Research

Energy balance

Loss of the lncRNA 116HG (found in the Prader-Willi syndrome locus) causes increased energy expenditure and a shift toward lipid oxidation (lower RER) during light/active hours in mice, independent of changes in food intake or physical activity.

This research highlights that energy expenditure is biologically regulated by specific genes (like 116HG) and circadian rhythms, not just by how much you eat or move. While this is a mouse model of a genetic disorder, it suggests that metabolic rate and substrate preference (fat vs. carbs) are active biological processes that can be dysregulated, independent of behavior.

GoodSupportsHIGH confidence
Snord116del mice exhibited increased energy expenditure corresponding to the dysregulation of diurnally expressed Mtor and circadian genes Clock, Cry1 and Per2... Snord116del mice exhibited a significant decrease in the RER compared with WT littermates during light hours... Snord116del mice also showed increased energy expenditure compared with WT mice during both light and dark hours... suggesting that the metabolic phenotype is due to the central dysregulation of energy expenditure, not changes in feeding or activity.
Weston T. Powell et al. · Human Molecular Genetics · 2013

Why this rating

High-quality genomic and metabolic phenotyping in a well-established mouse model, though translational to humans requires caution.

Source

A Prader–Willi locus lncRNA cloud modulates diurnal genes and energy expenditure

Weston T. Powell et al. · Human Molecular Genetics · 2013

DOI 10.1093/hmg/ddt281

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DOI resolved against Crossref · corpus check 2026-06-10

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