HDL high density lipoprotein | |
what organ makes cholesterol | liver |
LDLs do what | transport newly synth chol from liver to cell |
HDLs do what | head out to cell and pick up xs cholesterol |
want LDL or HDL to be higher? | want HDLs to be higher (doing clean up, LDLs are dropping off chol that can accumulate in bvessels) |
Statin drugs do what | decrease chol production by liver |
glucagon acts on what cells | hepatocytes in liver |
actions of glucagon | *glycogenolysis *gluconeogenesis |
Effect of glucagon on glucose | raises blood glucose to normal, if rises to hyperglycemia is negative feedback of release of this hormone |