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高脂肪饮食与 I-FABP 相关,作为代谢变化驱动的 Wistar 大鼠肠道屏障功能障碍的生物标志物。

Association of a high-fat diet with I-FABP as a biomarker of intestinal barrier dysfunction driven by metabolic changes in Wistar rats.

机构信息

Department of Physiology, The Islamia University of Bahawalpur, Bahawalpur, 63100, Pakistan.

Institute of Physiology and Pharmacology, University of Agriculture, Faisalabad, 38040, Pakistan.

出版信息

Lipids Health Dis. 2023 May 27;22(1):68. doi: 10.1186/s12944-023-01837-9.

Abstract

BACKGROUND

The epithelial lining of the gut expresses intestinal fatty-acid binding proteins (I-FABPs), which increase in circulation and in plasma concentration during intestinal damage. From the perspective of obesity, the consumption of a diet rich in fat causes a disruption in the integrity of the gut barrier and an increase in its permeability.

HYPOTHESIS

There is an association between the expression of I-FABP in the gut and various metabolic changes induced by a high-fat (HF) diet.

METHODS

Wistar albino rats (n = 90) were divided into three groups (n = 30 per group), viz. One control and two HF diet groups (15 and 30%, respectively) were maintained for 6 weeks. Blood samples were thus collected to evaluate the lipid profile, blood glucose level and other biochemical tests. Tissue sampling was conducted to perform fat staining and immunohistochemistry.

RESULTS

HF diet-fed rats developed adiposity, insulin resistance, leptin resistance, dyslipidemia, and increased expression of I-FABP in the small intestine compared to the control group. Increased I-FABP expression in the ileal region of the intestine is correlated significantly with higher fat contents in the diet, indicating that higher I-FABP expression occurs due to increased demand of enterocytes to transport lipids, leading to metabolic alterations.

CONCLUSION

In summary, there is an association between the expression of I-FABP and HF diet-induced metabolic alterations, indicating that I-FABP can be used as a biomarker for intestinal barrier dysfunction.

摘要

背景

肠道的上皮衬里表达肠道脂肪酸结合蛋白(I-FABP),在肠道损伤期间,其在循环和血浆浓度中增加。从肥胖的角度来看,摄入高脂肪饮食会破坏肠道屏障的完整性并增加其通透性。

假说

肠道中 I-FABP 的表达与高脂肪(HF)饮食引起的各种代谢变化之间存在关联。

方法

将 Wistar 白化大鼠(n = 90)分为三组(每组 n = 30),即维持 1 个对照组和 2 个 HF 饮食组(分别为 15%和 30%)6 周。因此收集血样以评估血脂谱、血糖水平和其他生化测试。进行组织取样以进行脂肪染色和免疫组织化学。

结果

与对照组相比,HF 饮食喂养的大鼠表现出肥胖、胰岛素抵抗、瘦素抵抗、血脂异常和小肠中 I-FABP 的表达增加。肠回肠区域中 I-FABP 的表达增加与饮食中更高的脂肪含量显著相关,表明更高的 I-FABP 表达是由于肠细胞对运输脂质的需求增加所致,导致代谢改变。

结论

总之,I-FABP 的表达与 HF 饮食诱导的代谢变化之间存在关联,表明 I-FABP 可用作肠道屏障功能障碍的生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c737/10223920/1e1f520c105c/12944_2023_1837_Fig1_HTML.jpg

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