Hormonal
Genetic deficiency of the circadian clock gene BMAL1 causes metabolic syndrome by impairing adipose tissue expansion, leading to elevated circulating fatty acids and subsequent ectopic fat accumulation in the liver and skeletal muscle.
This research highlights that metabolic health depends heavily on the capacity of adipose tissue to store fat. If fat cells cannot expand or function correctly (due to genetic or environmental factors), fat spills over into the liver and muscles, causing metabolic issues. Maintaining healthy adipose tissue function is crucial for preventing ectopic fat.
Deficient of the Bmal1 gene in mice resulted in elevation of the respiratory quotient value, indicating that BMAL1 is involved in the utilization of fat as an energy source. Indeed, lack of Bmal1 reduced the capacity of fat storage in adipose tissue, resulting in an increase in the levels of circulating fatty acids, including triglycerides, free fatty acids, and cholesterol. Elevation of the circulating fatty acids level induced the formation of ectopic fat in the liver and skeletal muscle in Bmal1 -/- mice.
Why this rating
High-quality controlled animal study with clear phenotypic outcomes, though not directly translatable to human intervention without caveats.
Source
Deficient of a Clock Gene, Brain and Muscle Arnt-Like Protein-1 (BMAL1), Induces Dyslipidemia and Ectopic Fat Formation
Shigeki Shimba et al. · PLoS ONE · 2011
DOI 10.1371/journal.pone.0025231
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