Key result
Probiotic supplementation with Lactobacillus acidophilus significantly reduced hepatic steatosis and restored lipolytic gene expression, liver functions, and antioxidants to normal levels in rabbits with HCD-induced NAFLD.
Why the study?
Does probiotic Lactobacillus acidophilus improve lipolytic gene expression, liver function, lipid profile, and antioxidant enzymes in rabbits with high-cholesterol diet-induced NAFLD?
Does probiotic Lactobacillus acidophilus improve lipolytic gene expression, liver function, lipid profile, and antioxidant enzymes in rabbits with high-cholesterol diet-induced NAFLD?
Absolute Event Rate: 20% vs 50%
p-value: p=≤0.05
Probiotic Lactobacillus acidophilus supplementation may protect against high-cholesterol diet-induced NAFLD by restoring lipolytic gene expression, liver functions, and antioxidant levels in a rabbit model.
L. acidophilus ameliorated HCD-induced NAFLD in rabbits; hypothesis-generating for human trials.
Nonalcoholic fatty liver disease (NAFLD) is a condition that affects about 24% of people worldwide. Increased liver fat, inflammation, and, in the most severe cases, cell death are all characteristics of NAFLD. However, NAFLD pathogenesis and therapy are still not clear enough. Thus, this study aimed to determine the effect of a high-cholesterol diet (HCD) inducing NAFLD on lipolytic gene expression, liver function, lipid profile, and antioxidant enzymes in rabbits and the modulatory effects of probiotic Lactobacillus acidophilus (L. acidophilus) on it. A total of 45 male New Zealand white rabbits, eight weeks old, were randomly divided into three groups of three replicates (5 rabbits/replicate). Rabbits in group I were given a basal diet; rabbits in group II were given a high-cholesterol diet that caused NAFLD; and rabbits in group III were given a high-cholesterol diet as well as probiotics in water for 8 weeks. The results showed that a high-cholesterol diet caused hepatic vacuolation and upregulated the genes for lipoprotein lipase (LPL), hepatic lipase (HL), and cholesteryl ester transfer protein (CETP). Downregulated low-density lipoprotein receptor (LDLr) gene, increased liver enzymes [alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH)], cholesterol, triglycerides (TG), low-density lipoprotein (LDL), glucose, and total bilirubin. On the other hand, it decreased high-density lipoprotein (HDL), total protein, albumin, and liver antioxidants [glutathione peroxidase (GPx), catalase (CAT), reduced glutathione (GSH), and superoxide dismutase (SOD)]. Supplementing with probiotics helped to return all parameters to normal levels. In conclusion, probiotic supplementation, especially L. acidophilus, protected against NAFLD, and restored lipolytic gene expression, liver functions, and antioxidants to normal levels.
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Aziz et al. (2023) studied Nonalcoholic fatty liver disease (NAFLD) (n=45). Probiotic Lactobacillus acidophilus vs. High-cholesterol diet (HCD) without probiotics was evaluated on Hepatic steatosis (percentage of fat within hepatocytes) (p=≤0.05). Probiotic supplementation with Lactobacillus acidophilus significantly reduced hepatic steatosis and restored lipolytic gene expression, liver functions, and antioxidants to normal levels in rabbits with HCD-induced NAFLD.
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