Differential Metabolomic Analysis of Liver Tissues from Rat Models of Parenteral Nutrition-Associated Liver Disease.

Parenteral nutrition (PN) is a life-saving therapy for patients with intestinal failure, but parenteral nutrition-associated liver disease (PNALD) limits its long-term use. The present study is aimed at determining which pathways are altered most notably in a rat model of PNALD. We randomly assigned male Sprague-Dawley (SD) rats into two different groups, whereby they received either enteral nutrition (EN) or PN. Liver tissues were harvested from all rats 7 days later for metabolomic profiling. The composition of primary conjugated bile acids was altered, the synthesis of polyunsaturated fatty acids was reduced, the conversion of pyruvate to acetyl-CoA was blocked, and the synthesis of phosphatidylcholine was inhibited in rats with PNALD. Riboflavin, which is involved in the electron transfer process in the mitochondrial electron transport chain, was remarkably decreased in PNALD rats. A deficiency of polyunsaturated fatty acids, riboflavin, choline, and taurine might be involved in the progression of PNALD. The implications of these findings for the field of medicine are that supplementation with polyunsaturated fatty acids, riboflavin, choline, and taurine might have potential as therapeutic strategies for PNALD and also shed light on the mechanisms of PNALD.

Superior Mesenteric Artery Syndrome Improved by Enteral Nutritional Therapy: A Retrospective Case-Series Study in a Single Institution.

INTRODUCTION: Superior mesenteric artery syndrome (SMAS) is a relatively rare cause of chronic duodenal obstruction, owing to the compression of the third portion of the duodenum. OBJECTIVES: This retrospective study aims to discuss the efficacy of enteral nutrition (EN) therapy in nutritional status and symptom improvement at a short-term follow-up for SMAS patients. METHODS: We retrospectively analyzed clinical data of patients diagnosed as SMAS and treated with EN from September 2012 to January 2019. RESULTS: Twenty-six patients were included (16 women; mean age 24.96 ± 11.77 years), none was excluded, and one was lost to follow-up. The patients' mean body weight was 40.94 ± 10.16 kg, mean weight loss 11.73 ± 7.58 kg, and mean body mass index (BMI) 14.82 ± 2.52 kg/m2. The mean duration of EN therapy was 10.10 ± 4.66 months. Serum level of nutritional indicators, BMI and body weight increased after EN therapy. During a median follow-up of 24 months (9-44) after EN therapy, the mean symptom score decreased from 24.28 ± 9.57 to 8.06 ± 8.29 (p < 0.0001), and 65% of patients' symptoms resolved and 15% of patients' symptoms improved. In total, 16 complications occurred, including tube blockage, peristomal wound infections, peristomal leakage, granulomas, and nasopharyngeal pain. CONCLUSION: EN therapy may be an effective option for SMAS patients. While it might not remove all symptoms, it can improve the nutritional status to support subsequent treatments.

N-3 polyunsaturated fatty acids ameliorate hepatic steatosis via the PPAR-α/CPT-1α pathway in a mouse model of parenteral nutrition.

Parenteral nutrition (PN) is one of the basic therapies for patients with intestinal failure; however, hepatic steatosis associated with PN limits the long-term use of PN. N-3 polyunsaturated fatty acids (PUFAs) have been used to improve clinical outcomes of patients receiving PN; however, the mechanisms by which n-3 PUFAs ameliorate hepatic steatosis remain unclear. In the present study, C57BL/6J mice were randomly assigned to three treatment groups, namely, enteral nutrition (EN), n-3 PUFAs, and n-6 PUFAs. Additionally, MK 886 was used to inhibit PPAR-α. After 7 days of intervention, mice were sacrificed, and liver tissue and serum samples were collected. Results from liver weight and liver triglyceride measurements and Oil Red O staining showed that n-3 PUFAs significantly reduced the liver triglyceride levels. In addition, treatment with n-3 PUFAs resulted in a greater decrease in serum triglyceride and low-density lipoprotein cholesterol levels compared to n-6 PUFAs. The key enzymes involved in FA oxidation, namely, PPAR-α and CPT-1α, were significantly restored at both the mRNA and protein levels in the n-3 PUFAs group. However, the benefits of n-3 PUFAs in improving serum and liver TG levels were abolished when the PPAR-α/CPT-1α pathway was blocked by MK 886. The results of this study indicated that n-3 PUFAs ameliorated the PN-associated hepatic steatosis by activating the PPAR-α/CPT-1α pathway. The present study provided a reliable scientific basis supporting the potential beneficial effects of n-3 PUFAs for improving hepatic steatosis in patients receiving long-term parenteral nutrition.