Sustained feeding of a diet high in fat resulted in a decline in the liver's insulin-degrading enzyme levels in association with the induction of oxidative and endoplasmic reticulum stress in adult male rats: Evaluation of 4-phenylbutyric acid

Autor: Fateme Binayi, Behnam Saeidi, Fatemeh Farahani, Mina Sadat Izadi, Farzaneh Eskandari, Fariba Azarkish, Mohammad Sahraei, Rasoul Ghasemi, Fariba Khodagholi, Homeira Zardooz
Jazyk: angličtina
Rok vydání: 2024
Předmět:
Zdroj: Heliyon, Vol 10, Iss 12, Pp e32804- (2024)
Druh dokumentu: article
ISSN: 2405-8440
DOI: 10.1016/j.heliyon.2024.e32804
Popis: The current study explored the impact of high fat diet (HFD) on hepatic oxidative and endoplasmic reticulum (ER) stress and its insulin degrading enzyme (IDE) content with the injection of 4-phenyl butyric acid (4-PBA) in adult male rats.Following the weaning period, male offspring were distributed among six distinct groups. The corresponding diet was used for 20 weeks, subsequently 4-PBA was administered for three consecutive days. Plasma glucose and insulin levels, HOMA-β (homeostasis model assessment of β-cell), hepatic ER and oxidative stress biomarkers and IDE protein content were assessed.Long-term ingestion of HFD (31 % cow butter) induced oxidative and ER stress in the liver tissue. Accordingly, a rise in the malondialdehyde (MDA) content and catalase enzyme activity and a decrease in the glutathione (GSH) content were detected within the liver of the HFD and HFD + DMSO groups. Consumption of this diet elevated the liver expression of binding immunoglobulin protein (BIP) and C/enhancer-binding protein homologous protein (CHOP) levels while reduced its IDE content. The HOMA-β decreased significantly. The injection of the 4-PBA moderated all the induced changes.Findings from this study indicated that prolonged HFD consumption led to a reduction in plasma insulin levels, likely attributed to pancreatic β cell malfunction, as evidenced by a decline in the HOMA-β index. Also, the HFD appears to have triggered oxidative and ER stress in the liver, along with a decrease in its IDE content.
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