Energy balance
Hepatic protein kinase Cbeta (PKCβ) deficiency mitigates late-onset obesity in mice by increasing energy expenditure through β3-adrenergic receptor signaling, independent of FGF21.
This research suggests that as we age, our liver may produce more PKCβ, which can suppress our body's ability to burn fat and heat (thermogenesis). While you cannot change your genetics, maintaining liver health through regular physical activity—which is shown to repress PKCβ expression—may help preserve your metabolic rate and resistance to age-related weight gain.
hepatocyte PKCβ deficiency (PKCβHep−/−) in mice significantly attenuates obesity in aged mice fed a high-fat diet... elevated energy expenditure... dependent on β3-adrenergic receptor signaling
Why this rating
High-quality genetic mouse model with rigorous metabolic phenotyping (CLAMS, mitochondrial respiration), though translational to humans is not directly established.
Source
Hepatic protein kinase Cbeta deficiency mitigates late-onset obesity
Yaoling Shu et al. · Journal of Biological Chemistry · 2023
DOI 10.1016/j.jbc.2023.104917
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