Maintaining intestinal structural integrity is a potential protective mechanism against inflammation in goose fatty liver.
Maintaining intestinal structural integrity is a potential protective mechanism against inflammation in goose fatty liver.
复制标题
维持肠道结构完整性是鹅脂肪肝炎症的潜在保护机制
DOI：
10.1016/j.psj.2020.08.052
复制
发表时间：
2020-11
期刊：
影响因子：
4.4
通讯作者：
Gong D
中科院分区：
文献类型：
--
作者：
Gu W;Wen K;Yan C;Li S;Liu T;Xu C;Liu L;Zhao M;Zhang J;Geng T;Gong D
过量饲养引起鹅肝严重脂肪变性，但不引起炎症，提示存在保护性成分。先前的研究表明，一些肠道微生物及其代谢产物损害肠道结构完整性和功能，从而在人类和小鼠非酒精性脂肪肝疾病的发展中引起炎症。因此，本研究推测鹅在过度饲养过程中肠道结构的完整性得以维持，这可能为鹅脂肪肝提供了一种抗炎症的保护机制。为了验证这一假设，选择48只70日龄健康朗德鹅公鹅，分别进行过饲（过饲组）和正常饲养（对照组）试验。血液和肠道（空肠，回肠和盲肠）样品收获的第12和第24天的过度喂养。试验结果表明，经过24 d的过量饲养，成功诱导出鹅脂肪肝。苏木精-伊红染色显示，2组小肠绒毛和隐窝排列整齐，肠结构完整，无病理症状。酶联免疫吸附试验和定量PCR分析表明，紧密连接和炎症相关基因的表达以及血浆脂多糖浓度组间无显着差异。与对照组相比，高饲组鹅回肠肥大，盲肠萎缩，这可能是由于鞘脂代谢的改变。凋亡通路的激活可能有助于盲肠避免坏死诱导的炎症。总之，健康完整的肠道为鹅脂肪肝提供了一层炎症保护。鞘脂代谢可能参与回肠和盲肠对过度摄食的适应。回肠的肥大使其成为鹅脂肪肝发生的重要因素。盲肠的萎缩和功能下降可能是由过度摄食诱导的细胞凋亡引起的。
Overfeeding causes severe steatosis but not inflammation in goose liver, suggesting existence of protective components. Previous studies have shown that some intestinal microbes and their metabolites damage intestinal structural integrity and function, thus causing inflammation in the development of human and mouse nonalcoholic fatty liver disease. Therefore, this study hypothesizes that intestinal structural integrity of goose is maintained during overfeeding, which may provide goose fatty liver a protective mechanism against inflammation. To test this hypothesis, 48 seventy-day-old healthy Landes male geese were overfed (as overfeeding group) or normally fed (as control group). Blood and intestine (jejunum, ileum, and cecum) samples were harvested on the 12th and 24th d of overfeeding. Data showed that goose fatty liver was successfully induced by 24 d of overfeeding. Hematoxylin-eosin staining analysis indicated that the arrangement of villi and crypts in the intestine was orderly, and the intestinal structure was intact with no pathological symptoms in the 2 groups. Enzyme-linked immunosorbent assay and quantitative PCR analysis indicated no significant differences in the expression of tight junction and inflammation-related genes as well as plasma lipopolysaccharide concentration between the groups. Ileal hypertrophy and cecal atrophy were observed in the overfed vs. control geese, probably because of change of sphingolipid metabolism. Activation of apoptotic pathway may help cecum avoid necrosis-induced inflammation. In conclusion, healthy and intact intestine provides a layer of protection for goose fatty liver against inflammation. Sphingolipid metabolism may be involved in the adaptation of ileum and cecum to overfeeding. The hypertrophy of ileum makes it an important contributor to the development of goose fatty liver. The atrophy and decline in the function of cecum may be caused by apoptosis induced by overfeeding.
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影响因子：
4.8
作者：
Fekry, Baharan;Jeffries, Kristen A.;Krupenko, Natalia I.
通讯作者：
Krupenko, Natalia I.
影响因子：
2.8
作者：
Kirpich IA;Marsano LS;McClain CJ
通讯作者：
McClain CJ
影响因子：
4.2
作者：
Hermier, D
通讯作者：
Hermier, D
DOI：
10.1016/0005-2760(94)90143-0
发表时间：
1994-02-10
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM
影响因子：
--
作者：
HERMIER, D;ROUSSELOTPAILLEY, D;SELLIER, N
通讯作者：
SELLIER, N
影响因子：
4.4
作者：
Hermier, D;Salichon, MR;Peresson, R
通讯作者：
Peresson, R