Apolipoprotein A-IV synthesis in rat intestine: regulation by dietary triglyceride

Apfelbaum, Terri F.; Davidson, Nicholas O.; Glickman, Robert M.

doi:10.1152/ajpgi.1987.253.1.1-a

Cited by 29 publications

(36 citation statements)

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“…These results suggested that the expression of apo A-IV in the jejunum, the site for absorption of dietary lipids, LOWERS ILEAL APO A-I AND A-IV mRNA 351 might be modulated by dietary fat at the pretranslational level. This suggestion was supported by the previous studies that showed that apo A-IV synthesis by rat small intestine increased in response to dietary lipid and might be under pretranslational control (19)(20)(21). In this study, however, apo A-IV mRNA was reduced by bile diversion in the ileum but not the jejunum.…”

Section: Discussionsupporting

confidence: 87%

Bile Diversion Lowers Apolipoprotein A-I and A-IV mRNA Levels in Rat Ileum.

Sonoyama

Nishikawa

Kiriyama

et al. 1994

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryWe recently reported that cholestyramine (a bile acid se questrant) lowered ileal apolipoprotein A-I mRNA level in rats. To obtain further information about this phenomenon, in this study, we investigated whether bile diversion lowers apolipoprotein A-I mRNA level in the ileum of rats. Bile-diverted rats were fed a diet with no added Na taurocholate (control diet) or with 0.4% Na taurocholate for 7 days. Sham-operated rats were also fed the control diet for the same period. Northern blot analysis revealed that the relative concentrations of jejunal apolipoprotein A-I and A-IV mRNA at the end of experimental period did not differ between groups while ileal apolipoprotein A-I and A-IV mRNA concentrations were significantly lower in bile-diverted rats fed the control and Na taurocholate-containing diets than in sham-operated rats. Plasma total and HDL cholesterol concentrations were the same in all groups. Relative concentration of apolipoprotein A-I in plasma also did not change. These results suggest that the bile plays an important role in ileal apolipoprotein gene expression at the pretranslational stage, but it is still unclear whether the effector is the bile acid or not. The unchanged concentration of plasma apolipoprotein A-I may have resulted from the constant secretion independent of synthesis in the intestine or the larger contribution from the liver which is another principal site for apolipo protein A-I expression.

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Section: Discussionsupporting

confidence: 87%

Bile Diversion Lowers Apolipoprotein A-I and A-IV mRNA Levels in Rat Ileum.

Sonoyama

Nishikawa

Kiriyama

et al. 1994

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…Normally, Apo A-IV is secreted primarily into the portal circulation from the small intestine and rises in response to high-fat meals (35). A lesser amount is produced by the liver.…”

Section: Discussionmentioning

confidence: 99%

Effects of Leptin Deficiency and Short-Term Repletion on Hepatic Gene Expression in Genetically Obese Mice

Ferrante¹,

Thearle²,

Liao

et al. 2001

Diabetes

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By supplying most organs of the body with metabolic substrates, the liver plays a central role in maintaining energy balance. Hepatic metabolism of glucose, fatty acids, and lipoproteins is disrupted in the leptin-deficient obese (Lep ob /Lep ob ) mouse, leading to hyperglycemia, steatosis, and hypercholesterolemia. Microarray expression profiles were used to identify transcriptional perturbations that underlie the altered hepatic physiology of Lep ob /Lep ob mice. A wide variety of genes involved in fatty acid metabolism are altered in expression, which suggests that both fatty acid synthesis and oxidation programs are activated in obese mice. The expression of a small subset of genes is upregulated by leptin deficiency, not modulated by caloric restriction, and markedly suppressed by short-term leptin treatment. Among these leptin-regulated genes, apolipoprotein A-IV is a strong candidate for mediating the atherogenic-resistant phenotype of Lep ob /Lep ob mice.

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“…Although a broad spectrum of physiological functions have been proposed for apoA-IV (5,6), the preponderance of evidence suggests that its primary biological function is related to intestinal lipid absorption. In humans, apoA-IV expression is restricted to the intestine and is specifically stimulated by triglyceride absorption (7)(8)(9)(10). The secretion of apoA-IV into mesenteric lymph rapidly increases during fat absorption in parallel with lymph triglycerides (11).…”

mentioning

confidence: 99%

apoA-IV tagged with the ER retention signal KDEL perturbs the intracellular trafficking and secretion of apoB

Gallagher

Weinberg

Shelness

2004

Journal of Lipid Research

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To examine the role of apolipoprotein A-IV (apoA-IV) in the intracellular trafficking and secretion of apoB, COS cells were cotransfected with microsomal triglyceride transfer protein (MTP), apoB-41 (amino terminal 41% of apoB), and either native apoA-IV or apoA-IV modified with the carboxy-terminal endoplasmic reticulum (ER) retention signal, KDEL (apoA-IV-KDEL). As expected, apoA-IV-KDEL was inefficiently secreted relative to native apoA-IV. Coexpression of apoB-41 with apoA-IV-KDEL reduced the secretion of apoB-41 by ‫ف‬ 80%. The apoA-IV-KDEL effect was specific, as neither KDEL-modified forms of human serum albumin or apoA-I affected apoB-41 secretion. Similar results were observed in McA-RH7777 rat hepatoma cells, which express endogenous MTP. The full inhibitory effect of apoA-IV-KDEL on apoB secretion was observed only for forms of apoB containing a minimum of the amino-terminal 25% of the protein (apoB-25). However, apoA-IV-KDEL inhibited the secretion of both lipid-associated and lipid-poor forms of apoB-25. Dual-label immunofluorescence microscopy of cells transfected with native apoA-IV and apoB-25 revealed that both apolipoproteins were localized to the ER and Golgi, as expected. However, when apoA-IV-KDEL was cotransfected with apoB-25, both proteins localized primarily to the ER. These data suggest that apoA-IV may physically interact with apoB in the secretory pathway, perhaps reflecting a role in modulating the process of triglyceride-rich lipoprotein assembly and secretion. -Gallagher, J. W., R. B. Weinberg, and G. S. Shelness. apoA-IV tagged with the ER retention signal KDEL perturbs the intracellular trafficking and secretion of apoB.

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Apolipoprotein A-IV synthesis in rat intestine: regulation by dietary triglyceride

Cited by 29 publications

References 0 publications

Bile Diversion Lowers Apolipoprotein A-I and A-IV mRNA Levels in Rat Ileum.

Bile Diversion Lowers Apolipoprotein A-I and A-IV mRNA Levels in Rat Ileum.

Effects of Leptin Deficiency and Short-Term Repletion on Hepatic Gene Expression in Genetically Obese Mice

apoA-IV tagged with the ER retention signal KDEL perturbs the intracellular trafficking and secretion of apoB

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