Iron deficiency transiently suppresses biliary neuronal nitric oxide synthase

Matthew I. Goldblatt, Deborah A. Swartz-Basile, Seong Ho Choi, Parvaneh Rafiee, Attila Nakeeb, Sushil K. Sarna, Henry A. Pitt

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background. Iron deficiency results in altered gall bladder and sphincter of Oddi (SO) motility and cholesterol crystal formation. In addition, gallbladder neuronal nitric oxide synthase (nNOS) has been shown to be markedly reduced after 8 weeks on an iron-deficient diet. However, the effects of prolonged iron deficiency on gallbladder and SO nNOS as well as crystal formation have not been determined. Therefore, we tested the hypothesis that iron deficiency would downregulate both gallbladder and SO nNOS expression and that nNOS downregulation and cholesterol crystal formation would progress over time. Materials and methods. Thirty-eight adult female prairie dogs were fed either an iron-supplemented (Fe+) (200 ppm) or an iron-deficient (Fe-) (8 ppm) diet for 8 weeks (Fe+ n = 9, Fe- n = 10) or 16 weeks (Fe+ n = 9, Fe- n = 10). Blood hemoglobin (HbG) was measured; gallbladder cholesterol crystals were counted; and cholesterol saturation indices (CSI) were calculated. Gallbladder and SO nNOS levels were measured by Western blot. Results. The Fe+ prairie dogs had significantly higher HbG than the Fe- animals (16.9 ± 0.6 g/dl vs 15.2 ± 0.5 g/dl, respectively, P < 0.05) after 8 weeks. This difference was even greater after 16 weeks (16.1 ± 0.4 g/dl vs 14.0 ± 0.5 g/dl, P < 0.01). At 8 weeks, more cholesterol crystals per 10 HPF were observed in the Fe- animals (0.4 ± 0.3 vs 1.6 ± 0.4 per 10 HPF, P < 0.05). This difference was even greater after 16 weeks (0.0 ± 0.0 vs 52.6 ± 25.3 per 10 HPF, P < 0.01). No difference in the CSI was observed in the four groups. Iron deficiency decreased the nNOS/β-actin protein levels in the gallbladder and SO at 8 weeks (57.0 ± 29.6 vs 7.4 ± 2.6, gallbladder, P < 0.05) (98.4 ± 39.7 vs 29.9 ± 11.0, SO, P = 0.09), but these levels returned to baseline at 16 weeks. Conclusions. We conclude that iron deficiency acutely suppresses gallbladder and SO nNOS, and that compensatory mechanisms return nNOS to baseline levels while cholesterol crystal formation increases over time.

Original languageEnglish (US)
Pages (from-to)123-128
Number of pages6
JournalJournal of Surgical Research
Volume98
Issue number2
DOIs
StatePublished - Jun 15 2001
Externally publishedYes

Fingerprint

Nitric Oxide Synthase Type I
Sphincter of Oddi
Gallbladder
Iron
Cholesterol
Sciuridae
Down-Regulation
Diet
Actins
Hemoglobins
Urinary Bladder
Western Blotting

Keywords

  • Gallbladder
  • Iron deficiency
  • Neuronal nitric oxide synthase
  • Prairie dog
  • Sphincter of Oddi

ASJC Scopus subject areas

  • Surgery

Cite this

Goldblatt, M. I., Swartz-Basile, D. A., Choi, S. H., Rafiee, P., Nakeeb, A., Sarna, S. K., & Pitt, H. A. (2001). Iron deficiency transiently suppresses biliary neuronal nitric oxide synthase. Journal of Surgical Research, 98(2), 123-128. https://doi.org/10.1006/jsre.2001.6196

Iron deficiency transiently suppresses biliary neuronal nitric oxide synthase. / Goldblatt, Matthew I.; Swartz-Basile, Deborah A.; Choi, Seong Ho; Rafiee, Parvaneh; Nakeeb, Attila; Sarna, Sushil K.; Pitt, Henry A.

In: Journal of Surgical Research, Vol. 98, No. 2, 15.06.2001, p. 123-128.

Research output: Contribution to journalArticle

Goldblatt, MI, Swartz-Basile, DA, Choi, SH, Rafiee, P, Nakeeb, A, Sarna, SK & Pitt, HA 2001, 'Iron deficiency transiently suppresses biliary neuronal nitric oxide synthase', Journal of Surgical Research, vol. 98, no. 2, pp. 123-128. https://doi.org/10.1006/jsre.2001.6196
Goldblatt MI, Swartz-Basile DA, Choi SH, Rafiee P, Nakeeb A, Sarna SK et al. Iron deficiency transiently suppresses biliary neuronal nitric oxide synthase. Journal of Surgical Research. 2001 Jun 15;98(2):123-128. https://doi.org/10.1006/jsre.2001.6196
Goldblatt, Matthew I. ; Swartz-Basile, Deborah A. ; Choi, Seong Ho ; Rafiee, Parvaneh ; Nakeeb, Attila ; Sarna, Sushil K. ; Pitt, Henry A. / Iron deficiency transiently suppresses biliary neuronal nitric oxide synthase. In: Journal of Surgical Research. 2001 ; Vol. 98, No. 2. pp. 123-128.
@article{920cf4d0e877495f8051abc684c7898d,
title = "Iron deficiency transiently suppresses biliary neuronal nitric oxide synthase",
abstract = "Background. Iron deficiency results in altered gall bladder and sphincter of Oddi (SO) motility and cholesterol crystal formation. In addition, gallbladder neuronal nitric oxide synthase (nNOS) has been shown to be markedly reduced after 8 weeks on an iron-deficient diet. However, the effects of prolonged iron deficiency on gallbladder and SO nNOS as well as crystal formation have not been determined. Therefore, we tested the hypothesis that iron deficiency would downregulate both gallbladder and SO nNOS expression and that nNOS downregulation and cholesterol crystal formation would progress over time. Materials and methods. Thirty-eight adult female prairie dogs were fed either an iron-supplemented (Fe+) (200 ppm) or an iron-deficient (Fe-) (8 ppm) diet for 8 weeks (Fe+ n = 9, Fe- n = 10) or 16 weeks (Fe+ n = 9, Fe- n = 10). Blood hemoglobin (HbG) was measured; gallbladder cholesterol crystals were counted; and cholesterol saturation indices (CSI) were calculated. Gallbladder and SO nNOS levels were measured by Western blot. Results. The Fe+ prairie dogs had significantly higher HbG than the Fe- animals (16.9 ± 0.6 g/dl vs 15.2 ± 0.5 g/dl, respectively, P < 0.05) after 8 weeks. This difference was even greater after 16 weeks (16.1 ± 0.4 g/dl vs 14.0 ± 0.5 g/dl, P < 0.01). At 8 weeks, more cholesterol crystals per 10 HPF were observed in the Fe- animals (0.4 ± 0.3 vs 1.6 ± 0.4 per 10 HPF, P < 0.05). This difference was even greater after 16 weeks (0.0 ± 0.0 vs 52.6 ± 25.3 per 10 HPF, P < 0.01). No difference in the CSI was observed in the four groups. Iron deficiency decreased the nNOS/β-actin protein levels in the gallbladder and SO at 8 weeks (57.0 ± 29.6 vs 7.4 ± 2.6, gallbladder, P < 0.05) (98.4 ± 39.7 vs 29.9 ± 11.0, SO, P = 0.09), but these levels returned to baseline at 16 weeks. Conclusions. We conclude that iron deficiency acutely suppresses gallbladder and SO nNOS, and that compensatory mechanisms return nNOS to baseline levels while cholesterol crystal formation increases over time.",
keywords = "Gallbladder, Iron deficiency, Neuronal nitric oxide synthase, Prairie dog, Sphincter of Oddi",
author = "Goldblatt, {Matthew I.} and Swartz-Basile, {Deborah A.} and Choi, {Seong Ho} and Parvaneh Rafiee and Attila Nakeeb and Sarna, {Sushil K.} and Pitt, {Henry A.}",
year = "2001",
month = "6",
day = "15",
doi = "10.1006/jsre.2001.6196",
language = "English (US)",
volume = "98",
pages = "123--128",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Iron deficiency transiently suppresses biliary neuronal nitric oxide synthase

AU - Goldblatt, Matthew I.

AU - Swartz-Basile, Deborah A.

AU - Choi, Seong Ho

AU - Rafiee, Parvaneh

AU - Nakeeb, Attila

AU - Sarna, Sushil K.

AU - Pitt, Henry A.

PY - 2001/6/15

Y1 - 2001/6/15

N2 - Background. Iron deficiency results in altered gall bladder and sphincter of Oddi (SO) motility and cholesterol crystal formation. In addition, gallbladder neuronal nitric oxide synthase (nNOS) has been shown to be markedly reduced after 8 weeks on an iron-deficient diet. However, the effects of prolonged iron deficiency on gallbladder and SO nNOS as well as crystal formation have not been determined. Therefore, we tested the hypothesis that iron deficiency would downregulate both gallbladder and SO nNOS expression and that nNOS downregulation and cholesterol crystal formation would progress over time. Materials and methods. Thirty-eight adult female prairie dogs were fed either an iron-supplemented (Fe+) (200 ppm) or an iron-deficient (Fe-) (8 ppm) diet for 8 weeks (Fe+ n = 9, Fe- n = 10) or 16 weeks (Fe+ n = 9, Fe- n = 10). Blood hemoglobin (HbG) was measured; gallbladder cholesterol crystals were counted; and cholesterol saturation indices (CSI) were calculated. Gallbladder and SO nNOS levels were measured by Western blot. Results. The Fe+ prairie dogs had significantly higher HbG than the Fe- animals (16.9 ± 0.6 g/dl vs 15.2 ± 0.5 g/dl, respectively, P < 0.05) after 8 weeks. This difference was even greater after 16 weeks (16.1 ± 0.4 g/dl vs 14.0 ± 0.5 g/dl, P < 0.01). At 8 weeks, more cholesterol crystals per 10 HPF were observed in the Fe- animals (0.4 ± 0.3 vs 1.6 ± 0.4 per 10 HPF, P < 0.05). This difference was even greater after 16 weeks (0.0 ± 0.0 vs 52.6 ± 25.3 per 10 HPF, P < 0.01). No difference in the CSI was observed in the four groups. Iron deficiency decreased the nNOS/β-actin protein levels in the gallbladder and SO at 8 weeks (57.0 ± 29.6 vs 7.4 ± 2.6, gallbladder, P < 0.05) (98.4 ± 39.7 vs 29.9 ± 11.0, SO, P = 0.09), but these levels returned to baseline at 16 weeks. Conclusions. We conclude that iron deficiency acutely suppresses gallbladder and SO nNOS, and that compensatory mechanisms return nNOS to baseline levels while cholesterol crystal formation increases over time.

AB - Background. Iron deficiency results in altered gall bladder and sphincter of Oddi (SO) motility and cholesterol crystal formation. In addition, gallbladder neuronal nitric oxide synthase (nNOS) has been shown to be markedly reduced after 8 weeks on an iron-deficient diet. However, the effects of prolonged iron deficiency on gallbladder and SO nNOS as well as crystal formation have not been determined. Therefore, we tested the hypothesis that iron deficiency would downregulate both gallbladder and SO nNOS expression and that nNOS downregulation and cholesterol crystal formation would progress over time. Materials and methods. Thirty-eight adult female prairie dogs were fed either an iron-supplemented (Fe+) (200 ppm) or an iron-deficient (Fe-) (8 ppm) diet for 8 weeks (Fe+ n = 9, Fe- n = 10) or 16 weeks (Fe+ n = 9, Fe- n = 10). Blood hemoglobin (HbG) was measured; gallbladder cholesterol crystals were counted; and cholesterol saturation indices (CSI) were calculated. Gallbladder and SO nNOS levels were measured by Western blot. Results. The Fe+ prairie dogs had significantly higher HbG than the Fe- animals (16.9 ± 0.6 g/dl vs 15.2 ± 0.5 g/dl, respectively, P < 0.05) after 8 weeks. This difference was even greater after 16 weeks (16.1 ± 0.4 g/dl vs 14.0 ± 0.5 g/dl, P < 0.01). At 8 weeks, more cholesterol crystals per 10 HPF were observed in the Fe- animals (0.4 ± 0.3 vs 1.6 ± 0.4 per 10 HPF, P < 0.05). This difference was even greater after 16 weeks (0.0 ± 0.0 vs 52.6 ± 25.3 per 10 HPF, P < 0.01). No difference in the CSI was observed in the four groups. Iron deficiency decreased the nNOS/β-actin protein levels in the gallbladder and SO at 8 weeks (57.0 ± 29.6 vs 7.4 ± 2.6, gallbladder, P < 0.05) (98.4 ± 39.7 vs 29.9 ± 11.0, SO, P = 0.09), but these levels returned to baseline at 16 weeks. Conclusions. We conclude that iron deficiency acutely suppresses gallbladder and SO nNOS, and that compensatory mechanisms return nNOS to baseline levels while cholesterol crystal formation increases over time.

KW - Gallbladder

KW - Iron deficiency

KW - Neuronal nitric oxide synthase

KW - Prairie dog

KW - Sphincter of Oddi

UR - http://www.scopus.com/inward/record.url?scp=0035876226&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035876226&partnerID=8YFLogxK

U2 - 10.1006/jsre.2001.6196

DO - 10.1006/jsre.2001.6196

M3 - Article

VL - 98

SP - 123

EP - 128

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 2

ER -