Abstract

The existing study aims to explore the different aspects of paracetamol (PCM) and high-fat high fructose diet (HFHF) produced non-diabetic and diabetic liver damage with references to multiple biochemical markers in the context of pharmacological therapies with respect to their adipogenic inhibition and hepatoprotective outcomes. Pterostilbene, Arbutin, and Purpurin were used for managing the HFHF and PCM-induced liver-related complications in rodents 28-week and 8-day models, respectively. The biochemical, oxidative stress parameters were measured for the assessment of elected interventions. For the sake of scientific credibility, the expression of fatty acid synthase, which is individualistically linked to diabetes-related fatty liver diseases, was assessed using real-time polymerase chain reaction. HFHF diet ingestion for 28 weeks noticeably (p < 0.05) caused a significant expansion of glucose levels in comparison to normal diet-treated investigational rodents, while the reverse was observed in intervention-treated sets in comparison to the HFHF-treated groups. The situation was upturned in the case of PCM-treated rodents as there was insignificant augmentation in the point of glucose which clearly depicted the distinction between non-diabetic and diabetic liver injury models. It is hypothesized that dropping free fatty acid levels through FAS inhibition will recover insulin resistance and assuage non-diabetic and diabetic liver injury models.

Key words: Diabetic liver injury; High fat high fructose model; Antiadipogenic effect, Health, Mortality, Pharmacy health.