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代谢和减重手术后,外周血单个核细胞激活后 Th1 反应减弱与糖酵解活性降低有关。

Reduced Th1 response is associated with lower glycolytic activity in activated peripheral blood mononuclear cells after metabolic and bariatric surgery.

机构信息

Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Ave. Morones Prieto 3000, 64710, Monterrey, NL, Mexico.

Swiss Hospital, SMG, Monterrey, NL, Mexico.

出版信息

J Endocrinol Invest. 2021 Dec;44(12):2819-2830. doi: 10.1007/s40618-021-01587-4. Epub 2021 May 15.

DOI:10.1007/s40618-021-01587-4
PMID:33991317
Abstract

BACKGROUND

Obesity promotes cellular immunometabolism changes that trigger the activation of macrophages and lymphocytes, leading to systemic inflammation. Activated leukocytes undergo metabolic reprogramming, increasing glycolytic activity.

OBJECTIVE

To examine whether the reduction in the inflammatory state associated with bariatric surgery is associated with decreased glycolytic activity in leukocytes. Setting Single-center, prospective observational study.

METHODS

This study involved 18 patients with obesity undergoing bariatric surgery. All measurements were performed preoperatively and six months postoperatively. Peripheral blood mononuclear cells and plasma were obtained to determine the glycolytic rate and mitochondrial membrane potential as surrogates of the metabolic switching and high-sensitivity C-reactive protein, adipokines, and CD69 expression as inflammatory and activation markers.

RESULTS

Glycolytic activity engaged by CD3/CD28 activation was reduced six months after bariatric surgery, associated with decreased levels of T helper (Th) 1 and Th17 signature cytokines. An overall reduction in inflammatory markers was observed, which correlated with a higher adiponectin/leptin ratio.

CONCLUSIONS

Metabolic and bariatric surgery-induced weight loss leads to reprogramming in T cells' metabolic machinery, resulting in reduced stimulation of glycolysis after activation, which may explain the decrease in systemic inflammation mediated by cytokines such as interferon-γ and interleukin-17A.

摘要

背景

肥胖会促进细胞免疫代谢变化,从而触发巨噬细胞和淋巴细胞的激活,导致全身炎症。活化的白细胞会经历代谢重编程,增加糖酵解活性。

目的

研究与减重手术相关的炎症状态的降低是否与白细胞糖酵解活性的降低有关。

设置

单中心前瞻性观察性研究。

方法

本研究纳入了 18 名接受减重手术的肥胖患者。所有测量均在术前和术后 6 个月进行。采集外周血单核细胞和血浆,以确定糖酵解率和线粒体膜电位作为代谢转换的替代指标,并检测高敏 C 反应蛋白、脂肪因子和 CD69 表达作为炎症和活化标志物。

结果

CD3/CD28 激活后糖酵解活性在减重手术后 6 个月降低,与 Th1 和 Th17 特征性细胞因子水平降低有关。观察到炎症标志物的总体减少,与脂联素/瘦素比值升高相关。

结论

代谢和减重手术引起的体重减轻会导致 T 细胞代谢机制的重新编程,导致激活后糖酵解的刺激减少,这可能解释了干扰素-γ和白细胞介素-17A 等细胞因子介导的全身炎症的减少。

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