Effects of Selenium-Enriched Probiotics on Lipid Metabolism, Antioxidative Status, Histopathological Lesions, and Related Gene Expression in Mice Fed a High-Fat Diet

Abstract

A total of 80 female albino mice were randomly allotted into five groups (n = 16) as follows: (A) normal control, (B) high-fat diet (HFD),; (C) HFD + probiotics (P), (D) HFD + sodium selenite (SS), and (E) HFD + selenium-enriched probiotics (SP). The selenium content of diets in groups A, B, C, D, and E was 0.05, 0.05, 0.05, 0.3, and 0.3 μg/g, respectively. The amount of probiotics contained in groups C and E was similar (Lactobacillus acidophilus 0.25 × 10(11)/mL and Saccharomyces cerevisiae 0.25 × 10(9)/mL colony-forming units (CFU)). The high-fat diet was composed of 15 % lard, 1 % cholesterol, 0.3 % cholic acid, and 83.7 % basal diet. At the end of the 4-week experiment, blood and liver samples were collected for the measurements of lipid metabolism, antioxidative status, histopathological lesions, and related gene expressions. The result shows that HFD significantly increased the body weights and liver damages compared to control, while P, SS, or SP supplementation attenuated the body weights and liver damages in mice. P, SS, or SP supplementation also significantly reversed the changes of alanine aminotransferase (AST), aspartate aminotransferase (ALT), total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), total protein (TP), high-density lipoprotein (HDL), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalasa (CAT), and malondialdehyde (MDA) levels induced by HFD. Generally, adding P, SS, or SP up-regulated mRNA expression of carnitine palmitoyltransferase-I (CPT1), carnitine palmitoyltransferase II (CPT2), acetyl-CoA acetyltransferase II (ACAT2), acyl-coenzyme A oxidase (ACOX2), and peroxisome proliferator-activated receptor alpha (PPARα) and down-regulated mRNA expression of fatty acid synthase (FAS), lipoprotein lipase (LPL), peroxisome proliferator-activated receptor gamma (PPARγ), and sterol regulatory element-binding protein-1 (SREBP1) involved in lipid metabolism. Among the group, adding SP has a maximum effect in improving lipid metabolism, antioxidative status, histopathological lesions, and related gene expression in mice fed a HFD.

Selenium and Selenoproteins in Adipose Tissue Physiology and Obesity

“…Particularly, sodium selenate in the supraphysiological dose of 0.72 mg/kg/day (8 weeks) significantly reduced adiposity in HFD-fed mice through down-regulation of PPARγ signaling and a concomitant reduction in diacylglycerol O-acyltransferase (DGAT) 2 and leptin expression, as well as improvement of insulin sensitivity [113]. In turn, physiological intake of sodium selenite (0.3 mg/kg diet for 4 weeks) in HFD-fed rats potentiated the effects of probiotic treatment on down-regulation of fatty acid synthase (FAS), lipoprotein lipase (LPL), PPARγ, and sterol regulatory element-binding protein (SREBP) 1, whereas expression of genes involved in lipid catabolism was increased in response to treatment [114]. Se-enriched Enterobacter exopolysaccharides significantly reduced adipose tissue inflammation by down-regulating IL6 and TNF expression both in vivo (HFD-fed diabetic KKAy mice) and in vitro (3T3-L1 adipocytes) through an AMPK/SirT1 pathway [115].…”

Towards Individualized Use of Probiotics and Prebiotics for Metabolic Syndrome and Associated Diseases Treatment: Does Pathophysiology-Based Approach Work and Can Anticipated Evidence Be Completed?

“…rhamnosus CCFM1107 decreased the level of cholesterol in the liver and serum of mice with alcoholic affection of liver [167]. After administration L. acidophilus to obese mice with damaged liver after cholesterol-enriched diet the reduction of cholesterol level both in serum and liver was observed [168]; and L. plantarum CAI6 and L. plantarum SC4 had a protective effect in models of CVD in hyperlipidemic mice by reducing the level of total and low-density lipoprotein cholesterol [169].…”

Trace Elements, PPARs, and Metabolic Syndrome

“…In the livers of HFD-induced NAFLD rats, selenium supplementation recovered dyslipidemia and improved liver function and hepatic steatosis by activating Ppar-α expression and subsequently elevating fatty acid oxidation [126]. Selenium-enriched probiotics have been confirmed to have a great effect in improving lipid metabolism, antioxidative status, and histopathological lesions in HFD-fed mice.…”

“…Selenium-enriched probiotics have been confirmed to have a great effect in improving lipid metabolism, antioxidative status, and histopathological lesions in HFD-fed mice. Among genes whose expression was altered in the liver, Ppar-α was upregulated [126]. IR plays a pivotal role in the pathogenesis of NALFD in the setting of IR syndrome or MetS [197].…”

“…An animal experiment in chicken pancreas illustrated the antagonistic effect of sodium selenite on cadmium-induced apoptosis, which involved the recovering of the impaired PPAR-γ/PI3K/Akt pathway by cadmium [121]. Besides, selenium-enriched probiotics (Lactobacillus acidophilus and Saccharomyces cerevisiae) have been reported to repress the gene expression of Ppar-γ, thereby improving lipid metabolism, in HFD-fed mice [126]. Conflicting results have emerged when comparing PPAR-γ modulation by selenium in various studies, whose reason may be that various sources of selenium (selenite and selenium-enriched probiotics) and diverse target organs/tissues (heart, liver, pancreas, and immune system) were considered in these studies.…”