Probiotic mixture improves fatty liver disease by virtue of its action on lipid profiles, leptin, and inflammatory biomarkers

Abstract

Background: A high fat diet has an essential role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). This condition is characterized by hepatic fat accumulation (steatosis) and is associated with obesity, diabetes, and fibrosis or cirrhosis of the liver. Probiotics may be useful in the treatment of steatosis. This study examined the effects of an ingested probiotic formulation on the lipid profiles, liver functions, leptin levels, and inflammatory marker levels of rats with NAFLD that had been induced via high fat and sucrose diet (HFSD).

Methods: Young male albino rats were randomly divided into three groups: a control group that was fed a standard diet; a second group that was fed a HFSD; and a third group that was given both a HFSD and ingestible probiotic mixtures. The groups were fed these diets for 16 weeks, and were then examined.

Results: HFSD-only rats showed hypertriglyceridemia, hypercholesterolemia, and elevated low density lipoprotein (LDL) levels, and their serum alanine transaminase (ALT) and bilirubin levels were significantly higher than those of the control group. Compared to rats on the standard diet, HFSD-only rats showed higher levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), increased serum leptin levels, and increased resistin hormone levels in the adipose tissues. In the third group, the inclusion of the probiotic mixture seemed to ameliorate the effects of the HFSD diet. The NAFD + probiotics group showed improved lipid profiles, better leptin and resistin levels, and better TNF-α and IL-6 levels than the NAFD-only group. They also showed no signs of NAFLD.

Conclusions: The probiotic mixture showed promise as a treatment for NAFLD pathogenesis, and may improve HFSD-induced steatosis through its effects on leptin, resistin, inflammatory biomarkers, and hepatic function markers. We also established that gut microbiota-mediated regulation of lipid profiles was dependent on dietary lipids and carbohydrates.

Keywords: HFSD; Inflammation; Leptin; Lipid profile; NAFLD biomarkers; Probiotics.

Fig. 1

Mechanisms of HFSD-induced gut microbial alterations (via ROS, IL-6, TNF-α, SCFA, and LPS) and metabolic dysfunctions, and subsequent improvements mediated by probiotics

Fig. 2

Histopathological results in the different groups of the experiment: a & b Microscopic analysis of the liver (H&E stain, magnification 20×) showed multiple fat globules between and within hepatocytes, with concomitant degenerative changes in hepatic cells within the HFSD group. Also NAFLD group revealed, macrovesicular steatosis (bold line arrow): major fat droplets are existing in hepatocytes; microvesicular steatosis (dotted arrow): minor fat droplets are present in hepatocytes. c Liver focal periportal inflammation (magnification 40×) and aggregation (cluster) of inflammatory cells (within dotted circles) in NAFLD group. d Typical histological structure of normal hepatic cells, with no inflammatory cells in the perivenular area, within the normal group. e View of hepatic cells with normal shape and lower fat globules in the HFSD and probiotic mixture groups