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脂肪因子在猫原代脂肪组织培养中对膳食脂肪酸的反应。

Adipokines secretion in feline primary adipose tissue culture in response to dietary fatty acids.

机构信息

Department of Pathobiology and Diagnostic Investigation, Diagnostic Center for Population and Animal Health College of Veterinary Medicine, Michigan State University, East Lansing, MI, 48824, USA.

Present address: Hebrew University Veterinary Teaching Hospital, Koret School of Veterinary Medicine, The Hebrew University of Jerusalem, P.O. Box 12, 76100, Rehovot, Israel.

出版信息

BMC Vet Res. 2019 Sep 6;15(1):324. doi: 10.1186/s12917-019-2065-8.

DOI:10.1186/s12917-019-2065-8
PMID:31492181
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6731618/
Abstract

BACKGROUND

Obesity in cats has been associated with alterations in adipokines including: adiponectin, interleukin-6 (IL6), and tumor necrosis factor-α (TNFα). Omega-3 polyunsaturated fatty acids have multiple beneficial effects on obesity-associated disorders, and therefore may alleviate these alterations. This study aimed to determine the effects of body condition, fat depot, troglitazone, and different fatty acids on secretion of adiponectin, IL6 and TNFα from adipose tissue of healthy cats. Subcutaneous and visceral adipose tissue samples were collected from 18 healthy intact female cats, and body condition score (Range 3-7/9) was determined. Concentrations of adiponectin were measured in mature adipocytes cultures and concentrations of IL6 and TNFα were measured in stromovascular cells cultures following treatment with control medium, troglitazone at 10 μM, eicosapentaenoic acid, arachidonic acid, or palmitic acid, at 25, 50, or 100 μM.

RESULTS

Stromovascular cells of visceral origin secreted higher concentrations of IL6 than corresponding cells of subcutaneous origin (P = 0.003). Arachidonic acid treatment at 25, 50, and 100 μM increased IL6 secretion in subcutaneous (P = 0.045, P = 0.002, and P < 0.001, respectively) and visceral (P = 0.034, P = 0.001, and P < 0.001, respectively) stromovascular cells. Eicosapentaenoic acid treatment increased TNFα secretion in subcutaneous stromovascular cells at 25, 50, and 100 μM (P = 0.002, P = 0.001, and P = 0.015, respectively) and in visceral stromovascular cells at 50 μM (P < 0.001). No significant effect on medium adiponectin concentration was observed following troglitazone treatment (P = 0.4) or fatty acids treatments at 25 (P = 0.2), 50 (P = 0.8), or 100 (P = 0.7) μM. Body condition score did not have significant effects on medium concentrations of adiponectin (P = 0.4), IL6 (P = 0.1), or TNFα (P = 0.8).

CONCLUSIONS

This study demonstrated higher basal secretion of IL6 from visceral compared to subcutaneous adipose tissue, a stimulatory effect of arachidonic acid on secretion of IL6 and a stimulatory effect of eicosapentaenoic acid on TNFα from feline adipose tissue.

摘要

背景

猫的肥胖与脂肪因子的改变有关,包括脂联素、白细胞介素-6(IL6)和肿瘤坏死因子-α(TNFα)。ω-3 多不饱和脂肪酸对肥胖相关疾病有多种有益作用,因此可能缓解这些改变。本研究旨在确定体况、脂肪库、曲格列酮和不同脂肪酸对健康猫脂肪组织分泌脂联素、IL6 和 TNFα 的影响。从 18 只健康的未去势雌性猫中采集皮下和内脏脂肪组织样本,并确定体况评分(范围 3-7/9)。在成熟脂肪细胞培养物中测量脂联素浓度,并在经对照培养基、10 μM 曲格列酮、25、50 或 100 μM 二十碳五烯酸、花生四烯酸或棕榈酸处理后,在基质血管细胞培养物中测量白细胞介素 6 和 TNFα 浓度。

结果

内脏来源的基质血管细胞分泌的 IL6 浓度高于相应的皮下来源细胞(P=0.003)。25、50 和 100 μM 花生四烯酸处理分别增加了皮下(P=0.045,P=0.002,P<0.001)和内脏(P=0.034,P=0.001,P<0.001)基质血管细胞中 IL6 的分泌。25、50 和 100 μM 二十碳五烯酸处理分别增加了皮下基质血管细胞中 TNFα 的分泌(P=0.002,P=0.001,P=0.015)和内脏基质血管细胞中 TNFα 的分泌(P<0.001)。曲格列酮处理(P=0.4)或 25(P=0.2)、50(P=0.8)或 100(P=0.7)μM 脂肪酸处理对培养基中脂联素浓度均无显著影响。体况评分对培养基中脂联素(P=0.4)、IL6(P=0.1)或 TNFα(P=0.8)的浓度无显著影响。

结论

本研究表明,与皮下脂肪组织相比,内脏脂肪组织中 IL6 的基础分泌水平更高,花生四烯酸对 IL6 的分泌有刺激作用,二十碳五烯酸对猫脂肪组织中 TNFα 的分泌有刺激作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a89e/6731618/3506cdbff299/12917_2019_2065_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a89e/6731618/85ebd90d88bc/12917_2019_2065_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a89e/6731618/171acbdcd264/12917_2019_2065_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a89e/6731618/3506cdbff299/12917_2019_2065_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a89e/6731618/85ebd90d88bc/12917_2019_2065_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a89e/6731618/171acbdcd264/12917_2019_2065_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a89e/6731618/3506cdbff299/12917_2019_2065_Fig3_HTML.jpg

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