Elevating adipose eosinophils in obese mice to physiologically normal levels does not rescue metabolic impairments.
Elevating adipose eosinophils in obese mice to physiologically normal levels does not rescue metabolic impairments.
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DOI：
10.1016/j.molmet.2017.12.004
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发表时间：
2018-03
影响因子：
8.1
通讯作者：
Hasty AH
中科院分区：
文献类型：
--
作者：
Bolus WR;Peterson KR;Hubler MJ;Kennedy AJ;Gruen ML;Hasty AH
肥胖是一种代谢紊乱，在世界范围内已达到流行病的程度，并导致患糖尿病、心血管疾病、哮喘、某些癌症和各种其他疾病的风险增加。肥胖及其合并症与脂肪组织（AT）功能受损有关。在过去的十年中，嗜酸性粒细胞被确定为适当AT功能的调节因子。我们的研究旨在确定肥胖小鼠中AT嗜酸性粒细胞的数量是否正常化，与那些瘦弱健康小鼠相比，是否会减少肥胖和/或改善代谢适应性。饲喂高脂饲料（HFD）的C57BL/6J小鼠同时给予重组白细胞介素-5 (rIL5) 8周，以增加AT嗜酸性粒细胞。代谢适应度通过评估体重增加、AT炎症、葡萄糖、脂质和混合膳食耐量、AT胰岛素信号、能量底物利用、能量消耗和白色AT北京能力来测试。用rIL5处理的肥胖hfd喂养小鼠的AT中嗜酸性粒细胞增加了约3倍，从而恢复到瘦健康小鼠的水平。然而，在上述综合代谢测定中，ril5处理的小鼠没有显著差异，尽管AT嗜酸性粒细胞增加。我们已经证明，将肥胖的AT嗜酸性粒细胞恢复到健康水平并不足以改善任何一系列代谢特征，否则肥胖会受到损害。因此，将嗜酸性粒细胞识别为AT功能的积极调节因子的机制比最初理解的更为复杂，需要进一步的研究来充分阐明。脂肪组织嗜酸性粒细胞随着高脂肪饮食引起的体重增加而下降。重组白细胞介素5治疗可恢复肥胖期间的脂肪嗜酸性粒细胞。恢复脂肪嗜酸性粒细胞并没有减少体重增加或脂肪量。恢复脂肪嗜酸性粒细胞不能恢复葡萄糖耐量或胰岛素信号。恢复脂肪嗜酸性细胞不会改变能量消耗或运动能力。通过rIL5管理将肥胖的脂肪嗜酸性粒细胞恢复到瘦脂肪水平是不足以恢复代谢健康的，看看作者对他们文章的看法
Obesity is a metabolic disorder that has reached epidemic proportions worldwide and leads to increased risk for diabetes, cardiovascular disease, asthma, certain cancers, and various other diseases. Obesity and its comorbidities are associated with impaired adipose tissue (AT) function. In the last decade, eosinophils have been identified as regulators of proper AT function. Our study aimed to determine whether normalizing the number of AT eosinophils in obese mice, to those of lean healthy mice, would reduce obesity and/or improve metabolic fitness. C57BL/6J mice fed a high fat diet (HFD) were simultaneously given recombinant interleukin-5 (rIL5) for 8 weeks to increase AT eosinophils. Metabolic fitness was tested by evaluating weight gain, AT inflammation, glucose, lipid, and mixed-meal tolerance, AT insulin signaling, energy substrate utilization, energy expenditure, and white AT beiging capacity. Eosinophils were increased ∼3-fold in AT of obese HFD-fed mice treated with rIL5, and thus were restored to levels observed in lean healthy mice. However, there were no significant differences in rIL5-treated mice among the above listed comprehensive set of metabolic assays, despite the increased AT eosinophils. We have shown that restoring obese AT eosinophils to lean healthy levels is not sufficient to allow for improvement in any of a range of metabolic features otherwise impaired in obesity. Thus, the mechanisms that identified eosinophils as positive regulators of AT function, and therefore systemic health, are more complex than initially understood and will require further study to fully elucidate. Adipose tissue eosinophils declined with high fat diet induced weight gain. Recombinant interleukin 5 treatment restored adipose eosinophils during obesity. Restoring adipose eosinophils didn't reduce weight gain or adipose mass. Restoring adipose eosinophils didn't rescue glucose tolerance or insulin signaling. Restoring adipose eosinophils didn't alter energy expenditure or beiging capacity. Restoring obese adipose eosinophils to lean adipose levels via rIL5 administration is not sufficient to regain metabolic fitness Watch what authors say about their articles
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影响因子：
82.9
作者：
Fischer K;Ruiz HH;Jhun K;Finan B;Oberlin DJ;van der Heide V;Kalinovich AV;Petrovic N;Wolf Y;Clemmensen C;Shin AC;Divanovic S;Brombacher F;Glasmacher E;Keipert S;Jastroch M;Nagler J;Schramm KW;Medrikova D;Collden G;Woods SC;Herzig S;Homann D;Jung S;Nedergaard J;Cannon B;Tschöp MH;Müller TD;Buettner C
通讯作者：
Buettner C
DOI：
10.4049/jimmunol.1301176
发表时间：
2013-12-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Hams E;Locksley RM;McKenzie AN;Fallon PG
通讯作者：
Fallon PG
影响因子：
4.4
作者：
Odemuyiwa, SO;Ghahary, A;Moqbel, R
通讯作者：
Moqbel, R
DOI：
10.1084/jem.20121964
发表时间：
2013-03-11
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Molofsky AB;Nussbaum JC;Liang HE;Van Dyken SJ;Cheng LE;Mohapatra A;Chawla A;Locksley RM
通讯作者：
Locksley RM
影响因子：
64.5
作者：
Qiu Y;Nguyen KD;Odegaard JI;Cui X;Tian X;Locksley RM;Palmiter RD;Chawla A
通讯作者：
Chawla A