CE and lipoproteins

• lipoprotein lipase (LPL): enzyme that stimulates lipolysis, breaks of TG into FA and glycerol, they can then enter cells
• VLDL: synthesized in liver, transport endogenous fats
• VLDLs made in liver ER with ApoB-100
• Fructose: stays in the liver, more lipogenic than glucose
• LPL recognizes Apo-CII on VLDLs to take up TAGS into skeletal muscle and adipose tissue
• Insulin: promotes uptake of TAGs into adipose tissue bc this is primary storage site
• Skeletal muscle and heart have access to FAs for fuel during fasted state
• steroid hormones are synthesized from cholesterol: sex hormones, cortisol, aldosterone
• bile acids are made from CE: makes it emulsifier for lipids during digestion
• Isoprenoids: made from CE precursors, makes up vitamin D
• CE synthesis: 3 acetyl-CoA combine to form HMG-CoA, then HMG-CoA turns to mevalonate by HMG-CoA reductase
• Statins: taget HMG-CoA reductase, blocks the synthesis of mevalonate
• HMGCR: catalytic domain is in cytosol, sterol-sensing domain is in the ER lumen. sterol-sensing responds to high CE, HMGCR will leave membrane and be degraded
• Mevalonate: goes into pathway to form vitamin D, steroid hormones, and bile acids
• HMGCR: active in dephosphorylated state, inactive when phosphorylated
• HMGCR: high CE: translocate out of ER membrane: low CE: transcription factor promotes its gene expression
• Dyslipidemia: abnormal blood lipids, low HDL, high LDL, high total-C, high TG. want high HDL and low LDL
• Foam cell: LDL combines with macrophage, HDL is protective bc it removes CE from the macrophage
• small LDL particle size is an increased risk factor for CVD