Noemí Cabré1, Fedra Luciano-Mateo1, Salvador Fernández-Arroyo1, Gerard Baiges-Gayà2, Anna Hernández-Aguilera1, Montserrat Fibla2, Raul Fernández-Julià3, Marta París4, Fàtima Sabench5, Daniel Del Castillo5, Javier A Menéndez6, Jordi Camps7, Jorge Joven8. 1. Department of Medicine and Surgery, Universitat Rovira i Virgili, Reus, Spain; Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain. 2. Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain. 3. Àrea Bàsica de Salut La Selva del Camp, Tarragona, Spain. 4. Department of Surgery, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain. 5. Department of Medicine and Surgery, Universitat Rovira i Virgili, Reus, Spain; Department of Surgery, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain. 6. Program Against Cancer Therapeutic Resistance (ProCURE), Metabolism and Cancer Group, Catalan Institute of Oncology, Girona, Spain; Girona Biomedical Research Institute (IDIBGI), Girona, Spain. 7. Department of Medicine and Surgery, Universitat Rovira i Virgili, Reus, Spain; Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain. Electronic address: jcamps@grupsagessa.com. 8. Department of Medicine and Surgery, Universitat Rovira i Virgili, Reus, Spain; Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain; The Southern Catalonia Campus of International Excellence, Tarragona, Spain. Electronic address: jjoven@grupsagessa.com.
Abstract
BACKGROUND & AIMS: Hepatic alterations, such as in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are frequently associated with obesity. To investigate the molecular mechanisms of these alterations and to identify molecules that could be used as potential therapeutic targets, we investigated the modulation of hepatic indices of oxidative stress and inflammation in obese patients undergoing laparoscopic sleeve gastrectomy (LSG). METHODS: Patients (n = 436) attending our obesity clinic underwent LSG for weight loss. We obtained a diagnostic intraoperative liver biopsy, and a sub-cohort (n = 120) agreed to a 1-year follow-up that included donation of blood samples and additional liver biopsies. Selected key molecules in blood and liver tissue were used to investigate the hepatic alterations in obesity, and their response to LSG. RESULTS: One year post-surgery, the prevalence of diabetes, dyslipidemia and hypertension decreased significantly. LSG improved liver histology features in all patients. Improvement was greater in severe cases of NAFLD including those with steatohepatitis, bridging fibrosis or cirrhosis. Significant pre-surgery differences in plasma, and liver markers of oxidative stress and inflammation (including chemokine C-C motif ligand 2, paraoxonase-1, galectin-3, and sonic hedgehog) were observed between patients with, and those without, NASH; post-surgery indicated consistent improvements in these parameters. CONCLUSION: Our study shows that the histology and liver function of patients with morbid obesity are significantly improved after LSG via mechanisms that involve the reduction of oxidative stress and inflammatory processes. These data encourage the use of LSG as a therapeutic option to improve, or resolve, NAFLD.
BACKGROUND & AIMS: Hepatic alterations, such as in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are frequently associated with obesity. To investigate the molecular mechanisms of these alterations and to identify molecules that could be used as potential therapeutic targets, we investigated the modulation of hepatic indices of oxidative stress and inflammation in obesepatients undergoing laparoscopic sleeve gastrectomy (LSG). METHODS:Patients (n = 436) attending our obesity clinic underwent LSG for weight loss. We obtained a diagnostic intraoperative liver biopsy, and a sub-cohort (n = 120) agreed to a 1-year follow-up that included donation of blood samples and additional liver biopsies. Selected key molecules in blood and liver tissue were used to investigate the hepatic alterations in obesity, and their response to LSG. RESULTS: One year post-surgery, the prevalence of diabetes, dyslipidemia and hypertension decreased significantly. LSG improved liver histology features in all patients. Improvement was greater in severe cases of NAFLD including those with steatohepatitis, bridging fibrosis or cirrhosis. Significant pre-surgery differences in plasma, and liver markers of oxidative stress and inflammation (including chemokine C-C motif ligand 2, paraoxonase-1, galectin-3, and sonic hedgehog) were observed between patients with, and those without, NASH; post-surgery indicated consistent improvements in these parameters. CONCLUSION: Our study shows that the histology and liver function of patients with morbid obesity are significantly improved after LSG via mechanisms that involve the reduction of oxidative stress and inflammatory processes. These data encourage the use of LSG as a therapeutic option to improve, or resolve, NAFLD.
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