Abstract
Hepato-renal dysfunctions associated with hyperlipidemia necessitates a continuous search for natural remedies. This study thus evaluated the effect of dietary chitosan on diet-induced hyperlipidemia in rats. A total of 30 male Wistar rats (90 ± 10) g were randomly allotted into six (6) groups (n = 5): Normal diet, High-fat diet (HFD), and Normal diet + 5% chitosan. The three other groups received HFD, supplemented with 1%, 3%, and 5% of chitosan. The feeding lasted for 6 weeks, after which the rats were sacrificed. The liver and kidneys were harvested for analyses. Hepatic alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) activity, and renal biomarkers (ALT, AST, urea, and creatinine) were assayed spectrophotometrically. Additionally, expression of hepatic and renal CD43 and p53 was estimated immunohistochemically. The HFD group had elevated bodyweight compared to normal which was reversed in the chitosan-supplemented groups. Hyperlipidemia caused a significant (p < 0.05) decrease in the hepatic (AST, ALT, and ALP) and renal (AST and ALT) activities, while renal urea and creatinine increased. Furthermore, the HFD group showed an elevated level of hepatic and renal CD43 while p53 expression decreased. However, groups supplemented with chitosan showed improved hepatic and renal biomarkers, as well as corrected the aberrations in the expressions of p53 and CD43. Conclusively, dietary chitosan inclusion in the diet (between 3% and 5%) could effectively improve kidney and liver functionality via abatement of inflammatory responses.
Highlights
Group 1: Control animals fed with Normal diet, group 2: High-fat diet (HFD) control received HFD only group 3: Normal diet supplemented with 5% chitosan
This study provides a possible mechanism underlining the protective in vivo effect of crab chitosan on the liver and kidneys of hyperlipidemic rats
The role of hyperlipidemia in the induction of oxidative stress has been linked to excessive production of ROS [3]
Summary
Hyperlipidemia (HLP) is a family of disorders that are characterized by abnormally high levels of lipids in the blood. It is the contributory factor to the induction and development of atherosclerosis and cardiovascular diseases (CVD) [1,2]. The ever-increasing prevalence of HLP might be responsible for the continuous upsurge in the demographic data of obesity and attendant organ dysfunction worldwide [3]. Chronic renal failure parallels the occurrence of premature atherosclerosis, and cardiovascular comorbidities and mortalities [4]. Clinical evidence suggests that atherosclerosis due to HLP predates renal failure [4]. HLP contributes to the onset of fatty liver disease which is Pathophysiology 2021, 28, 224–237.
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