We read with great interest the mechanistic study comparing short-term hypocaloric ketogenic versus non-ketogenic diets in individuals with metabolic dysfunction-associated steatotic liver disease (MASLD), which integrated proton magnetic resonance spectroscopy-quantified intrahepatic triglyceride (IHTG) with isotope tracer-based flux phenotyping and targeted plasma metabolomics [1]. The authors reported greater relative reductions in IHTG with the ketogenic diet compared with the non-ketogenic diet, accompanied by larger decreases in the homeostasis model assessment of insulin resistance (HOMA-IR).
We read with great interest the mechanistic study comparing short-term hypocaloric ketogenic versus non-ketogenic diets in individuals with metabolic dysfunction-associated steatotic liver disease (MASLD), which integrated proton magnetic resonance spectroscopy-quantified intrahepatic triglyceride (IHTG) with isotope tracer-based flux phenotyping and targeted plasma metabolomics [1]. The authors reported greater relative reductions in IHTG with the ketogenic diet compared with the non-ketogenic diet, accompanied by larger decreases in the homeostasis model assessment of insulin resistance (HOMA-IR).