| Journal | Biochemistry and biophysics reports |
| Study Type | Clinical Study |
| Population | Human participants |
This item covers developments relevant to cannabis medicine and clinical practice. Clinicians monitoring evidence in this area should review the source material.
The endocannabinoid system (ECS) and the autophagy receptor p62 are both implicated in metabolic regulation and obesity, yet the mechanisms linking these pathways remain unclear. Here, we investigated whether p62 modulates CB1 receptor (CB1R) turnover or function and whether CB1R contributes to the metabolic phenotype of p62 knockout (KO) mice. In primary cortical neurons from wild-type mice, inhibition of autophagic flux with Bafilomycin A1 led to substantial CB1R accumulation, demonstrating that CB1R is a subject to autophagy-dependent degradation. CB1R agonist stimulation partially reduced this accumulation, suggesting receptor activation influences turnover. In vivo, p62 deficiency did not significantly alter CB1R protein abundance in the brain or hypothalamus, although hypothalamic ERK1/2 signaling downstream of CB1R was modestly attenuated. P62 KO mice displayed late-onset obesity without hyperphagia, early hypoactivity, and elevated hypothalamic 2-arachidonoylglycerol (2-AG) lev
“This is a development worth tracking. The clinical implications will become clearer as more evidence accumulates.”
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