Betaine for nonalcoholic fatty liver disease: Results of a randomized placebo-controlled trial
| Autor: | Schuyler O. Sanderson, Keith D. Lindor, Paul Angulo, Craig J. McClain, Matthew C. Cave, Consuelo Soldevila-Pico, Manal F. Abdelmalek, Chen Liu, Jill Keach, Theresa L. Chen, Joy Peter |
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| Rok vydání: | 2009 |
| Předmět: |
Adult
Male medicine.medical_specialty Pathology Placebo-controlled study Placebo Gastroenterology chemistry.chemical_compound Betaine Adipokines Double-Blind Method Internal medicine Nonalcoholic fatty liver disease medicine Humans Aged Hepatology medicine.diagnostic_test Adiponectin business.industry Fatty liver Middle Aged medicine.disease S-Adenosylhomocysteine Fatty Liver chemistry Liver biopsy Cytokines Female Steatosis business |
| Zdroj: | Hepatology. 50:1818-1826 |
| ISSN: | 0270-9139 |
| Popis: | Based on animal studies and pilot studies in humans, betaine, a methyl donor for the remethylation of homocysteine, may be a therapeutic agent for nonalcoholic steatohepatitis (NASH). We evaluated the safety and efficacy of betaine for patients with NASH and whether betaine positively modified factors postulated to be “second hits” and underlying mechanisms of NASH. We conducted a randomized placebo-control study of 55 patients with biopsy-proven NASH who received either oral betaine (20 g daily) or placebo for 12 months. Pre- and posttreatment variables were analyzed using the paired t test or Wilcoxon rank test. Treatment groups were comparable at baseline. Of the 35 patients (17 betaine, 18 placebo) who completed the study, 34 patients (16 betaine, 18 placebo) underwent posttreatment liver biopsy. Patients randomized to betaine had a decrease in steatosis grade. No intra- or intergroup differences or changes in nonalcoholic fatty liver disease activity score or fibrosis stage were noted. Elevations of insulin, glucose, and proinflammatory cytokines and the reduced antioxidant status noted in NASH patients did not improve with betaine therapy. The antiinflammatory agent adiponectin was significantly reduced in both groups and did not change with therapy. Lastly, S-adenosylhomocysteine was approximately twice normal and was not reduced by betaine therapy. Conclusion: Compared to placebo, betaine improved hepatic steatosis and may protect against worsening steatosis. High-dose betaine supplementation failed to reduce S-adenosylhomocysteine and did not positively affect any of the second hit mechanisms postulated to contribute to NASH that we studied. Although betaine has been proven effective in treating hepatic steatosis in several animal models, translating novel therapeutic options noted in animal studies to humans with NASH will prove challenging. (HEPATOLOGY 2009.) |
| Databáze: | OpenAIRE |
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