Increased lymph alkaline phosphatase after fat feeding: Effects of medium chain triglycerides and inhibition of protein synthesis

Glickman, Robert M.; Alpers, David H.; Drummey, Gladys D.; Isselbacher, Kurt J.

doi:10.1016/0304-4165(70)90296-5

Cited by 72 publications

(20 citation statements)

References 16 publications

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“…Intestinal Protein Synthesis Inhibition and Lymph Chylomicron Size 361 nificant decrease in the amount of oleic acid-14C recovered in lymph (Table I), both in this study and earlier (13) (Fig. 2), triglyceride/phospholipid ratios (Table II), and by electron microscopy Fig.…”

Section: Discussionsupporting

confidence: 71%

Fat Absorption During Inhibition of Protein Synthesis: Studies of Lymph Chylomicrons

Glickman¹,

Kirsch²,

Isselbacher³

1972

J. Clin. Invest.

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Section: Discussionsupporting

confidence: 71%

Fat Absorption During Inhibition of Protein Synthesis: Studies of Lymph Chylomicrons

Glickman¹,

Kirsch²,

Isselbacher³

1972

J. Clin. Invest.

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“…IAP is associated with the brush-border membrane of intestinal epithelial cells (20,62); it is thought to transport dietary lipids as a component of the surfactant-like particles that surround the neutral fat droplets in the villous enterocytes during fat absorption (32,33,64). Moreover, fatty meals increase the levels of IAP in serum and lymph (15,35). Mice homozygous for Akp3 null mutation showed faster body weight gain when fed a high-fat diet, as well as an increased lipid clearance, after a single oral administration of corn oil (38,40).…”

Section: Discussionmentioning

confidence: 99%

Pdx1inactivation restricted to the intestinal epithelium in mice alters duodenal gene expression in enterocytes and enteroendocrine cells

Chen

Fang²,

Davis

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Null mutant mice lacking the transcription factor pancreatic and duodenal homeobox 1 (Pdx1) are apancreatic and survive only a few days after birth. The role of Pdx1 in regulating intestinal gene expression has therefore yet to be determined in viable mice with normal pancreatic development. We hypothesized that conditional inactivation of Pdx1 restricted to the intestinal epithelium would alter intestinal gene expression and cell differentiation. Pdx1 flox/flox; VilCre mice with intestine-specific Pdx1 inactivation were generated by crossing a transgenic mouse strain expressing Cre recombinase, driven by a mouse villin 1 gene promoter fragment, with a mutant mouse strain homozygous for loxP site-flanked Pdx1. Pdx1 protein is undetectable in all epithelial cells in the intestinal epithelium of Pdx1 flox/flox; VilCre mice. Goblet cell number and mRNA abundance for mucin 3 and mucin 13 genes in the proximal small intestine are comparable between Pdx1 flox/flox; VilCre and control mice. Similarly, Paneth cell number and expression of Paneth cell-related genes Defa1, Defcr-rs1, and Mmp7 in the proximal small intestine remain statistically unchanged by Pdx1 inactivation. Although the number of enteroendocrine cells expressing chromogranin A/B, gastric inhibitory polypeptide (Gip), or somatostatin (Sst) is unaffected in the Pdx1 flox/flox; VilCre mice, mRNA abundance for Gip and Sst is significantly reduced in the proximal small intestine. Conditional Pdx1 inactivation attenuates intestinal alkaline phosphatase (IAP) activity in the duodenal epithelium, consistent with an average 91% decrease in expression of the mouse enterocyte IAP gene, alkaline phosphatase 3 (a novel Pdx1 target candidate), in the proximal small intestine following Pdx1 inactivation. We conclude that Pdx1 is necessary for patterning appropriate gene expression in enterocytes and enteroendocrine cells of the proximal small intestine.

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“…The cause ofreduced serum albumin, alanine aminotransferase, and alkaline phosphatase values is unknown, although impaired synthesis or release into the serum may account for these small changes (59).…”

Section: Discussionmentioning

confidence: 99%

Regulation of hepatic transport of bile salt. Effect of protein synthesis inhibition on excretion of bile salts and their binding to liver surface membrane fractions.

Gonzalez¹,

Sutherland²,

Simon³

1979

J. Clin. Invest.

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The overall transport ofbile salts across the hepatocyte is characterized as a carrier-mediated process whose rate-limiting step is biliary secretion. Specific bile salt binding proteins have been identified in liver surface membrane fractions and were postulated to represent the initial interaction in bile salt translocation across both the sinusoidal and canalicular membranes. To test this hypothesis, cycloheximide was administered to rats to inhibit hepatic protein synthesis. 16

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Increased lymph alkaline phosphatase after fat feeding: Effects of medium chain triglycerides and inhibition of protein synthesis

Cited by 72 publications

References 16 publications

Fat Absorption During Inhibition of Protein Synthesis: Studies of Lymph Chylomicrons

Fat Absorption During Inhibition of Protein Synthesis: Studies of Lymph Chylomicrons

Pdx1inactivation restricted to the intestinal epithelium in mice alters duodenal gene expression in enterocytes and enteroendocrine cells

Regulation of hepatic transport of bile salt. Effect of protein synthesis inhibition on excretion of bile salts and their binding to liver surface membrane fractions.

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