[Nutritional Management of Nonalcoholic fatty liver disease (NAFLD)]. / Interventions nutritionnelles dans la prise en charge de la stéatose et la stéatohépatite non alcoolique.

Nonalcoholic fatty liver disease (NAFLD) is strongly associated with obesity and insulin resistance. There is currently no pharmacological treatment validated in steatosis. The combination of weight loss and adequate physical activity can improve liver steatosis. In randomized trials and cohort studies, a weight loss of at least 7% and a diet approaching the Mediterranean diet have been associated with an improvement in hepatic fat content, an improvement in hepatic biomarkers, and regression of histological signs of steatosis. Bariatric surgery by losing weight can lead to an improvement in hepatic fat content.

Four Weeks of Preoperative Omega-3 Fatty Acids Reduce Liver Volume: a Randomised Controlled Trial.

PURPOSE: Weight loss before bariatric surgery with a low-calorie diet (LCD) has several advantages, including reduction of liver volume and an improved access to the lesser sac. Disadvantages include performing surgery in a state of undernutrition, side effects, costs and patient compliance. Omega-3 fatty acids may serve as an alternative to reduce liver steatosis. MATERIALS AND METHODS: A randomised controlled open-label trial was done to compare the effects of a LCD with Modifast (800 kcal/day) during 2 weeks with 2 g of omega-3 fatty acids a day and a normal diet (2000 kcal/day) during 4 weeks. Total liver volume (TLV) and volume of the left liver lobe (LLL), visceral fat area (VFA) and muscle area (SMA) at the L3-L4 level were measured with MRI before and after preoperative treatment. RESULTS: Sixty-two morbidly obese women undergoing laparoscopic Roux-en-Y gastric bypass surgery (LRYGB) were recruited. In both groups, there was a significant decrease in LLL, TLV and VFA. For LLL and TLV reduction, the LCD had a significantly larger effect (p < 0.05). Only in the LCD group was there a significant decrease in SMA with significantly more side effects and worse compliance. CONCLUSION: Both the LCD and omega-3 diet reduced LLL, TLV and VFA. The LCD outperformed the omega-3 diet in LLL and TLV reduction, but induced significant loss of SMA and had worse compliance due to more side effects. Omega-3 fatty acids may provide a safe and more patient-friendly alternative for a LCD and further research is indicated. TRIAL REGISTRATION: The study is registered at www.clinicaltrials.gov (NCT02206256).

Preoperative 4-week supplementation with omega-3 polyunsaturated fatty acids reduces liver volume and facilitates bariatric surgery in morbidly obese patients.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a very common condition among obese patients that may lead to the enlargement of the liver, that in turn impairs the access to the gastro-esophageal junction during laparoscopic bariatric surgery. Omega-3 polyunsaturated fatty acids (Ω-3 PUFAs) supplementation has been shown to reduce nutritional hepatic steatosis. The aim of this study was to assess the effects of a 4-week course of oral Ω-3 PUFAs supplementation on the volume of the liver. METHODS: 20 morbidly obese patients were administered oral Ω-3 PUFAs (1,500 mg daily) for 4 weeks before undergoing the laparoscopic Roux-en-Y gastric bypass (LRYGBP) without any dietary restriction. The volume of the left hepatic lobe was estimated by liver ultrasonography at baseline and at the end of treatment. The degree of difficulty to access the gastro-esophageal junction was appreciated subjectively by the operating surgeon. RESULTS: All patients completed the study and no side effect was reported. The mean volume of the left hepatic lobe decreased by 20% from 598 ± 97 to 484 ± 118 cm(3) after the treatment (p = 0.002). The access to the gastro-esophageal junction was reported as simple, with easy retraction of the left hepatic lobe by the operating surgeon in all cases. CONCLUSIONS: This study demonstrates that a 4-week course of oral Ω-3 PUFAs supplementation results in a significant reduction in liver size that facilitates the LRYGBP.

Management of nonalcoholic steatohepatitis: an evidence-based approach.

Nonalcoholic fatty liver disease (NAFLD) and its progressive form, nonalcoholic steatohepatitis (NASH), are an increasingly common cause of chronic liver disease in the developed world, with NASH projected to be the leading cause of liver transplantation in the United States by 2020. This review of NASH management addresses current data from the perspective of levels of evidence for therapeutic options in NASH, including lifestyle modification, drug therapies, and bariatric surgery. In particular, behavioral therapies to assist patients in adopting lifestyle changes are highlighted and a research agenda for future NASH management is presented.

Hepatic ratio of phosphatidylcholine to phosphatidylethanolamine predicts survival after partial hepatectomy in mice.

UNLABELLED: A major predictor of failed liver resection and transplantation is nonalcoholic fatty liver disease (NAFLD). NAFLD is linked to a wide spectrum of diseases including obesity and diabetes that are increasingly prevalent in Western populations. Thus, it is important to develop therapies aimed at improving posthepatectomy outcomes in patients with NAFLD, as well as to improve the evaluation of patients slated for hepatic surgery. Decreased hepatic phosphatidylcholine (PC) content and decreased ratio of hepatic PC to phosphatidylethanolamine (PE) have previously been linked to NAFLD. To determine if decreased hepatic PC/PE could predict survival after hepatectomy, we used mouse models lacking key enzymes in PC biosynthesis, namely, phosphatidylethanolamine N-methyltransferase and hepatic-specific CTP:phosphocholine cytidylyltransferase α. These mice were fed a high-fat diet to induce NAFLD. We then performed a 70% partial hepatectomy and monitored postoperative survival. We identified hepatic PC/PE to be inversely correlated with the development of steatosis and inflammation in the progression of NAFLD. Decreased hepatic PC/PE before surgery was also strongly associated with decreased rates of survival after partial hepatectomy. Choline supplementation to the diet increased hepatic PC/PE in Pemt(-/-) mice with NAFLD, decreased inflammation, and increased the survival rate after partial hepatectomy. CONCLUSION: Decreased hepatic PC/PE is a predictor of NAFLD and survival following partial hepatectomy. Choline supplementation may serve as a potential therapy to prevent the progression of NAFLD and to improve postoperative outcome after liver surgery.

Heat shock preconditioning inhibits CD4+ T lymphocyte activation in transplanted fatty rat livers.

Heat shock preconditioning (HPc) of fatty donor livers significantly increases recipient survival in rats. We investigated to what extent the blockade of Kupffer cells by gadolinium chloride (GdCl3) can mimic the effect of HPc and the involvement of liver CD4+ T lymphocytes in HPc. Fatty liver was experimentally induced in Lewis rats by a choline- and methionine-deficient diet. Fatty liver donors were pretreated with HPc (42.5 degrees C for 10 min), the Kupffer cell inhibitor GdCl3, or placebo (sham group). Donors were then harvested, stored in University of Wisconsin preservation solution for 12 h at 4 degrees C, and transplanted into normal syngeneic rats. Hepatic injury (alanine aminotransferase) and serum cytokines (interleukin-12p70, tumor necrosis factor-alpha, and interleukin-10) of recipients increased at 3 h, then decreased, and increased again at 24 h after transplantation. HPc treatment diminished both the early and later phases of this biphasic response and improved recipient survival. GdCl3 reduced these cytokines in the early but not the later phase and did not reduce neutrophil accumulation or improve the recipient survival. HPc, but not GdCl3 treatment, also reduced the number of liver CD4+ T lymphocytes and their interferon-gamma production. We conclude that HPc, but not GdCl3 treatment, prevents biphasic liver injury and the activation of liver CD4+ T lymphocytes in transplanted fatty donor livers.