Tyrosine hydroxylase deletion in Ntsr1 neurons confers resistance to diet-induced weight gain: an energy-balance analysis

Ntsr1Cre;Thflox mice resist diet-induced weight gain on HFD without increased energy expenditure, activity, thermogenesis, or detectable fecal energy/fat changes, unlike prior feeding findings.

• Why it matters: High-fat diet disrupts circadian feeding and promotes obesity, but the neural pathways that translate diet exposure into energy-balance outcomes are unclear.
• What they did: The study compared Ntsr1Cre;Thflox cKO and controls using food intake measures, indirect calorimetry, activity, body temperature, fecal energy and nonesterified fatty acids, and gut microbiome profiling across SCD and HFD cohorts.
• The result: DIO resistance occurred despite no genotype increase in energy expenditure, activity, or body temperature; fecal output was lower on HFD in one replication cohort, while fecal mass, energy density, and nonesterified fatty acids were unchanged in an independent bomb-calorimetry cohort.

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