Effects of acute inflammation on plasma retinol, retinol-binding protein, and its mRNA in the liver and kidneys of vitamin A-sufficient rats

Francisco J. Rosales, Steven J. Ritter, Reza Zolfaghari, John Edgar Smith, A. Catharine Ross

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Abstract

The acute inflammatory response to tissue injury and infection is associated with low concentrations of plasma retinol and its specific transport proteins, retinol-binding protein (RBP) and transthyretin (TTR). To examine the kinetics and mechanism of hyporetinemia, we have induced acute inflammation with lipopolysaccharide (LPS, from Pseudomonas aeruginosa) in rats with adequate stores of vitamin A. Twenty-four h after treatment with LPS (50 μg i.p. per 100 g body weight) or saline and food withdrawal, plasma retinol equalled 0.72 ± 0.06 μmol/L (mean ± SEM) in five LPS-treated rats versus 1.35 ± 0.1 μmol/L in five saline-treated rats (P < 0.01). Plasma, liver, and kidney RBP and TTR concentrations ere also significantly reduced, but liver and kidney retinol concentrations did not differ between treatment groups. The relative abundance of RBP mRNA in liver (LPS treatment compared to saline treatment) was reduced as early as 12 h (0.44 ± 0.15, n = 4 pairs, P < 0.02), and continued to be reduced at 24 h (0.57 ± 0.12, n = 5 pairs, P < 0.02). In the kidney this ratio did not change significantly due to LPS treatment. The relative abundance of cellular retinol-binding protein (CRBP) mRNA in liver and kidney also was not affected by LPS treatment. We infer from these data that inflammation-induced hyporetinemia results from a reduction in the hepatic synthesis of RBP and secretion of the retinol-RBP complex. Moreover, the results imply that plasma retinol concentration is a poor indicator of vitamin A status during inflammation.

Original languageEnglish (US)
Pages (from-to)962-971
Number of pages10
JournalJournal of Lipid Research
Volume37
Issue number5
StatePublished - May 1 1996

Fingerprint

Retinol-Binding Proteins
Vitamin A
Liver
Rats
Inflammation
Kidney
Plasmas
Messenger RNA
Prealbumin
Cellular Retinol-Binding Proteins
Protein Binding
Pseudomonas aeruginosa
Lipopolysaccharides
Carrier Proteins
Body Weight
Tissue
Food
Scanning electron microscopy
Kinetics
Wounds and Injuries

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Endocrinology
  • Cell Biology

Cite this

Rosales, Francisco J. ; Ritter, Steven J. ; Zolfaghari, Reza ; Smith, John Edgar ; Ross, A. Catharine. / Effects of acute inflammation on plasma retinol, retinol-binding protein, and its mRNA in the liver and kidneys of vitamin A-sufficient rats. In: Journal of Lipid Research. 1996 ; Vol. 37, No. 5. pp. 962-971.
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abstract = "The acute inflammatory response to tissue injury and infection is associated with low concentrations of plasma retinol and its specific transport proteins, retinol-binding protein (RBP) and transthyretin (TTR). To examine the kinetics and mechanism of hyporetinemia, we have induced acute inflammation with lipopolysaccharide (LPS, from Pseudomonas aeruginosa) in rats with adequate stores of vitamin A. Twenty-four h after treatment with LPS (50 μg i.p. per 100 g body weight) or saline and food withdrawal, plasma retinol equalled 0.72 ± 0.06 μmol/L (mean ± SEM) in five LPS-treated rats versus 1.35 ± 0.1 μmol/L in five saline-treated rats (P < 0.01). Plasma, liver, and kidney RBP and TTR concentrations ere also significantly reduced, but liver and kidney retinol concentrations did not differ between treatment groups. The relative abundance of RBP mRNA in liver (LPS treatment compared to saline treatment) was reduced as early as 12 h (0.44 ± 0.15, n = 4 pairs, P < 0.02), and continued to be reduced at 24 h (0.57 ± 0.12, n = 5 pairs, P < 0.02). In the kidney this ratio did not change significantly due to LPS treatment. The relative abundance of cellular retinol-binding protein (CRBP) mRNA in liver and kidney also was not affected by LPS treatment. We infer from these data that inflammation-induced hyporetinemia results from a reduction in the hepatic synthesis of RBP and secretion of the retinol-RBP complex. Moreover, the results imply that plasma retinol concentration is a poor indicator of vitamin A status during inflammation.",
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Effects of acute inflammation on plasma retinol, retinol-binding protein, and its mRNA in the liver and kidneys of vitamin A-sufficient rats. / Rosales, Francisco J.; Ritter, Steven J.; Zolfaghari, Reza; Smith, John Edgar; Ross, A. Catharine.

In: Journal of Lipid Research, Vol. 37, No. 5, 01.05.1996, p. 962-971.

Research output: Contribution to journalArticle

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T1 - Effects of acute inflammation on plasma retinol, retinol-binding protein, and its mRNA in the liver and kidneys of vitamin A-sufficient rats

AU - Rosales, Francisco J.

AU - Ritter, Steven J.

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AU - Ross, A. Catharine

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N2 - The acute inflammatory response to tissue injury and infection is associated with low concentrations of plasma retinol and its specific transport proteins, retinol-binding protein (RBP) and transthyretin (TTR). To examine the kinetics and mechanism of hyporetinemia, we have induced acute inflammation with lipopolysaccharide (LPS, from Pseudomonas aeruginosa) in rats with adequate stores of vitamin A. Twenty-four h after treatment with LPS (50 μg i.p. per 100 g body weight) or saline and food withdrawal, plasma retinol equalled 0.72 ± 0.06 μmol/L (mean ± SEM) in five LPS-treated rats versus 1.35 ± 0.1 μmol/L in five saline-treated rats (P < 0.01). Plasma, liver, and kidney RBP and TTR concentrations ere also significantly reduced, but liver and kidney retinol concentrations did not differ between treatment groups. The relative abundance of RBP mRNA in liver (LPS treatment compared to saline treatment) was reduced as early as 12 h (0.44 ± 0.15, n = 4 pairs, P < 0.02), and continued to be reduced at 24 h (0.57 ± 0.12, n = 5 pairs, P < 0.02). In the kidney this ratio did not change significantly due to LPS treatment. The relative abundance of cellular retinol-binding protein (CRBP) mRNA in liver and kidney also was not affected by LPS treatment. We infer from these data that inflammation-induced hyporetinemia results from a reduction in the hepatic synthesis of RBP and secretion of the retinol-RBP complex. Moreover, the results imply that plasma retinol concentration is a poor indicator of vitamin A status during inflammation.

AB - The acute inflammatory response to tissue injury and infection is associated with low concentrations of plasma retinol and its specific transport proteins, retinol-binding protein (RBP) and transthyretin (TTR). To examine the kinetics and mechanism of hyporetinemia, we have induced acute inflammation with lipopolysaccharide (LPS, from Pseudomonas aeruginosa) in rats with adequate stores of vitamin A. Twenty-four h after treatment with LPS (50 μg i.p. per 100 g body weight) or saline and food withdrawal, plasma retinol equalled 0.72 ± 0.06 μmol/L (mean ± SEM) in five LPS-treated rats versus 1.35 ± 0.1 μmol/L in five saline-treated rats (P < 0.01). Plasma, liver, and kidney RBP and TTR concentrations ere also significantly reduced, but liver and kidney retinol concentrations did not differ between treatment groups. The relative abundance of RBP mRNA in liver (LPS treatment compared to saline treatment) was reduced as early as 12 h (0.44 ± 0.15, n = 4 pairs, P < 0.02), and continued to be reduced at 24 h (0.57 ± 0.12, n = 5 pairs, P < 0.02). In the kidney this ratio did not change significantly due to LPS treatment. The relative abundance of cellular retinol-binding protein (CRBP) mRNA in liver and kidney also was not affected by LPS treatment. We infer from these data that inflammation-induced hyporetinemia results from a reduction in the hepatic synthesis of RBP and secretion of the retinol-RBP complex. Moreover, the results imply that plasma retinol concentration is a poor indicator of vitamin A status during inflammation.

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