Key result
Rimonabant reduces adipokines and inflammatory cytokines in the liver and adipose tissue of NAFLD mice.
Why the study?
In high-fat diet-induced NAFLD, increased endocannabinoid system activity contributes significantly to steatosis, prompting investigation into whether cannabinoid receptor type 1 blockade affects adipokine and proinflammatory cytokine content in adipose and hepatic tissue.
Does rimonabant reduce adipokine and proinflammatory cytokine concentrations in adipose and hepatic tissue in mice with high-fat diet-induced NAFLD?
Does rimonabant reduce adipokine and proinflammatory cytokine concentrations in adipose and hepatic tissue in mice with high-fat diet-induced NAFLD?
p-value: p=<0.01
Cannabinoid receptor 1 blockade with rimonabant improves adipokine profiles, reduces proinflammatory cytokines, and ameliorates hepatic steatosis and insulin resistance in a mouse model of NAFLD.
CB1 blockade attenuates adipokine and cytokine dysregulation in murine NAFLD; leaves open whether peripheral antagonists merit human trials.
In high-fat diet (HFD) induced nonalcoholic fatty liver disease (NAFLD), there is an increase in the endocannabinoid system activity, which significantly contributes to steatosis development. The aim of our study was to investigate the effects of cannabinoid receptor type 1 blockade on adipokine and proinflammatory cytokine content in adipose and hepatic tissue in mice with NAFLD. Male mice C57BL/6 were divided into a control group fed with a control diet for 20 weeks (C, n = 6) a group fed with a HFD for 20 weeks (HF, n = 6), a group fed with a control diet and treated with rimonabant after 18 weeks (R, n = 9), and a group fed with HFD and treated with rimonabant after 18 weeks (HFR, n = 10). Rimonabant significantly decreased leptin, resistin, apelin, visfatin, interleukin 6 (IL-6), and interferon-γ (IFN-γ) concentration in subcutaneous and visceral adipose tissue in the HFR group compared to the HF group (p < 0.01). Rimonabant reduced hepatic IL-6 and IFN-γ concentration as well as plasma glucose and insulin concentration and the homeostatic model assessment index in the HFR group compared to the HF group (p < 0.01). It can be concluded that the potential usefulness of CB1 blockade in the treatment of HFD-induced NAFLD is due to modulation of the adipokine profile and proinflammatory cytokines in both adipose tissues and liver as well as glucose metabolism.
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Jorgačević et al. (2019) studied Nonalcoholic fatty liver disease (NAFLD) (n=31). Rimonabant vs. Vehicle (saline, 0.9% NaCl) was evaluated on Adipokine and proinflammatory cytokine concentrations in adipose and hepatic tissue (p=<0.01). Rimonabant significantly decreased leptin, resistin, apelin, visfatin, IL-6, and IFN-γ concentrations in adipose tissue and liver in mice with high-fat diet-induced NAFLD.
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