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
Wednesday, June 8, 2005
Tuesday, June 7, 2005
Ruger 10-22 Wooden Bullpup Stock
pathophysiology of lipid metabolism
Central Europe: about 40% of energy taken as fat, some polyunsaturated fatty acids (FA) are essential (10 g / d of linoleic acid, 2 g / d alpha -linolenic acid) -> -> Eicosanoids
storage v. fats + metabolites d. d. adipose tissue glucose in adipocytes, lipolysis of cAMP when required
transport as free FS, to albumin or lipoproteins in of cholesterol, triglycerides, phospholipids and proteins (apolipoproteins);
triglyceride: chylomicrons (triglycerides from food -> liver), VLDL (endogenous TG -> liver)
High cholesterol: LDL, low HDL
VLD -> reduction of IDL, LDL
cholesterol metabolism :
exogenously about 0.5 g / d, endogenously about 1 g / d;
about 40% absorbed
intracellular synthesis of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMG-CoA reductase)
high serum LDL, high dietary cholesterol intake - less> endogenous synthesis (suppression d. LDL . receptor inhibition d. HMG-CoA reductase in the liver cell)
still hypercholesterolemia Possible: saturates inhibited by LDL degradation, suppression d. d. LDL-receptor activity;
excretion: with biliary cholesterol or bile acids ; breakdown products of steroidal hormones, Hautsbschilferung
VLDL, IDL and LDL - atherogenic>
HDL -> protective
Exogenous pathway - intestinal :
triglycerides : pancreatic lipase in the duodenum, upper jejunum, absorption, re-assembled, m. Apo B -> chylomicrons (CM) -> lymph;
absorption d. glycerides induced Education v. AI, AII, AIV + in mucosa and liver in ApoB48 mucosa (essential f. CM-formation, but can not bind to LDL receptor);!
compound m. B48 on MTP = microsomal Triglyceridtransferprotein;
Apo C and E in the transfer of lymph HDL to CM
ApoCII stimulates LPL (lipoprotein lipase) on endothelial cells, - hydroysiert> triglycerides and removed from CM; liver takes CMR = Chylomikronenremnants of LRP (Apo -E-binding receptor)
cholesterol: from food + bile; absorption 25-75%;
unesterified -> in micelles m. Bile acids, triglycerides and phospholipids, possibly by spec. Sterol transporter
IZ Date: esterified to 80%
Central Europe: about 40% of energy taken as fat, some polyunsaturated fatty acids (FA) are essential (10 g / d of linoleic acid, 2 g / d alpha -linolenic acid) -> -> Eicosanoids
storage v. fats + metabolites d. d. adipose tissue glucose in adipocytes, lipolysis of cAMP when required
transport as free FS, to albumin or lipoproteins in of cholesterol, triglycerides, phospholipids and proteins (apolipoproteins);
triglyceride: chylomicrons (triglycerides from food -> liver), VLDL (endogenous TG -> liver)
High cholesterol: LDL, low HDL
VLD -> reduction of IDL, LDL
cholesterol metabolism :
exogenously about 0.5 g / d, endogenously about 1 g / d;
about 40% absorbed
intracellular synthesis of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMG-CoA reductase)
high serum LDL, high dietary cholesterol intake - less> endogenous synthesis (suppression d. LDL . receptor inhibition d. HMG-CoA reductase in the liver cell)
still hypercholesterolemia Possible: saturates inhibited by LDL degradation, suppression d. d. LDL-receptor activity;
excretion: with biliary cholesterol or bile acids ; breakdown products of steroidal hormones, Hautsbschilferung
VLDL, IDL and LDL - atherogenic>
HDL -> protective
Exogenous pathway - intestinal :
triglycerides : pancreatic lipase in the duodenum, upper jejunum, absorption, re-assembled, m. Apo B -> chylomicrons (CM) -> lymph;
absorption d. glycerides induced Education v. AI, AII, AIV + in mucosa and liver in ApoB48 mucosa (essential f. CM-formation, but can not bind to LDL receptor);!
compound m. B48 on MTP = microsomal Triglyceridtransferprotein;
Apo C and E in the transfer of lymph HDL to CM
ApoCII stimulates LPL (lipoprotein lipase) on endothelial cells, - hydroysiert> triglycerides and removed from CM; liver takes CMR = Chylomikronenremnants of LRP (Apo -E-binding receptor)
cholesterol: from food + bile; absorption 25-75%;
unesterified -> in micelles m. Bile acids, triglycerides and phospholipids, possibly by spec. Sterol transporter
IZ Date: esterified to 80%
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