Multisystemic effects of the herbal formulation cholesterol defence in high-fat diet-induced dyslipidaemic rats

Abstract

Aim: This study evaluated the multisystemic effects of the herbal formulation cholesterol defence, in high-fat diet-induced dyslipidaemic rats. Methodology: A total of 35 male albino rats weighing between 160 to 180g were used for the study. The rats were weighed and grouped into 5 groups of 7 rats each. They were fed high fat diet for 6 weeks. 2 weeks before commencement of treatments and then 4 weeks alongside the treatments. Group 1 was negative control and group 2 positive control. Group 3 was administered metformin, group 4 administered CholesDefence, and group 5 administered a combination of metformin and cholesDefence. Fasting plasma glucose (FPG) was determined using Glucose oxidase method. Fasting plasma insulin (FPI) and C-reactive protein (CRP) levels were quantitatively determined by a rat-specific sandwich-enzyme linked immunosorbent assay (ELISA) method. Insulin resistance (IR) was determined using the homeostatic model assessment for insulin resistance (HOMA-IR) method. Total Cholesterol (TC), Triglyceride (TG) and High Density Lipoprotein Cholesterol (HDL-C) were determined by enzymatic methods. Low Density Lipoprotein Cholesterol (LDL-C) was calculated from the Friedewald’s equation. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined using the Reitman-Frankel method. Alkaline phosphatase (ALP) was determined using the Colorimetric endpoint method. Phytochemical analysis was done on the herbal tablet using classical methods. Results: The results revealed the presence of flavonoids, cardiac glycosides, saponins, tannins and terpenoids in the herbal tablet. FPG, insulin and HOMA-IR values were significantly higher in the positive control group, compared to the negative control and treatment groups. Metformin and CholesDefence significantly reduced FPG levels. Metformin significantly reduced insulin and HOMA-IR values, which were significantly higher in the group 3 administered CholesDefence, compared to the negative control. ALT, AST and ALP were significantly higher in the positive control, but was significantly reduced to normal levels by the treatments. CRP was significantly reduced by metformin, but not by CholesDefence. Metformin and the combination therapy significantly improved TC, TG, HDL-C, but had no impact on LDL-C levels. CholesDefence had no effect on TC, HDL-C, and LDL-C levels, but significantly reduced TG levels. Conclusion: Dyslipidaemia induced by high-fat diet elevated glucose and insulin levels, causing significant insulin resistance. It impacted the liver, leading to elevated liver enzymes and systemic inflammation. CholesDefence and its combination therapy was not as effective as metformin in improving the dyslipidaemia, hyperinsulinaemia, insulin resistance and the resulting inflammation. It however had equipotent anti-hyperglycaemic and hepatoprotective effects compared to metformin.