Journal of translational medicine · 2026
Adipose tissue plays a crucial role in obesity-induced postoperative neurocognitive disorders.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Tropis Clémence, Labaste François, Sallese Marie, Dortignac Alizée, Pereira Ophélie, Gonidec Sophie Le, Ferré Fabrice, Pey Vincent, Billerach Raphaëlle, Bouisset Guillaume, Dahan Lionel, Valet Philippe, Minville Vincent, Dray Cédric
Аннотация
BACKGROUND: Postoperative neurocognitive disorder (PND) is characterized by cognitive deficits that emerge after surgery. Although often reversible within weeks or months, PND can persist and lead to significant central dysfunction and an increased risk of dementia. Given that obesity is a chronic low-grade inflammatory condition previously associated with structural and functional brain alterations, we hypothesized and demonstrated that it could be a significant risk factor for PND.
METHODS: We assessed the incidence of PND and cognitive performance in obese individuals undergoing cardiac or orthopedic surgeries. In parallel, we developed a preclinical model combining diet-induced obesity in mice with surgically induced tibial fracture. Pharmacological (ketoprofen), surgical (adipose tissue ablation), and behavioral (calorie restriction) interventions were used to target obesity-associated inflammation.
RESULTS: Compared with nonobese individuals, obese patients presented a greater incidence of early postoperative cognitive changes and lower cognitive performance (p < 0.009). In mice, the combination of obesity and surgery results in exacerbated signs of PND. Importantly, obesity-related PND in mice was prevented by interventions that reduced central and systemic inflammation.
CONCLUSIONS: These findings identify obesity-driven fat mass and inflammation as strong risk factors for PND for the first time. Targeting obesity-associated inflammatory mechanisms may represent an effective strategy to reduce the incidence of this debilitating postoperative condition.
METHODS: We assessed the incidence of PND and cognitive performance in obese individuals undergoing cardiac or orthopedic surgeries. In parallel, we developed a preclinical model combining diet-induced obesity in mice with surgically induced tibial fracture. Pharmacological (ketoprofen), surgical (adipose tissue ablation), and behavioral (calorie restriction) interventions were used to target obesity-associated inflammation.
RESULTS: Compared with nonobese individuals, obese patients presented a greater incidence of early postoperative cognitive changes and lower cognitive performance (p < 0.009). In mice, the combination of obesity and surgery results in exacerbated signs of PND. Importantly, obesity-related PND in mice was prevented by interventions that reduced central and systemic inflammation.
CONCLUSIONS: These findings identify obesity-driven fat mass and inflammation as strong risk factors for PND for the first time. Targeting obesity-associated inflammatory mechanisms may represent an effective strategy to reduce the incidence of this debilitating postoperative condition.