Key result
Hepatocyte Kctd17 inhibition improved glucose tolerance and hepatic steatosis in high-fat diet-fed mice by preventing Oga degradation and subsequent Chrebp stabilization.
Why the study?
The mechanisms underlying obesity-induced type 2 diabetes and NAFLD are incompletely understood, prompting investigation into whether elevated hepatocyte Kctd17 plays a causal role.
Inhibition of hepatocyte Kctd17 improves glucose tolerance and hepatic steatosis in obesity models by preventing Chrebp stabilization, suggesting a potential therapeutic target for T2D and NAFLD.
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Kctd17 inhibition improves metabolic parameters in obese mice; leaves open translation to human T2D or NAFLD therapy.
Oh et al. (2022) studied Obesity-induced type 2 diabetes and NAFLD. Hepatocyte Kctd17 inhibition vs. Control was evaluated on Glucose tolerance and hepatic steatosis. Hepatocyte Kctd17 inhibition improved glucose tolerance and hepatic steatosis in high-fat diet-fed mice by preventing Oga degradation and subsequent Chrebp stabilization.