Validation experiment designed to validate causal mechanisms targeting Hmgcs2, Oxct1 in C57BL/6J diet-induced obese mice. Primary outcome: body weight loss, systemic ketosis, and tissue-specific metabolic gene expression
This experiment assessed the therapeutic potential of different ketogenic diet formulations in C57BL/6J diet-induced obese (DIO) mice. Two KD formulations were tested: 80% fat and 90% fat. Researchers measured metabolic parameters including fasting glucose, body weight changes, systemic ketosis markers, and adipose tissue distribution. Gene expression analysis focused on hepatic transcriptional programs for fatty acid oxidation and ketogenesis, as well as intestinal ketone metabolism genes (Hmgcs2, Oxct1). The study revealed that 80% KD lowered fasting glucose without weight reduction, while 90% KD promoted systemic ketosis, significant weight loss, and adipose reduction. Interestingly, hepatic ketogenesis programs were suppressed under 90% KD despite elevated BHB, while intestinal Hmgcs2 was strongly induced with Oxct1 upregulated specifically in obesity.
Therapeutic KD feeding (80% vs 90% fat) with assessment of metabolic parameters, body composition, and tissue-specific gene expression
Dose-dependent anti-obesity effects with distinct tissue-specific metabolic adaptations
Weight loss, sustained ketosis, and appropriate metabolic gene expression changes
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