Obesity and metabolic syndrome in circadian Clock mutant mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal study in mice
PubMed 15845877 · doi:10.1126/science.1108750
What was done
Researchers evaluated feeding behavior, metabolic markers, and hypothalamic peptide gene expression in homozygous Clock mutant mice.
What was found
The abstract reports no numerical values. Homozygous Clock mutant mice exhibited an attenuated diurnal feeding rhythm, hyperphagia, and obesity. They developed metabolic syndrome characterized by hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia, along with attenuated hypothalamic expression of peptides involved in energy balance.
Why it matters
This study demonstrates a direct genetic link between the molecular circadian clock network and metabolic homeostasis in mammals.
Limits
The study was conducted entirely in an animal model, which may not directly translate to human physiology. The abstract provides no sample sizes, numerical data, or effect sizes.
Cited by
- supports Mice lacking a functional circadian clock due to gene mutations or knockouts develop obesity, diabetes, and cardiovascular diseases.