Inimical impact of high-fat diet on expression of heme oxygenase-1, trace metals content, and associated intestinal histopathology

Author:

Sheikh Nadeem1ORCID,Shakeel Shakira1,Akhtar Tasleem2ORCID,Khawar Muhammad Babar3

Affiliation:

1. Institute of Zoology, University of the Punjab Cell and Molecular Biology Lab, , Q-A Campus, Lahore 54590 , Pakistan

2. University of Health Sciences Lahore Department of Pharmacology, , 54600 , Pakistan

3. University of Narowal Applied Molecular Biology and Biomedicine Lab, Department of Zoology, , Narowal 51600 , Pakistan

Abstract

AbstractA high-fat diet (HFD) is one of the most prominent causative factors for obesity and metabolic inflammation. The effects of HFD overconsumption on intestinal histology, expression of haem oxygenase-1 (HO-1), and transferrin receptor-2 (TFR2) remain elusive. The present study was conducted to analyze the effect of HFD on these parameters. To develop the HFD-induced obese model, rat colonies were divided into 3 groups; the control group was reared on normal rat chow, whereas groups I and II were given HFD for 16 weeks. Hematoxylin and eosin (H & E) staining revealed marked epithelial changes, inflammatory cell infiltrates, and destruction of mucosal architecture in both experimental groups as compared to the control group. Sudan Black B staining showed a high triglyceride deposition in the intestinal mucosa of animals fed on HFD. Atomic absorption spectroscopy revealed a decrease in tissue copper (Cu) and selenium (Se) concentration in both HFD experimental groups. Whereas the cobalt (Co) and manganese (Mn) levels were comparable to controls. The mRNA expression levels of HO-1 and TFR2 were found to be significantly upregulated in HFD groups compared to the control group. Hence, HFD consumption leads to histopathological changes and altered gene expression in the rodent intestine. So, one should remove HFD from daily meals to avoid related metabolic complications.

Funder

Higher Education Commission, Pakistan

Publisher

Oxford University Press (OUP)

Subject

Health, Toxicology and Mutagenesis,Toxicology

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