School of Medicine, University of Auckland, Auckland, New Zealand.
School of Medicine, University of Auckland, Auckland, New Zealand.
Cytokine. 2019 Aug;120:107-114. doi: 10.1016/j.cyto.2019.04.011. Epub 2019 May 1.
While a plethora of studies have been conducted to investigate the associations between pro-inflammatory cytokines and obesity, the inter-relationship between pro-inflammatory cytokines and intra-pancreatic fat deposition (IPFD) has been poorly investigated. In the present study, circulating levels of C-C motif chemokine ligand 2 (CCL2), interleukin-6 (IL-6), leptin, and tumor necrosis factor-alpha (TNFα) were measured in 90 individuals after acute pancreatitis (AP) as well as 21 healthy non-obese individuals. Magnetic resonance imaging was used to quantify IPFD and visceral-to-subcutaneous fat volume ratio by two independent raters. Linear regression analyses were performed to investigate the associations between IPFD and each cytokine, adjusting for demographic, metabolic, and pancreatitis-related factors, as well as abdominal fat distribution. In healthy non-obese individuals, IPFD was not significantly associated with any of the studied cytokines in both the unadjusted and adjusted models. In individuals after AP, IPFD was significantly associated with leptin in the models adjusted for age and sex (β = 0.063 [95% confidence interval: 0.007, 0.119], P = 0.026); age, sex, visceral-to-subcutaneous fat volume ratio, glycated hemoglobin, and pancreatitis-related factors (β = 0.056 [95% confidence interval: 0.000, 0.111], P = 0.049). Also, IPFD was significantly associated with TNFα in the unadjusted model (β = 0.102 [95% confidence interval: 0.002, 0.202], P = 0.045) and the model adjusted for age, sex, visceral-to-subcutaneous fat volume ratio, glycated hemoglobin, and pancreatitis-related factors (β = 0.128 [95% confidence interval: 0.034, 0.223], P = 0.008). The associations between IPFD and IL-6, CCL2 were not statistically significant, in both the unadjusted and adjusted models. These findings indicate that leptin and TNFα are associated with IPFD independent of abdominal fat distribution and other covariates in individuals after AP. The role of IPFD in low-grade inflammation warrants further investigations.
虽然有大量研究探讨了促炎细胞因子与肥胖之间的关系，但促炎细胞因子与胰腺内脂肪沉积（IPFD）之间的相互关系尚未得到充分研究。本研究在 90 名急性胰腺炎（AP）患者和 21 名健康非肥胖个体中测量了 C 型趋化因子配体 2（CCL2）、白细胞介素 6（IL-6）、瘦素和肿瘤坏死因子-α（TNFα）的循环水平。使用磁共振成像由两名独立的评估者来定量 IPFD 和内脏到皮下脂肪体积比。进行线性回归分析，以调查 IPFD 与每种细胞因子之间的关联，调整人口统计学、代谢和胰腺炎相关因素以及腹部脂肪分布。在健康非肥胖个体中，在未调整和调整模型中，IPFD 与研究的细胞因子均无显著相关性。在 AP 后个体中，在调整年龄和性别后的模型中，IPFD 与瘦素显著相关（β=0.063[95%置信区间：0.007，0.119]，P=0.026）；年龄、性别、内脏到皮下脂肪体积比、糖化血红蛋白和胰腺炎相关因素（β=0.056[95%置信区间：0.000，0.111]，P=0.049）。此外，在未调整模型中，IPFD 与 TNFα 显著相关（β=0.102[95%置信区间：0.002，0.202]，P=0.045），在调整年龄、性别、内脏到皮下脂肪体积比、糖化血红蛋白和胰腺炎相关因素后的模型中也显著相关（β=0.128[95%置信区间：0.034，0.223]，P=0.008）。在未调整和调整模型中，IPFD 与 IL-6、CCL2 之间的相关性均无统计学意义。这些发现表明，在 AP 后个体中，瘦素和 TNFα 与 IPFD 相关，与腹部脂肪分布和其他协变量无关。IPFD 在低度炎症中的作用值得进一步研究。
