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Duodenal-Jejunal Bypass Improves Non-alcoholic Fatty Liver Disease Independently of Weight Loss in Rodents with Diet-Induced Obesity.

Nonalcoholic fatty-liver disease (NAFLD) is the most common cause of liver-related mortality. NAFLD is associated with obesity, hepatic fat accumulation and insulin-resistance, all of which contribute to its pathophysiology. Weight-loss is the main therapy for NAFLD and metabolic surgery is the most effective treatment for morbid obesity and its metabolic comorbidities. Although has been reported that Roux-en-Y gastric bypass can reverse NAFLD, it is unclear if such effects result from reduced weight, from a less calorie-intake or from the direct influence of surgery on mechanisms contributing to NAFLD. We aim to investigate whether gastrointestinal (GI) bypass surgery can induce direct effects on hepatic fat accumulation and insulin-resistance, independently of weight reduction. Twenty Wistar rats under a high-fat diet underwent duodenal-jejunal-bypass (DJB) or sham-operation and were pair-fed (PF) for 15 weeks after surgery to obtain a matched weight. Outcome measures include ectopic fat deposition, expression of genes and proteins involved in fat metabolism, insulin-signaling and gluconeogenesis in liver and muscle. Despite no differences in body-weight and calorie-intake, DJB showed lower ectopic fat accumulation, improved peripheral and hepatic insulin-sensitivity, and enhanced lipid droplet degradation. In both tissues DJB increased insulin-signaling while hepatic key enzymes involved in gluconeogenesis and de novo lipogenesis were decreased. These findings suggest that DJB can reverse, independently of weight loss, ectopic fat deposition and insulin-resistance, two features of NAFLD that share a mutual pathway, in which Perilipin-2 (PLIN2) seems to be the main player, supporting further investigation into strategies that target the gut to treat metabolic liver diseases.