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Bio 203 metabolism

metabolism review

QuestionAnswer
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
Created by: lorrelaws
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