Adeli 25 28
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Adeli 25 28
- 1. Postulated Mechanisms of Insulin ResistancePostulated Mechanisms of Insulin Resistance PTP-1BPTP-1B Mass & ActivityMass & Activity Impaired Phosphorylation ofImpaired Phosphorylation of Insulin Receptor, IRS-1Insulin Receptor, IRS-1 PI-3 Kinase ActivityPI-3 Kinase Activity Attenuated Insulin SignalingAttenuated Insulin Signaling Reduced Phosphorylation of ApoB orReduced Phosphorylation of ApoB or an apoB-chaperonean apoB-chaperone Enhanced Stability and Accelerated Assembly of ApoBEnhanced Stability and Accelerated Assembly of ApoB Overproduction of VLDLOverproduction of VLDL ER-60MTP
- 2. Intestine Contribution of the Intestinal LipoproteinsContribution of the Intestinal Lipoproteins to Metabolic Dyslipidemia in Insulin Resistanceto Metabolic Dyslipidemia in Insulin Resistance Liver ApoB48 ApoB100 Intestinal Lipoprotein Metabolism
- 3. DietaryDietary CholesterolCholesterol DietaryDietary FatFat LuminalLuminal TriglycerideTriglyceride LipasesLipases Bile AcidsBile Acids Fatty AcidsFatty Acids Mocellar CholesterolMocellar Cholesterol Fatty AcidsFatty Acids CholrdyrtolCholrdyrtol ApoB48 + TG + CEApoB48 + TG + CE TGTG CMCM ABCA1ABCA1 ABCG5ABCG5 ABCG8ABCG8 Fatty Acid TransportersFatty Acid Transporters Intestinal Epithelial CellIntestinal Epithelial Cell (Intake)(Intake) (Uptake)(Uptake) (Chylomicron(Chylomicron Assembly)Assembly) (Cholesterol(Cholesterol Excretion)Excretion) Intestinal Lipid Absorption (Trigleride(Trigleride Synthesis)Synthesis)
- 4. Hypothesis III: Fasting and postprandial hyperlipidemia in insulin resistant states may be attributable in part to intestinal oversecretion of apoB-48 containing lipoproteins Experimental Approach: • Dietary induction of an insulin resistant state in the hamster by high fructose feeding • Isolation of adult viable villi from Syrian hamster small intestine. • -In Vivo Studies to assess production rate of intestinal (apoB48- containing) lipoproteins • -Ex Vivo Studies to assess intestinal apoB48 lipoprotein synthesis and secretion, mechanisms of chylomicron assembly, role of de novo lipogenesis in intestinal lipoprotein secretion in the fasting and postprandial states
Hinweis der Redaktion
- Key point: The process of cholesterol absorption is complex and currently only partly understood. Cholesterol absorption is a complex, multistep process. Methods of affecting these processes include reducing dietary cholesterol by decreasing intake. Bile acid sequestrants such as cholestyramine and colestipol bind to bile acids, blocking their normal resorption. This increases bile acid excretion resulting in a net cholesterol loss.4,10 The packaging of cholesterol in micelles can be reduced through the use of plant stanol esters, such as sitostanol. These esters are structurally similar to cholesterol and competitively compete with cholesterol for incorporation into micelles.2,5,11,12 Since cholesterol must be packaged in micelles in order to cross the basement membrane of enterocytes, this effectively decreases cholesterol uptake and increases cholesterol secretion. ABCG5 and ABCG8 are proteins involved in sterol excretion.13 ABCA1 is up-regulated by cellular cholesterol and functions to transport cholesterol out of the cell.7-9