pathophysiology of lipid metabolism, continued
IZ cholesterol esterified by ACAT mainly absorbed through MTP and in CM Affairs.
esterification dep. v. intracellular long-chain fatty acids (activated by CoA) -> effect on absorption, protein binding
= SREBP (sterol response element) 1a, 1c, 2; as inactive precursor molecules in the RES by LXR (liver X receptor) activated - > in the nucleus, activate enzymes f. fatty acid synthesis, Triglyceridbindung, phospholipid
Endogenous pathway - Liver
triglycerides :
SREBP1c regulates fatty acid and triglyceride synthesis, VLDL
newly synthesized from acetate, FS, degradation products d. CMR secreted in the blood substrate for LPL ->
IDL, -> either removed B, E receptor in the liver again, or HL (hepatic lipase), triglycerides and phospholipids from interior surface -> to LDL
SREBP1c regulates lipogenic effect of insulin in hepatic v.: glucokinase expression increased, phosphoenol pyruvate carboxykinase (gluconeogenesis) decreased;
insulin resistance: hyperinsulinemia; SREBP1c erhebl. stimulation - increased> fatty acid synthesis -> fatty liver
LDL cholesterol
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