FSHN 150 1st Edition Lecture 18Outline of Last LectureII. Health dangers of excessive trans fatty acidsIII. Saturated fatty acidsIV. MonounsaturatedV. PolyunsaturatedVI. Essential Fatty acidsVII. Trans fatVIII. Fat DigestionIX. Fat AbsorptionX. Transport of digested fatXI. LipoproteinsOutline of Current LectureI. ChylomicronsII. Very Low Density LPIII. Low Density LD(LDL)IV. High Density LP (HDL)V. HypercholesterolemiaVI. Lipid MetabolismVII. MedicationsVIII. Hormonal Control of TGCurrent LectureI. ChylomicronsA. formed in SI, enters lymphatic system via bloodB. carries dietary lipids and FSV tissuesC. TGD. Tg removed mostly storedE. Remnants picked up and recycled by liveII. Very Low Density LPA. formed by liver also from chylomicrons remnants in liveB. TG rich sourceC. Transport lipids(hepatic fat) to tissuesD. TG used for energy and storageIII. Low Density LD(LDL)A. high in cholesterol low in TGB. deliver cholesterol to body cellsC. LDL cleared by liver and other tissuesD. Diets low in sat. fat and cholesterol encourage liver uptake of LDLIV. High Density LP (HDL)A. made by liverB. high in protein low in TG moderate in cholesterolC. lowers CVDV. HypercholesterolemiaA. high in cholesterol deposits in the tissuesB. heart attack and death common before age 15C. no LDL receptors on cells D. added normal LDL to a cell medium caused cholesterol synthesis to stopE. discovery of LDL receptors led to how the body controls cholesterolVI. Lipid MetabolismA. fuel and storageB. fatty acids used for enegy or stored as TGC. in muscle FA metabolized to ATPD. In Adipose: after a meal excess energy FA to TGi. between meals some TG to FAii. feasting: fat to TG CHO to FA to TG protein to FA to TGiii. fasting: TG to FA + glycerol to body cellsiv. low CHO means incomplete burning of fat (ketone bodies)VII. MedicationsA. work to lower LDL in one of two waysB. Statins vs sterolsVIII. Hormonal Control of TGA. insulin increases storage of TG in adiposeB. Glucagon and epinephrine lowers adipose