The Effect of Cysteamine Bitartrate on Adiponectin Multimerization in Non-Alcoholic Fatty Liver Disease and Healthy Subjects
Dohil R et al. – Cysteamine impacts adiponectin multimerization. Long–term cysteamine therapy increases levels of all multimers, whereas, in vitro short–term exposure causes a rapid increase in LMW and reduction in MMW multimers in nonalcoholic fatty liver disease (NAFLD) and healthy controls. Cysteamine may be a potential therapeutic agent for conditions associated with insulin–resistance, oxidative stress, and depressed adiponectin levels.
- Sera from 10 children with biopsy-proven NAFLD treated with cysteamine were assayed for adiponectin multimers at baseline, after 24 weeks of treatment, and again 16 weeks after discontinuing treatment.
- Pretreatment sera from subjects with NAFLD and from adult controls without NAFLD controls (n = 8) were incubated in cysteamine and multimers were measured 1 hour later.
- A cysteamine/adiponectin multimer dose-response curve was created.
- Following 24 weeks of cysteamine therapy, the mean percentage increase for high, medium (MMW), and low (LMW) molecular weight multimers and total adiponectin from baseline was 53% (P = .02), 19% (P = .02), 29.4% (P = .03), and 49.3% (P = .05), respectively.
- Levels returned to baseline at 16 weeks after stopping therapy, unlike hepatic transaminase levels which remained low.
- Sera from 0 week, incubated in cysteamine for 1 hour, showed a significant mean percent increase in LMW adiponectin levels and a mean percent reduction in MMW levels compared with baseline in adults with and without NAFLD.