ABSTRACT
INTRODUCTION AND OBJECTIVES: Appropriate nutritional support may improve energy metabolism in alcoholic liver cirrhosis (ALC) patients. We explored the effect of a late evening snack (LES) and oral amino acid (OAA) capsules on energy metabolism and the Fischer ratio in ALC. PATIENTS AND METHODS: Ninety-one ALC patients were enrolled and randomly divided into three groups: 31 patients in the LES and OAA group, 32 in the LES group, and 28 controls. Respiratory quotient (RQ), carbohydrate oxidation rate (CHO%), fat oxidation rate (FAT%), serum isoleucine and the Fischer ratio were measured at baseline and at months 1, 3, and 6 of follow-up. RESULTS: The RQ in the LES and OAA group was 0.79 ± 0.06, 0.80 ± 0.04, 0.82 ± 0.04, and 0.82 ± 0.04 at baseline and at months 1, 3, and 6 of follow-up, respectively. These values were significantly higher than those in the LES group (P < 0.05). The RQ in the LES group was significantly higher than that in the control group at month 1 and month 6 (P < 0.05). CHO% in the LES and OAA group was significantly increased and FAT% was significantly decreased at month 3 of follow-up (P < 0.05). In the LES and OAA group, serum isoleucine and the Fischer ratio were markedly increased compared with the LES group and control group (P < 0.05). CONCLUSIONS: LES can significantly increase the RQ in ALC. LES and OAA were more effective than LES alone in improving serum isoleucine and the Fischer ratio.
Subject(s)
Amino Acids , Liver Cirrhosis, Alcoholic , Humans , Liver Cirrhosis/metabolism , Snacks , Capsules , IsoleucineABSTRACT
This study investigates the effect of the overexpression of the placental growth factor (PGF) and hyperoxia on lung development and determines whether anti-PGF antibody ameliorates hyperoxia-mediated impairment of lung development in newborn rats. After exposure to normoxic conditions for seven days, newborn rats subjected to normoxia were intraperitoneally or intratracheally injected with physiological saline, adenovirus-negative control (Ad-NC), or adenovirus-PGF (Ad-PGF) to create the Normoxia, Normoxia+Ad-NC, and Normoxia+Ad-PGF groups, respectively. Newborn rats subjected to hyperoxia were intraperitoneally injected with physiological saline or anti-PGF antibodies to create the Hyperoxia and Hyperoxia+anti-PGF groups, respectively. Our results revealed significant augmentation in the levels of PGF and its receptor Flt-1 in the lung tissues of newborn rats belonging to the Normoxia+Ad-PGF or Hyperoxia groups. PGF overexpression in these groups caused lung injury in newborn rats, while anti-PGF antibody treatment significantly cured the hyperoxia-induced lung injury. Moreover, PGF overexpression significantly increased TNF-α and Il-6 levels in the bronchoalveolar lavage (BAL) fluid of the Normoxia+Ad-PGF and Hyperoxia groups. However, their levels were significantly reduced in the BAL fluid of the Hyperoxia+anti-PGF group. Immunohistochemical analysis revealed that PGF overexpression and hyperoxia treatment significantly increased the expression of the angiogenesis marker, CD34. However, its expression was significantly decreased upon administration of anti-PGF antibodies (compared to the control group under hyperoxia). In conclusion, PGF overexpression impairs lung development in newborn rats while its inhibition using an anti-PGF antibody ameliorates the same. These results provided new insights for the clinical management of bronchopulmonary dysplasia in premature infants.
Subject(s)
Antibodies, Monoclonal/metabolism , Autoantibodies/metabolism , Hyperoxia/metabolism , Lung Injury/metabolism , Placenta Growth Factor/metabolism , Animals , Animals, Newborn , Antibodies, Monoclonal/immunology , Autoantibodies/immunology , Disease Models, Animal , Female , Hyperoxia/complications , Hyperoxia/diagnostic imaging , Lung Injury/diagnostic imaging , Lung Injury/pathology , Microscopy, Electron, Scanning , Placenta Growth Factor/immunology , Pregnancy , RatsABSTRACT
This study investigates the effect of the overexpression of the placental growth factor (PGF) and hyperoxia on lung development and determines whether anti-PGF antibody ameliorates hyperoxia-mediated impairment of lung development in newborn rats. After exposure to normoxic conditions for seven days, newborn rats subjected to normoxia were intraperitoneally or intratracheally injected with physiological saline, adenovirus-negative control (Ad-NC), or adenovirus-PGF (Ad-PGF) to create the Normoxia, Normoxia+Ad-NC, and Normoxia+Ad-PGF groups, respectively. Newborn rats subjected to hyperoxia were intraperitoneally injected with physiological saline or anti-PGF antibodies to create the Hyperoxia and Hyperoxia+anti-PGF groups, respectively. Our results revealed significant augmentation in the levels of PGF and its receptor Flt-1 in the lung tissues of newborn rats belonging to the Normoxia+Ad-PGF or Hyperoxia groups. PGF overexpression in these groups caused lung injury in newborn rats, while anti-PGF antibody treatment significantly cured the hyperoxia-induced lung injury. Moreover, PGF overexpression significantly increased TNF-α and Il-6 levels in the bronchoalveolar lavage (BAL) fluid of the Normoxia+Ad-PGF and Hyperoxia groups. However, their levels were significantly reduced in the BAL fluid of the Hyperoxia+anti-PGF group. Immunohistochemical analysis revealed that PGF overexpression and hyperoxia treatment significantly increased the expression of the angiogenesis marker, CD34. However, its expression was significantly decreased upon administration of anti-PGF antibodies (compared to the control group under hyperoxia). In conclusion, PGF overexpression impairs lung development in newborn rats while its inhibition using an anti-PGF antibody ameliorates the same. These results provided new insights for the clinical management of bronchopulmonary dysplasia in premature infants.