Research

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.

GoodSupportsHIGH confidence
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
Yaoling Shu et al. · Journal of Biological Chemistry · 2023

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

mechanism_only · n=24Cited 7×
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DOI resolved against Crossref · corpus check 2026-06-10

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