Iron deficiency diminishes gallbladder neuronal nitric oxide synthase

Deborah A. Swartz-Basile, Matthew I. Goldblatt, Cindy Blaser, Philip A. Decker, Steven A. Ahrendt, Sushil K. Sarna, Henry A. Pitt

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Background. Iron deficiency has been demonstrated in the prairie dog to result in cholesterol crystal formation and altered biliary motility. Gallbladder filling and emptying are influenced by both inhibitory and excitatory stimuli, with nitric oxide (NO) playing a key role in normal relaxation. Iron is a cofactor for nitric oxide synthase. Therefore, we tested the hypothesis that iron deficiency would result in diminished levels of gallbladder neuronal nitric oxide synthase (nNOS) but would not influence the gallbladder's response to excitatory stimuli. Materials and methods. Twenty adult female prairie dogs were fed either an iron-supplemented (Fe+) (200 ppm) control diet (n = 10) or an iron-deficient (Fe-) (8 ppm) diet (n = 10) for 8 weeks. Fasting gallbladder volume was measured. Gallbladder muscle strips were harvested for response to excitatory stimuli and measurement of nNOS protein levels by Western blotting. Muscle strip response to a spectrum of doses of cholecystokinin, acetylcholine, and electrical field stimuli was determined, and the areas under the response curves were calculated. Results. Gallbladder volume increased in the iron-deficient prairie dogs compared with the iron-supplemented group (1.45 ± 0.27 mL vs 0.80 ± 0.13 mL, P < 0.05). Iron deficiency diminished the ratio of gallbladder nNOS to β-actin protein levels (0.05 ± 0.01 vs 3.48 ± 1.02, P < 0.05) but resulted in a normal response to excitatory stimuli. Conclusions. We conclude that diminished gallbladder neuronal nitric oxide synthase contributes to the gallbladder stasis that occurs with iron deficiency. This phenomenon may contribute to the increased incidence of gallstones in premenopausal women. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)26-31
Number of pages6
JournalJournal of Surgical Research
Volume90
Issue number1
DOIs
StatePublished - May 1 2000
Externally publishedYes

Fingerprint

Nitric Oxide Synthase Type I
Gallbladder
Iron
Sciuridae
Gallbladder Emptying
Diet
Muscles
Cholecystokinin
Gallstones
Nitric Oxide Synthase
Acetylcholine
Area Under Curve
Actins
Fasting
Nitric Oxide
Proteins
Western Blotting
Cholesterol

Keywords

  • Gallbladder
  • Iron deficiency
  • Motility
  • Nitric oxide synthase

ASJC Scopus subject areas

  • Surgery

Cite this

Swartz-Basile, D. A., Goldblatt, M. I., Blaser, C., Decker, P. A., Ahrendt, S. A., Sarna, S. K., & Pitt, H. A. (2000). Iron deficiency diminishes gallbladder neuronal nitric oxide synthase. Journal of Surgical Research, 90(1), 26-31. https://doi.org/10.1006/jsre.2000.5827

Iron deficiency diminishes gallbladder neuronal nitric oxide synthase. / Swartz-Basile, Deborah A.; Goldblatt, Matthew I.; Blaser, Cindy; Decker, Philip A.; Ahrendt, Steven A.; Sarna, Sushil K.; Pitt, Henry A.

In: Journal of Surgical Research, Vol. 90, No. 1, 01.05.2000, p. 26-31.

Research output: Contribution to journalArticle

Swartz-Basile, DA, Goldblatt, MI, Blaser, C, Decker, PA, Ahrendt, SA, Sarna, SK & Pitt, HA 2000, 'Iron deficiency diminishes gallbladder neuronal nitric oxide synthase', Journal of Surgical Research, vol. 90, no. 1, pp. 26-31. https://doi.org/10.1006/jsre.2000.5827
Swartz-Basile DA, Goldblatt MI, Blaser C, Decker PA, Ahrendt SA, Sarna SK et al. Iron deficiency diminishes gallbladder neuronal nitric oxide synthase. Journal of Surgical Research. 2000 May 1;90(1):26-31. https://doi.org/10.1006/jsre.2000.5827
Swartz-Basile, Deborah A. ; Goldblatt, Matthew I. ; Blaser, Cindy ; Decker, Philip A. ; Ahrendt, Steven A. ; Sarna, Sushil K. ; Pitt, Henry A. / Iron deficiency diminishes gallbladder neuronal nitric oxide synthase. In: Journal of Surgical Research. 2000 ; Vol. 90, No. 1. pp. 26-31.
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abstract = "Background. Iron deficiency has been demonstrated in the prairie dog to result in cholesterol crystal formation and altered biliary motility. Gallbladder filling and emptying are influenced by both inhibitory and excitatory stimuli, with nitric oxide (NO) playing a key role in normal relaxation. Iron is a cofactor for nitric oxide synthase. Therefore, we tested the hypothesis that iron deficiency would result in diminished levels of gallbladder neuronal nitric oxide synthase (nNOS) but would not influence the gallbladder's response to excitatory stimuli. Materials and methods. Twenty adult female prairie dogs were fed either an iron-supplemented (Fe+) (200 ppm) control diet (n = 10) or an iron-deficient (Fe-) (8 ppm) diet (n = 10) for 8 weeks. Fasting gallbladder volume was measured. Gallbladder muscle strips were harvested for response to excitatory stimuli and measurement of nNOS protein levels by Western blotting. Muscle strip response to a spectrum of doses of cholecystokinin, acetylcholine, and electrical field stimuli was determined, and the areas under the response curves were calculated. Results. Gallbladder volume increased in the iron-deficient prairie dogs compared with the iron-supplemented group (1.45 ± 0.27 mL vs 0.80 ± 0.13 mL, P < 0.05). Iron deficiency diminished the ratio of gallbladder nNOS to β-actin protein levels (0.05 ± 0.01 vs 3.48 ± 1.02, P < 0.05) but resulted in a normal response to excitatory stimuli. Conclusions. We conclude that diminished gallbladder neuronal nitric oxide synthase contributes to the gallbladder stasis that occurs with iron deficiency. This phenomenon may contribute to the increased incidence of gallstones in premenopausal women. (C) 2000 Academic Press.",
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AB - Background. Iron deficiency has been demonstrated in the prairie dog to result in cholesterol crystal formation and altered biliary motility. Gallbladder filling and emptying are influenced by both inhibitory and excitatory stimuli, with nitric oxide (NO) playing a key role in normal relaxation. Iron is a cofactor for nitric oxide synthase. Therefore, we tested the hypothesis that iron deficiency would result in diminished levels of gallbladder neuronal nitric oxide synthase (nNOS) but would not influence the gallbladder's response to excitatory stimuli. Materials and methods. Twenty adult female prairie dogs were fed either an iron-supplemented (Fe+) (200 ppm) control diet (n = 10) or an iron-deficient (Fe-) (8 ppm) diet (n = 10) for 8 weeks. Fasting gallbladder volume was measured. Gallbladder muscle strips were harvested for response to excitatory stimuli and measurement of nNOS protein levels by Western blotting. Muscle strip response to a spectrum of doses of cholecystokinin, acetylcholine, and electrical field stimuli was determined, and the areas under the response curves were calculated. Results. Gallbladder volume increased in the iron-deficient prairie dogs compared with the iron-supplemented group (1.45 ± 0.27 mL vs 0.80 ± 0.13 mL, P < 0.05). Iron deficiency diminished the ratio of gallbladder nNOS to β-actin protein levels (0.05 ± 0.01 vs 3.48 ± 1.02, P < 0.05) but resulted in a normal response to excitatory stimuli. Conclusions. We conclude that diminished gallbladder neuronal nitric oxide synthase contributes to the gallbladder stasis that occurs with iron deficiency. This phenomenon may contribute to the increased incidence of gallstones in premenopausal women. (C) 2000 Academic Press.

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