Rachel Botchlett

TL;DR: It is suggested that metformin protects against obesity-associated NAFLD largely through direct effects on decreasing hepatocyte fat deposition and on inhibiting inflammatory responses in both hepatocytes and macrophages.

TL;DR: An AMP-activated protein kinase (AMPK)-independent mechanism for BBR to suppress obesity-associated inflammation and improve hepatic steatosis is revealed and actions on improving aspects of NAFLD are largely attributable to BBR suppression of inflammation, which is independent of AMPK.

TL;DR: Mechanistically, the beneficial effects of metformin on hepatic aspects are mediated through both adenosine monophosphate-activated protein kinase (AMPK)-dependent and AMPK-independent pathways and may also benefit patients with other chronic liver diseases.

TL;DR: Examining the association between the circulating levels of indole and liver fat content in human subjects and exploring the mechanisms underlying indole actions in mice with diet‐induced NAFLD found it to be largely unknown whether and how indole acts to protect againstNAFLD.

TL;DR: These findings are consistent with the hypothesis that oxidative stress triggers nNOSμ translocation from the sarcolemma and FoxO3a dephosphorylation as an early event during mechanical unloading, and serve as a biological switch for nN OS to initiate morphological changes in skeletal muscle fibers.