Sustained function in atrophying liver tissue after portal branch ligation in the rat.

TY - JOUR

T1 - Sustained function in atrophying liver tissue after portal branch ligation in the rat.

AU - Mueller, Lars

AU - Grotelueschen, Rainer

AU - Meyer, Jannine

AU - Vashist, Yogesh K

AU - Abdulgawad, Awad

AU - Wilms, Christian

AU - Hillert, Christian

AU - Rogiers, Xavier

AU - Broering, Dieter C

PY - 2003

Y1 - 2003

N2 - BACKGROUND: Preoperative segmental portal vein occlusion has become a common method to prevent liver failure after extended hepatic resection. To date, it is not elucidated whether atrophy by portal deprivation with concomitant contralateral regeneration leads to impaired liver function. We addressed this question by examining the expression of liver function proteins related to glucose homeostasis and acute-phase response in a corresponding animal model. MATERIALS AND METHODS: Male Wistar rats were subjected to either portal branch ligation (PBL), partial hepatectomy (PH), or sham operation (SO). The mRNA expression and chronological distribution of glucose-6-phosphatase (G6P), glucagon receptor (GR), glceraldehyd-3-phosphate-dehydrogenase (GAPDH), albumin, fibronectin, and C1-esterase-inhibitor (C1-Inh) genes were examined by Northern-blot hybridizations. Determinations of serum-glucose and glycogen staining by periodic acid and Schiff were performed to analyze changes in glucose mobilization and storage. RESULTS: In regenerating liver tissue after PH and PBL, we detected a selective reduction of transcripts encoding G6P during the prereplicative period 6 and 12 h after surgery and a contemporary drop in serum glucose levels. This impairment proved to be more distinct after PH than after PBL. Compared with the residual liver after PH, the level of glycogen disappearance was lower after PBL in the regenerating lobe. In the portal-deprived liver tissue, the expression of genes coding for G6P, GR, GAPDH, albumin, fibronectin, and C1-Inh was not altered compared with the SO group. CONCLUSIONS: Overall, portal-deprived liver tissue undergoing atrophy retains its liver-specific differentiation and function and helps to maintain homeostasis during the fast regeneration of the non-occluded liver lobe.

AB - BACKGROUND: Preoperative segmental portal vein occlusion has become a common method to prevent liver failure after extended hepatic resection. To date, it is not elucidated whether atrophy by portal deprivation with concomitant contralateral regeneration leads to impaired liver function. We addressed this question by examining the expression of liver function proteins related to glucose homeostasis and acute-phase response in a corresponding animal model. MATERIALS AND METHODS: Male Wistar rats were subjected to either portal branch ligation (PBL), partial hepatectomy (PH), or sham operation (SO). The mRNA expression and chronological distribution of glucose-6-phosphatase (G6P), glucagon receptor (GR), glceraldehyd-3-phosphate-dehydrogenase (GAPDH), albumin, fibronectin, and C1-esterase-inhibitor (C1-Inh) genes were examined by Northern-blot hybridizations. Determinations of serum-glucose and glycogen staining by periodic acid and Schiff were performed to analyze changes in glucose mobilization and storage. RESULTS: In regenerating liver tissue after PH and PBL, we detected a selective reduction of transcripts encoding G6P during the prereplicative period 6 and 12 h after surgery and a contemporary drop in serum glucose levels. This impairment proved to be more distinct after PH than after PBL. Compared with the residual liver after PH, the level of glycogen disappearance was lower after PBL in the regenerating lobe. In the portal-deprived liver tissue, the expression of genes coding for G6P, GR, GAPDH, albumin, fibronectin, and C1-Inh was not altered compared with the SO group. CONCLUSIONS: Overall, portal-deprived liver tissue undergoing atrophy retains its liver-specific differentiation and function and helps to maintain homeostasis during the fast regeneration of the non-occluded liver lobe.

M3 - SCORING: Zeitschriftenaufsatz

VL - 114

SP - 146

EP - 155

JO - J SURG RES

JF - J SURG RES

SN - 0022-4804

IS - 2

M1 - 2

ER -