Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver

Nobuyuki Morikawa, Makoto Suematsu, Takanori Kyokane, Nobuhito Goda, Yusuke Kumamoto, Taro Okitsu, Yuzuru Ishimura, Masaki Kitajima

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Although discontinuous total parenteral nutrition (d-TPN) has recently been favored for clinical use over continuous total parenteral nutrition (c- TPN) to ameliorate liver dysfunction, mechanisms for the protection against postoperative liver dysfunction remain unknown. This study aimed to examine differences in mitochondrial function in d-TPN-and c-TPN-pretreated livers during ischemia-reperfusion. Rat livers pretreated with d-TPN or c-TPN were perfused with Krebs-Ringer buffer and were exposed to 25% low-flow hypoxia followed by reperfusion. Intrahepatic mitochondrial membrane potential (ΔΨ) and cell viability were assessed by dual-color digital microfluorography using rhodamine 123 (Rh123) and propidium iodide (PI), respectively. In response to hypoxia, livers pretreated with c-TPN, d-TPN, and an ordinary chow diet exhibited a significant ΔΨ reduction among the entire lobules. Upon reperfusion, the regional ΔΨ values further decreased in the c-TPN liver, whereas those in the d-TPN-treated or chow-treated livers displayed a rapid recovery toward the control levels. The severity of cell injury did not differ among the groups, showing that the reperfusion-induced ΔΨ drop in the c-TPN-pretreated liver is not a consequence of cell injury. Differences in the ΔΨ drop among the groups appear to occur irrespective of those in the glycogen storage, because the livers undergoing d-TPN display a marked ΔΨ recovery even when reperfused at the end of a fasted state. These results indicate that c-TPN, but not d-TPN, jeopardizes mitochondrial re- energization and suggest that a circadian pattern of the TPN serves as a potentially beneficial strategy to reduce the risk of postischemic mitochondrial dysfunction in the liver.

Original languageEnglish
Pages (from-to)1289-1299
Number of pages11
JournalHepatology
Volume28
Issue number5
DOIs
Publication statusPublished - 1998

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Total Parenteral Nutrition
Liver
Reperfusion
Liver Diseases
Rhodamine 123
Propidium
Mitochondrial Membrane Potential
Wounds and Injuries
Glycogen
Cell Survival
Buffers
Ischemia
Color
Diet

ASJC Scopus subject areas

  • Hepatology

Cite this

Morikawa, N., Suematsu, M., Kyokane, T., Goda, N., Kumamoto, Y., Okitsu, T., ... Kitajima, M. (1998). Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver. Hepatology, 28(5), 1289-1299. https://doi.org/10.1002/hep.510280518

Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver. / Morikawa, Nobuyuki; Suematsu, Makoto; Kyokane, Takanori; Goda, Nobuhito; Kumamoto, Yusuke; Okitsu, Taro; Ishimura, Yuzuru; Kitajima, Masaki.

In: Hepatology, Vol. 28, No. 5, 1998, p. 1289-1299.

Research output: Contribution to journalArticle

Morikawa, N, Suematsu, M, Kyokane, T, Goda, N, Kumamoto, Y, Okitsu, T, Ishimura, Y & Kitajima, M 1998, 'Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver', Hepatology, vol. 28, no. 5, pp. 1289-1299. https://doi.org/10.1002/hep.510280518
Morikawa, Nobuyuki ; Suematsu, Makoto ; Kyokane, Takanori ; Goda, Nobuhito ; Kumamoto, Yusuke ; Okitsu, Taro ; Ishimura, Yuzuru ; Kitajima, Masaki. / Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver. In: Hepatology. 1998 ; Vol. 28, No. 5. pp. 1289-1299.
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