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Peroxisome Proliferator Activator α Agonist Clofibrate Induces Pexophagy in Coconut Oil-Based High-Fat Diet-Fed Rats

Peroxisome Proliferator Activator α Agonist Clofibrate Induces Pexophagy in Coconut Oil-Based High-Fat Diet-Fed Rats


Introduction

In the realm of nutritional science and metabolic research, understanding the mechanisms of cellular processes such as pexophagy is crucial. Pexophagy, the selective degradation of peroxisomes through autophagy, plays a vital role in maintaining cellular homeostasis. This blog explores the latest findings on how clofibrate, a well-known PPARα agonist, influences pexophagy in rats subjected to a high-fat diet (HFD) based on coconut oil. These insights potentially pave the way for novel therapeutic strategies targeting metabolic disorders.

Methodology

The study meticulously divided rats into distinct groups to evaluate the impact of a coconut oil-based HFD. One group received clofibrate, allowing for a comparative analysis of pexophagy markers between treated and untreated subjects. The selected markers, including NBR1, p62, and LAMP2, provided a comprehensive assessment of the pexophagy process.



Effects of High-Fat Diet and Clofibrate

Feeding rats a high-fat diet resulted in noticeable hepatic steatosis, characterized by an accumulation of fat in liver cells. This condition served as a foundation for assessing clofibrate's efficacy. When administered clofibrate, a remarkable alteration in the expression of pexophagy-related genes was observed, suggesting a potent induction of peroxisome proliferation.

Role of Pexophagy Markers

The expression levels of pexophagy markers such as NBR1 and p62 were significantly modulated following clofibrate treatment, indicating enhanced degradation of peroxisomes. Additionally, LAMP2, a crucial lysosomal membrane protein, showed increased activity, further corroborating the upregulation of pexophagic pathways.

Implications on Mammalian Pexophagy

Ultrastructural observations provided deeper insights into clofibrate's impact on cellular architecture, revealing increased prevalence of autophagic vesicles engulfing peroxisomes. Such findings suggest that PPARα agonists like clofibrate could regulate peroxisome turnover, offering potential applications in addressing metabolic conditions linked to impaired peroxisome function.

Conclusion

The research underscores the pivotal role clofibrate plays in modulating pexophagy within the context of a high-fat diet. By elucidating the molecular pathways influenced by PPARα agonists, this study lays the groundwork for developing targeted therapeutic approaches for metabolic diseases. Clofibrate's ability to stimulate peroxisome turnover presents promising avenues for future exploration in metabolic and cellular health research.

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